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Croup

This page is about clinical aspects of the disease.  For microbiologic aspects of the causative organism(s), see Human parainfluenza virus.

For patient information click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Synonyms and keywords: Tracheolaryngobronchitis; laryngotracheobronchitis; laryngo-tracheo-bronchitis; croup syndrome; barking cough; acute laryngotracheitis

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Croup is an upper respiratory disease entailing swelling of the trachea caused by infection from human parainfluenza virus – an enveloped, single stranded negative sense RNA virus with four distinct serotypes. Development of viral croup results from infiltration of histiocytes, lymphocytes, plasma cells, and neutrophils white blood cells primarily by human parainfluenza viruses (HPIV). The infiltration from HPIV causes inflammation by the up-regulated production of cytokines, localized in the trachea. HPIV-response Immunoglobulin E (IgE) release inhibits histamine, contributing to the inflammation of the trachea and leading to swelling of the larynx, trachea, and large bronchi that obstructs the airways, leading to croup. Known as “barking cough“, croup manifests through symptoms including a “bark-like” cough, stridor, hoarseness, respiratory distress, and common cold symptoms such as runny nose and low-grade fever. Croup symptoms typically manifest after 2-7 days of human parainfluenza virus infection, usually lasting between 24-48 hours with only rare instances reported of up to 7 days. They will typically resolve without treatment, excepting the most severe cases that pose the threat of respiratory failure. Croup must be differentiated from other upper respiratory diseases and conditions that cause airway obstruction around the larynx, as well as those that present similar symptoms to influenza. Croup is a very common disease and is almost always found in children between 6 months and 6 years of age, but rare cases have been reported in children as young as 3 months and as old as 15 years. Primary measures of preventing croup involve preventing the spread of human parainfluenza virus. This is accomplished by maintaining personal hygiene, such as washing hands frequently, and limiting exposure to patients with croup or other respiratory illness. Medical therapies to treat croup are dependent on the classification of the particular case: mild, moderate, severe, and imminent respiratory failure. For mild croup, glucocorticoid therapy is usually sufficient to alleviate symptoms, typically administering nebulized dexmethasone and budesonide. For more severe cases, nebulized racemic and L-epinephrine is administered in conjunction with glucocorticoids. Hospitalization and intubation is very rare and is usually only used when the respiratory distress is life-threatening. Common physical examination findings of croup are primarily chest and lung abnormalities. This includes inspiratory stridor, expiratory wheezing, suprasternal and intercostal indrawing, sternal wall retractions, and desynchronized chest and abdominal wall expansion. Low-grade fever can be present, as well as cyanosis in severe cases. Diagnosis of croup is dependent on x-ray imaging of the chest and neck, with diagnostic images indicative of croup including evidence of steeple sign: narrowing of the subglottic lumen in the neck. It also includes a visibly distended hypopharynx in some cases. Prognosis of croup is usually good, with mild and moderate croup usually resolving itself without treatment. Severe cases of croup can have poor prognosis, if untreated, due to the possibility of respiratory failure. All classifications of croup have good prognosis with appropriate treatment.

Historical Perspective

Diptheritic croup reports date back to the Homer-era of Ancient Greece, speculating to have emerged in the 12th century B.C.E. The Viral-based croup was discovered in 1826 by French medical doctor Pierre Bretonneau. Initial therapies included cold water mist to soothe pain as well as tracheotomy for patients with severe cases requiring hospitalization. In the 1970s, nebulized Epinephrine emerged as a therapy. Glucocorticoid therapies emerged in the late 1980s’ and 1990’s. Preventative therapy emerged with successful immunization of individuals against diptheritic croup with the development of influenza and diptheria vaccines.

Pathophysiology

Development of croup results from infiltration of white blood cells through the human parainfluenza virus (HPIV). HPIV expels its nucleocapsid into the recipient cell cytoplasm. The viral transcription then occurs through the HPIV RNA-dependent RNA polymerase. The viral mRNAs are translated into viral proteins, leading to the replication of the genome into the negative-sense RNA strand, which is then encapsidated by the nucleoprotein and used for further transcription and replication. The inflammation response to HPIV occurs from the up-regulation of cytokines and the released Immunoglobulin E inhibiting histamine. The resultant swelling of the larynx, trachea, and large bronchi obstructs the airways, which leads to croup.

