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32 Hemoptysis inChildren: ENT-Related Etiologies
419
If a chest x-ray reveals an atypical mass, a bronchoscopic evaluation can be performed as an outpatient. To rule out neoplasm, outpatient beroptic bronchoscopy
may also be necessary for patients with a normal chest radiograph and risk factors
for lung cancer or recurrent hemoptysis. A high-resolution CT scan is warranted
when sputum and bronchoscopy fail to reveal pathology despite a clinical suspicion
of malignancy. A high-resolution CT scan is also justied when a chest X-ray indicates peripheral or other parenchymal illness [2].
32.2.2 Massive Hemoptysis
Massive hemoptysis fatality rates vary according to the severity and cause of the
bleeding. Massive hemoptysis, dened as more than 1000mL of blood lost in 24h,
is associated with an 80% fatality rate [7]. These individuals need immediate attention and a pulmonologist’s opinion. Hemostasis of catastrophic or life-threatening
proportions requires close medical attention. Because asphyxiation, not bleeding to
death, is the leading cause of mortality, it is crucial to keep the airway open.
Resuscitation measures such as providing more oxygen and uids are essential.
Since immediate surgical intervention may be required [2], getting help from a cardiothoracic surgeon is recommended.
32.3 Differential Diagnosis ofHemoptysis
Source other than the lower respiratory tract
• Upper airway (nasopharyngeal) bleeding
• Gastrointestinal bleeding [2]
Tracheobronchial source
• Neoplasm (bronchogenic carcinoma, endobronchial metastatic tumor, Kaposi’s sarcoma,
bronchial carcinoid)
• Bronchitis (acute or chronic)
• Bronchiectasis
• Broncholithiasis
• Airway trauma
• Foreign body [2]
Pulmonary parenchymal source
• Lung abscess
• Pneumonia
• Tuberculosis
• Mycetoma (“fungus ball”)
• Goodpasture’s syndrome
• Idiopathic pulmonary hemosiderosis
• Wegener’s granulomatosis
• Lupus pneumonitis
• Long contusion [2]
Primary vascular source
420
• Arteriovenous malformation.
• Pulmonary embolism.
• Elevated pulmonary venous pressure (especially mitral stenosis).
• Pulmonary artery rupture secondary to balloon-tip pulmonary artery catheter
manipulation [2]
Miscellaneous and rare causes
• Pulmonary endometriosis
• Systemic coagulopathy or use of anticoagulants or thrombolytic agents [2]
M. O. Korkmaz et al.
32.4 Diagnostic Evaluation
Critical blood tests (complete blood count and coagulation prole) and a chest
radiograph are the initial stages in the assessment for most children presenting with
hemoptysis. The results of the history and physical are used to make further diagnoses [3].
32.4.1 History
If the etiology of the hemoptysis is unclear, a complete medical history should be
obtained when the patient has stabilized. The following six ndings may help in
determining the etiology of hemoptysis:
32.4.1.1 Infection Warning Signs
• Tracheobronchitis, pneumonia, and bronchiectasis are frequently diagnosed
when blood is present in mucopurulent sputum.
• Pneumonia is suspected when there is a fever, chills, and purulent, bloody sputum.
• Anaerobic lung abscess is suspected when sputum has a putrid odor.
32.4.1.2 Choking
Even if the choking event happened days or weeks before the hemoptysis, a foreign
body in the trachea or airway should be considered.
32.4.1.3 Exposures
These risk factors have been linked to hemoptysis:
• Illegal narcotics, especially cocaine, and similar inhalants.
• Nicotine or cannabis smoking can cause pneumonia-like lung symptoms [8].
• Phenytoin, retinoic acid, amiodarone, propylthiouracil, and penicillamine are all
linked to an increased risk of alveolar hemorrhage.
• Medications that lower platelet counts or otherwise interfere with normal platelet
function.
• Breathing in nitrogen dioxide fumes from broken ice resurfacing and ventilation
equipment at a hockey rink.
32 Hemoptysis inChildren: ENT-Related Etiologies
421
• Travel and exposure—Find out whether they have ever visited or lived where TB
is common or have had any recent contact with homeless people, inmates, institutions, or migrant workers. Inquire about any trips to regions known to harbor
endemic mycoses or comparable exposures (such as participation in archaeological digs or spelunking) [3].
32.4.1.4 Underlying Medical Problems
Symptoms or diagnoses that point to a more serious medical issue are considered
“underlying medical problems” [3].
• Trauma.
• Easy bruising, menorrhagia, or a history of bleeding that suggests a problem
(such as von Willebrand disease).
• Degenerative lung or heart disease.
• Bronchiectasis is sometimes linked to systemic symptoms of collagen vascular
diseases or vasculitis syndromes.
• Hematuria, which may be indicative of pulmonary-renal syndrome.
32.4.2 Physical Examination
Hemoptysis may be diagnosed based on several clues gleaned from a thorough
physical examination, some of which are included in this section.
• Chest or neck bruises (a sign of trauma).
• Crepitus indicates obstruction of the airway.
• Hemangioma or telangiectasia (both of which point to arteriovenous
malformations).
• Clubbed ngers (which may indicate chronic obstructive pulmonary illness, pulmonary arteriovenous malformations, or congenital heart defects).
• A lost tooth can be inhaled, especially if the kid is sleeping. It can cause bleeding
in the oral cavity or nasopharynx, elevating the possibility of foreign body
aspiration.
• Infectious conditions, foreign body aspiration, and localized airway, or parenchymal hemorrhage can all lead to aberrant breath sounds.
32.4.3 Laboratory Evaluation
Patients experiencing hemoptysis of at least moderate severity (5 mL blood) and
unclear etiology should see a pediatric pulmonologist. These people should have
routine testing for [3] conditions:
Undiagnosed hemoptysis in children [3]:
• A complete blood count.
422
M. O. Korkmaz et al.
• Coagulation tests must be performed to rule out von Willebrand disease (plasma
von Willebrand factor antigen, von Willebrand factor activity, and factor VIII
activity).
• Sputum should be cultured for bacteria, fungi, and viruses, and acid-fast bacilli
should be stained if possible.
• Screening for hematuria using urinalysis.
32.4.4 Imaging
Radiographs of the chest taken traditionally should include at least two different
angles. Parenchymal and alveolar opacities may be seen on radiographs if there has
been a hemorrhage, and these opacities may be widespread or localized to one area
of the lungs. Similar symptoms may present themselves in cases of nonpulmonary
blood aspiration.
Some of the characteristics that point to a particular cause of bleeding are [3]:
Hyperination, volume loss, or localized pneumonia are all symptoms of endo-
bronchial blockage that a foreign body may cause if it is radiopaque.
• Cavitations (which may indicate TB, a fungal infection, or granulomatosis with
polyangiitis).
• Bronchiectasis—until the condition is well advanced, plain radiography has limited sensitivity for identifying bronchiectasis. A “tram-track” look has been associated with severe bronchiectasis.
Radiographs may seem normal in as much as one-third of infants with hemopty-
sis [9, 10].
Patients with moderate or severe hemoptysis for whom a focused history, physi-
cal, and chest radiograph have failed to yield an explanation should undergo additional evaluation using computed tomography (CT) of the chest with contrast by
multidetector CT angiography [3].
The CT angiography procedure should be tailored to view the bronchial arteries
since they are the most common sites of pulmonary bleeding. This method should
be enough if you are checking for pulmonary embolism in the pulmonary arterial
circulation [11]. Alveolar hemorrhage often presents as “ground-glass” opacities in
the perivascular regions, and CT angiography will also allow evaluation of the airways and lung parenchyma. The CT scan has the potential to detect airway and
vascular abnormalities.
Pulmonary arteriography should be investigated if a signicant suspicion of vas-
cular abnormalities remains despite a negative CT scan. Bronchial arteriography
may help pinpoint the source of bleeding and make bronchial artery embolization
(BAE) [12] more effective in cases of signicant hemoptysis.
32 Hemoptysis inChildren: ENT-Related Etiologies
423
32.5 Hemoptysis: 32.5% ofCases had anENT Cause
32.5.1 Respiratory Illness
Sixty to seventy percent of instances of hemoptysis may be attributed to infection.
Infection produces inammation and edema of the supercial mucosa, which can
result in the rupture of the supercial blood vessels. Bronchitis was the leading
cause of hemoptysis in a retrospective analysis [13] of inpatient and outpatient cases
in the United States, followed by pneumonia (10%) and TB (8%). Most cases of
hemoptysis are caused by infection with bacteria like Staphylococcus aureus or
Pseudomonas aeruginosa or fungi like Aspergillus species. Severe hemoptysis can
also be caused by viruses like inuenza [14]. Patients with human immunodeciency virus (HIV) infection are more likely to develop pulmonary Kaposi’s sarcoma [2, 15], one of numerous illnesses that can cause hemoptysis.