Causes

Human parainfluenza virus is an enveloped, single stranded negative sense RNA virus with four distinct serotypes. The virus genome consists of approximately 15,000 nucleotides used to encode six structural proteins; they function to attach, enter, and fuse with the host cell, forming a complex with the RNA genome. Human parainfluenza virus is a member of the paramyxoviridae family. It is a member of one of two genuses depending on the serotype: Respirovirus or rubulavirus. Human parainfluenza virus infects the body by infiltrating white blood cells. It is transmitted through respiratory droplets through the air, as well as physical contact with an infected individual or contaminated physical surface.

Classification

Croup is classified by severity of symptoms. The Westley Score system quantifies symptoms from a score of 0-5. The sum of the symptom score stratifies croup into mild, moderate, severe, or indicative of total respiratory failure.

Differentiating Croup from Other Diseases

Croup must be differentiated from other upper respiratory diseases and conditions that cause upper airway obstruction around the larynx, as well as those that present similar symptoms to influenza.

Epidemiology and Demographics

Annually, the incidence of croup is approximately 532/100,000 individuals, peaking in the fall of each year. Croup is primarily found in children between 6 months and 6 years of age, but rare cases have been reported in children as young as 3 months and as old as 15 years. Males are 1.5 times more likely to develop croup.

Risk Factors

Risk factors for croup include being male and between 6 months and 6 years old, family history of the disease, living in a densely populated region, traveling to or from developing countries, and lacking an influenza vaccine.

Natural History, Complications and Prognosis

Croup symptoms typically manifest after 2-7 days of human parainfluenza virus infection. Symptoms will typically last between 24-48 hours; very rarely they will last up to 7 days. They will typically resolve without treatment, excepting the most severe cases that pose the threat of respiratory failure. Prognosis is good in mild and moderate croup with and without treatment. Severe croup and impending respiratory failure classifications have poor prognosis, if left untreated, due to life-threatening airway obstruction. With treatment, all manifestations of croup have a good prognosis. Complications of croup stem from airway obstruction, including respiratory failure and respiratory distress. They also stem from infections due to immunocompromise from the causative human parainfluenza virus and corticosteroid therapy; these include bacterial tracheitis, atelectasis, pneumonia, pulmonary edema, and epiglottitis.

Diagnosis

History and Symptoms

Symptoms of croup include: barking cough, stridor, hoarseness, difficulty breathing, and common cold symptoms. Family history of history of croup in the patient can help determine and differentiate a croup diagnosis.

Physical Examination

Common physical examination findings of croup are primarily chest and lung abnormalities. This includes inspiratory stridor, expiratory wheezing, suprasternal and intercostal indrawing, sternal wall retractions, and desynchronized chest and abdominal wall expansion. Additionally, croup patients often appear ill, similarly to common cold patients, and lethargic. Low-grade fever can be present, as well as cyanosis in severe cases.

Laboratory Findings

Laboratory findings may include abnormal white blood cell counts as well as markers for inflammation.

X Ray

X Ray findings in croup patients include evidence of steeple sign: narrowing of the subglottic lumen in the neck. It also includes a visibly distended hypopharynx in some cases.

Other Diagnostic Studies

Croup’s exact cause can be determined by a nasopharyngeal swab. It is not usually performed since it is not usually necessary for diagnosis, as well as presenting patient distress and having no impact on management and treatment.

Treatment

Medical Therapy

The primary medical therapy used to treat croup depends on the severity of the case. For mild croup, glucocorticoid therapy is primarily used to alleviate symptoms by reducing tracheal swelling and inflammation. The main corticosteroids used are dexamethasone and/or budesonide, administered orally or, rarely, via a parenteral method. These are usually effective beginning 6 hours post-treatment. For moderate and severe croup, epinephrine is used in conjunction with glucocorticoids. The primary epinephrine therapies used are racemic epinephrine or L-epinephrine, both in nebulized form. Epinephrine alleviates symptoms within 10-30 minutes, but they usually return within 2 hours, requiring repeated dosing for long-term relief. Hospitalization is rarely required and is primarily used for observation and symptom management in children. Intubation is a rare necessary treatment for hospitalized children with the most severe croup cases.

Prevention

Primary measures of preventing croup involve maintaining personal hygiene, such as washing hands frequently, and limiting exposure to patients with croup or other respiratory illness. Prevention for rarer causes of croup include vaccinations for haemophilus influenzae (Hib), measles, and diptheria.

References


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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Diptheritic croup reports date back to the Homer-era of Ancient Greece, speculating to have emerged in the 12th century B.C.E. The Viral-based croup was discovered in 1826 by French medical doctor Pierre Bretonneau. Initial therapies included cold water mist to soothe pain as well as tracheotomy for patients with severe cases requiring hospitalization. In the 1970s, nebulized Epinephrine emerged as a therapy. Glucocorticoid therapies emerged in the late 1980s’ and 1990’s. Preventative therapy emerged with successful immunization of individuals against diptheritic croup with the development of influenza and diptheria vaccines.

Discovery

  • The first reported cases of diptheritic croup date back to Ancient Greece, speculated to the 12th century B.C.E.[1]
  • Viral croup was discovered and differentiated from diptheritic croup in 1826 by French medical doctor Pierre Bretonneau[1]

Landmark Events in the Development of Treatment Strategies

References

  1. ↑ 1.0 1.1 Feigin, Ralph D. (2004). Textbook of pediatric infectious diseases. Philadelphia: Saunders. p. 252. ISBN 0-7216-9329-6.
  2. ↑ 2.0 2.1 2.2 Marchessault V (2001). “Historical review of croup”. Paediatr Child Health. 6 (10): 721–3. PMC 2805983. PMID 20084146.
  3. ↑ Kairys SW, Olmstead EM, O’Connor GT (1989). “Steroid treatment of laryngotracheitis: a meta-analysis of the evidence from randomized trials”. Pediatrics. 83 (5): 683–93. PMID 2654865.
  4. ↑ Klassen TP, Feldman ME, Watters LK, Sutcliffe T, Rowe PC (1994). “Nebulized budesonide for children with mild-to-moderate croup”. N. Engl. J. Med. 331 (5): 285–9. doi:10.1056/NEJM199408043310501. PMID 8022437.
  5. ↑ Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.


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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Development of croup results from infiltration of white blood cells through the human parainfluenza virus (HPIV). HPIV expels its nucleocapsid into the recipient cell cytoplasm. The viral transcription then occurs through the HPIV RNA-dependent RNA polymerase. The viral mRNAs are translated into viral proteins, leading to the replication of the genome into the negative-sense RNA strand, which is then encapsidated by the nucleoprotein and used for further transcription and replication. The inflammation response to HPIV occurs from the up-regulation of cytokines and the released Immunoglobulin E inhibiting histamine. The resultant swelling of the larynx, trachea, and large bronchi obstructs the airways, which leads to croup.

Pathogenesis

Transmission

  • Croup may develop after human parainfluenza virus is transmitted primarily by coughing, releasing infected secretions through respiratory droplets or contaminated surfaces or objects.[7]

References

  1. ↑ Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
  2. ↑ 2.0 2.1 2.2 2.3 Henrickson, K. J. (2003). “Parainfluenza Viruses”. Clinical Microbiology Reviews. 16 (2): 242–264. doi:10.1128/CMR.16.2.242-264.2003. ISSN 0893-8512.
  3. ↑ Schomacker, Henrick; Schaap-Nutt, Anne; Collins, Peter L; Schmidt, Alexander C (2012). “Pathogenesis of acute respiratory illness caused by human parainfluenza viruses”. Current Opinion in Virology. 2 (3): 294–299. doi:10.1016/j.coviro.2012.02.001. ISSN 1879-6257.
  4. ↑ Schaap-Nutt, Anne; Liesman, Rachael; Bartlett, Emmalene J.; Scull, Margaret A.; Collins, Peter L.; Pickles, Raymond J.; Schmidt, Alexander C. (2012). “Human parainfluenza virus serotypes differ in their kinetics of replication and cytokine secretion in human tracheobronchial airway epithelium”. Virology. 433 (2): 320–328. doi:10.1016/j.virol.2012.08.027. ISSN 0042-6822.
  5. ↑ Welliver RC, Sun M, Rinaldo D (1985). “Defective regulation of immune responses in croup due to parainfluenza virus”. Pediatr. Res. 19 (7): 716–20. doi:10.1203/00006450-198507000-00016. PMID 2991841.
  6. ↑ Baron, Samuel (1996). Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston. ISBN 0-9631172-1-1.
  7. ↑ “Human Parainfluenza Viruses | Clinical Overview of HPIVs | CDC”.