In children without pulmonary, cardiac, hematologic, or neoplastic illness, infec-
tion is the leading cause of hemoptysis.
Infections, including TB, aspergilloma, and acute endemic mycoses, are com-
mon causes of hemoptysis. Hemoptysis is not prevalent in children with these infections since cavitary illness is rare in this age group [16, 17].
In addition, hemoptysis can be caused by a pulmonary infection with a common
community-acquired bacterium, such as Staphylococcus, Streptococcus, Klebsiella,
or Pseudomonas [18, 19]. Signicant bleeding can be a symptom of the inuenza
virus, especially the H1N1 strain of the disease [20–22]. Evidence suggests that the
immunothrombosis pathophysiology of pneumonia caused by coronavirus disease
2019 (COVID-19) can lead to alveolar bleeding [23, 24].
Finally, any acute respiratory illness that induces vigorous coughing might result
in mild hemoptysis (blood-streaked sputum) due to mechanical stress on the airway.
Hemoptysis of this sort typically resolves on its own [3].
32.5.2 Aspiration ofaNon-native Body
Children under three are at the most risk for foreign body aspiration. Most children
aspirate do not have symptoms associated with the incident until days or weeks
later, when they may appear with wheezing (typically monophonic and occasionally
unilateral), persistent cough, pneumonia, or hemoptysis [25]. A history of choking
strongly suggests foreign body aspiration. However, the patient may not remember
the episode when they present [3].
32.5.3 Trauma
Suctioning past the tracheal entrance of the tube can cause mucosal damage to the
central airways and bloody sputum in children who have an endotracheal tube or
tracheostomy. Very minimal bleeding occurs; this is not considered clinically
424
M. O. Korkmaz et al.
signicant. Humidication, soft suction catheters, and controlled suction lengths
can help protect the mucosa from further injury and possibly even stop bleeding.
Children who require a tracheostomy for an extended period may also experience
granulation tissue formation, resulting in mild hemoptysis [3].
Bronchoscopy results may include mucosal abrasions or granulation tissue in
around 10% of these children, indicating that the bleeding is more extensive than
initially thought.
It is incredibly uncommon for signicant hemoptysis to develop as a result of an
airway tube eroding into a big vessel in the mediastinum or tracheal wall; nonetheless, some case reports describe presentations with bouts of non-massive “sentinel”
bleeding [26–28]. Patients who have undergone a tracheostomy should have any
signs of profuse bleeding assessed immediately by a surgical expert, usually using
beroptic endoscopy [3].
Adult studies show that bleeding during transbronchial biopsies occurs in
0.26–5.0% of instances and is seldom signicant in these people.
32.5.4 Hemoptysis Mimics
Hemoptysis is the term used to describe the expectoration of blood from the lungs.
True hemoptysis [3] might be confused with bleeding from the upper respiratory
tract, the oropharynx or nasopharynx, or the upper digestive tract (for example,
from esophageal varices related to cirrhosis).
Children who produce injuries that seem like pulmonary bleeding on themselves
have been described as having “factitious hemoptysis” [29]. A patient who appears
with hemoptysis, odd symptoms, and a negative assessment [30] should be evaluated for Munchausen syndrome (or Munchausen syndrome via proxy).
References
1. Cahill BC, Ingbar DH.Massive hemoptysis. Assessment and management. Clin Chest Med.
1994;15:147–67.
2. Bidwell JL, Pachner RW. Hemoptysis: diagnosis and management. Am Fam Physician.
2005;72(7):1253–60.
3. Stillwell PC, Kupfer O. Hemoptysis in children. In: Mallory GB, Hoppin AG, editors. .
UpToDate. Last updated: Feb 13, 2023.
4. Vece TJ, de Guzman MM, Langston C, Fan LL.Diffuse alveolar hemorrhage in children. In:
Wilmott RW, Deterding R, Li A, Ratjen F, Sly P, editors. Kendig’s disorders of the respiratory
tract in children. 9th ed. Philadelphia, PA: Elsevier; 2018. p.893.
5. Davidson K, Shojaee S.Managing massive hemoptysis. Chest. 2020;157:77.
6. Flume PA, Mogayzel PJ Jr, Robinson KA, etal. Cystic brosis pulmonary guidelines: pulmonary complications: hemoptysis and pneumothorax. Am J Respir Crit Care Med. 2010;182:298.
7. Jean-Baptiste E.Clinical assessment and management of massive hemoptysis. Crit Care Med.
2000;28:1642–7.
8. Reynolds C, Staples H. Hemoptysis in an adolescent with EVALI. Pediatr Pulmonol.
2022;57:2875.
32 Hemoptysis inChildren: ENT-Related Etiologies
9. Pianosi P, Al-sadoon H.Hemoptysis in children. Pediatr Rev. 1996;17:344.
10. Lichtenberger JP 3rd, Digumarthy SR, Abbott GF, etal. Diffuse pulmonary hemorrhage: clues
to the diagnosis. Curr Probl Diagn Radiol. 2014;43:128.
11. Marquis KM, Raptis CA, Rajput MZ, etal. CT for evaluation of hemoptysis. Radiographics.
2021;41:742.
12. Noë GD, Jaffé SM, Molan MP.CT and CT angiography in massive haemoptysis with emphasis on pre-embolization assessment. Clin Radiol. 2011;66:869.
13. Reisz G, Stevens D, Boutwell C, Nair V.The causes of hemoptysis revisited. A review of the
etiologies of hemoptysis between 1986 and 1995. Mo Med. 1997;94:633–5.
14. Bond D, Vyas H.Viral pneumonia and hemoptysis. Crit Care Med. 2001;29:2040–1.
15. Nelson JE, Forman M.Hemoptysis in HIV-infected patients. Chest. 1996;110:737–43.
16. Shaffer JP, Barson W, Luquette M, etal. Massive hemoptysis as the presenting manifestation
in a child with histoplasmosis. Pediatr Pulmonol. 1997;24:57.
17. Morris SK, Giroux RJP, Consunji-Araneta R, et al. Epidemiology, clinical features and outcomes of incident tuberculosis in children in Canada in 2013-2016: results of a national surveillance study. Arch Dis Child. 2021;106:1165.
18. Chiel L, Welsh S, Andren K, et al. Pediatric hemoptysis without bronchiectasis or cardiac
disease: etiology, recurrence, and mortality. J Pediatr. 2019;214:66.
19. Carteaux G, Contou D, Voiriot G, etal. Severe hemoptysis associated with bacterial pulmonary infection: clinical features, signicance of parenchymal necrosis, and outcome. Lung.
2018;196:33.
20. Haura L, Warachit B, Makkoch J, Poovorawan Y.Hemoptysis in children with pandemic inuenza H1N1 2009 infection. Southeast Asian J Trop Med Public Health. 2009;40:1259.
21. Del Bianco R, Santos MS, Ribeiro MC, etal. Clinical aspects of inuenza A (H1N1) in HIVinfected individuals in São Paulo during the pandemic of 2009. Braz J Infect Dis. 2011;15:170.
22. Gilbert CR, Vipul K, Baram M.Novel H1N1 inuenza A viral infection complicated by alveolar hemorrhage. Respir Care. 2010;55:623.
23. Potus F, Mai V, Lebret M, et al. Novel insights on the pulmonary vascular consequences of
COVID-19. Am J Physiol Lung Cell Mol Physiol. 2020;319:L277.
24. Fireizen Y, Shahriary C, Imperial ME, et al. Pediatric P-ANCA vasculitis following
COVID-19. Pediatr Pulmonol. 2021;56:3422.
25. Foltran F, Ballali S, Rodriguez H, etal. Inhaled foreign bodies in children: a global perspective on their epidemiological, clinical, and preventive aspects. Pediatr Pulmonol. 2013;48:344.
26. Ghai B, Makkar JK, Bakshi J, etal. Survival of a child without sequelae after tracheoarterial
stula. Paediatr Anaesth. 2007;17:588.
27. Ideno S, Shinto A, Matsuoka T, et al. Two cases of emergency extracorporeal membrane
oxygenation support in children suffering from Tracheo-innominate artery stula. Masui.
2016;65:146.
28. Jesus LE, Silva EWGMD, Balieiro M, et al. Post-tracheostomy tracheoinnominate stula:
endovascular treatment. Rev Paul Pediatr. 2021;40:e2020229.
29. Sood M, Clarke JR, Murphy MS.Covert biting of the buccal mucosa masquerading as haematemesis or haemoptysis in children. Acta Paediatr. 1999;88:1038.
30. Bjornson CL, Kirk VG.Munchausen’s syndrome presenting as hemoptysis in a 12-year-old
girl. Can Respir J. 2001;8:439.
425
Part IV
Pediatric Pulmonology Disease Specific Upper
Respiratory Tract Involvement
Airway Inflammation: United Airway
inChildren
MahirSerbes, RenatoCutrera, andDeryaAltıntaş
33.1 Introduction
United airway disease (UAD) in children describes the shared epidemiologic,
pathophysiologic, and clinical evidence that revealed the strong relationship among
the most frequent and chronic inammatory diseases of the upper and lower airways
including allergic rhinitis (AR), chronic rhinosinusitis (CRS), and asthma
(Table33.1) [2, 4]. This concept proposes that these diseases are manifestations of
a single unied airway inammatory process and inammation in one part of the
airway will likely stimulate a similar reaction throughout the rest of the airway. Due
to recent scientic improvements in the knowledge of mechanisms for chronic
inammation of both upper and lower airways, the concept of a single disease has
been replaced by syndromes encompassing complex biological networks of distinct
and interrelating inammatory pathways (endotypes) with variable clinical presentations (phenotypes) [3].
The aim of this section was to provide a better understanding of the common
pathophysiologic mechanisms of airway inammation supporting the link between
the so-called UAD in children.
33
M. Serbes · D. Altıntaş (*)
Department of Pediatric Immunology and Allergy, Cukurova University, School of Medicine,
Adana, Turkey
R. Cutrera
Department of Pediatric Medicine, IRCCS Bambino Gesù Children’s Hospital, Rome, Italy
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
H. Yüksel et al. (eds.), Pediatric Airway Diseases, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-74853-0_33
429
430
Clinical evidence
– The treatment of AR can improve asthma
be useful for long-term management of
asthma patients complicated by AR [8]
symptoms [2]
– Leukotriene receptor antagonists are known to
anti-IgE antibody omalizumab improved nasal
and bronchial symptoms and reduced
unscheduled visits due to asthma [8]
treating both rhinitis and asthma [8]
– The recombinant, humanized, monoclonal
– Allergen immunotherapy is effective for
M. Serbes et al.
and lower airways is suggested to be via a
bone marrow-derived systemic
inammatory response [6]
membrane thickening, the typical hallmark
of the lower airway remodeling, not only
– The communication between the upper
Epidemiologic evidence Pathophysiologic evidence
– The prevalence of AR
a
Histological evidence
– The mucosa of the upper and lower
Table 33.1 Evidence and mechanisms of the nose and lung interaction supporting UAD
– The presence of epithelial basement
appears to be at least triple
the prevalence of asthma,
and 19–38% of patients
with AR have concomitant
asthma, and 30–80% of
asthmatics have AR [2, 3]
airways is similar, with
pseudostratied epithelium with
columnar, ciliated cells located on a
basement membrane. In the
submucosa, there are vessels, mucus
glands, broblasts, and some
highlighted the importance of the presence
of IgE in the bronchial mucosa, as in the
nasal mucosa inlocal allergic rhinitis [8]
found that sputum eosinophilia was
associated with a 52 times increase in the
in asthmatic patients but also in atopic
patients without asthma and patients with
AR [7]
– In non-allergic asthma, it has been
CRS manifest asthma, a
prevalence of approximately
2–3 times greater than that
of the general population.
CRSwNP is more
commonly associated with
– About 20% of patients with
moving air in and out of the lungs
inammatory cells [1]
foreign substances
– Both act as transport systems
– Both provide defense against inhaled
odds of nasal eosinophilia
– In a 2010 cross-sectional study, it was
lower tract respiratory
– Specic antibodies to SAEs can induce
disorders, such as asthma
and nonspecic bronchial
hyper-reactivity [2]
– Comorbid rhinitis/
basophil degranulation and mast cell
activation, providing another possible
mechanism by which S aureus could
contribute to chronic type 2 inammation
[3, 4]
rhinosinusitis worsens
asthma outcomes [3, 4]
and the presence of specic
IgE to S. aureus
enterotoxins (SAEs) were
signicantly higher in those
patients who had both
CRSwNP and asthma
– Colonization with S aureus
(66.7% and 53.8%,
respectively) [5]
The absence of smooth muscles in the upper airways and the lack of extensive subepithelial capillaries, arterial systems, and venous cavernous sinusoids in
CRSwNP chronic rhinosinusitis with nasal polyps
a
the lower airways are the histological differences between upper and lower airways