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Causes

Causes

This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Croup.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Human parainfluenza virus is an enveloped, single stranded negative sense RNA virus with four distinct serotypes. The virus genome consists of approximately 15,000 nucleotides used to encode six structural proteins; they function to attach, enter, and fuse with the host cell, forming a complex with the RNA genome. Human parainfluenza virus is a member of the paramyxoviridae family. It is a member of one of two genuses depending on the serotype: Respirovirus or Rubulavirus. Human parainfluenza virus infects the body by infiltrating white blood cells. It is transmitted through respiratory droplets through the air, as well as physical contact with an infected individual or contaminated physical surface.

Microbiological Characteristics

  • Human parainfluenza virus (HPIV) is an enveloped, single stranded negative sense RNA virus.[2]
  • Human parainfluenza virus is comprised of four distinct serotypes:[3]
    • HPIV-1
    • HPIV-2
    • HPIV-3
    • HPIV-4
Protein Location Function
hemagglutinin Envelope Attachment and cell entry
fusion protein Envelope Fusion and cell entry
matrix protein Within the envelope Assembly
nucleoprotein Nucleocapsid Forms a complex with the RNA genome
phosphoprotein Nucleocapsid Forms as a part of the RNA polymerase complex
large protein Nucleocapsid Forms as a part of the RNA polymerase complex
  • Human parainfluenza virus is a member of the paramyxoviridae family.
  • The genus for human parainfluenza virus depends on its serotype:[4]
    • Respirovirus: HPIV-1 & HPIV-3
    • Rubulavirus: HPIV-2 & HPIV-4

Transmission

  • Human parainfluenza virus is primarily transmitted by the following:[5]
    • Airborne respiratory droplets from coughing and sneezing
    • Close physical contact with an infected individual
    • Physical contact with a contaminated surface

Virology

References

  1. ↑ “phil.cdc.gov”.
  2. ↑ Vainionpää R, Hyypiä T (1994). “Biology of parainfluenza viruses”. Clin. Microbiol. Rev. 7 (2): 265–75. PMC 358320. PMID 8055470.
  3. ↑ Baron, Samuel (1996). Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston. ISBN 0-9631172-1-1.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Henrickson, K. J. (2003). “Parainfluenza Viruses”. Clinical Microbiology Reviews. 16 (2): 242–264. doi:10.1128/CMR.16.2.242-264.2003. ISSN 0893-8512.
  5. ↑ “Human Parainfluenza Viruses | Transmission of HPIVs | CDC”.
  6. ↑ Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.


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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Croup is classified by severity of symptoms. The Westley Score system quantifies symptoms from a score of 0-5. The sum of the symptom score stratifies croup into mild, moderate, severe, or indicative of total respiratory failure.

Classification of Croup

Croup is classified by severity of symptoms through the Westley score of assessing croup severity, demonstrated in the table below:[1][2]

Feature 0 1 2 3 4 5
Chest wall retraction None Mild Moderate Severe
Stridor None With agitation At rest
Cyanosis None With agitation At rest
Level of consciousness Normal Disoriented
Air entry Normal Decreased Markedly decreased


The score is aggregated into a qualitative croup classification:[1][2]

Classification Score Features
Mild ≤2 Characteristic barking cough and hoarseness
Moderate 3-5 Cough, hoarseness, and stridor
Severe 6-11 Cough, hoarseness, stridor, and visible chest indrawing
Respiratory Failure ≥12 Failure of respiratory system

References

  1. ↑ 1.0 1.1 Johnson D (2009). “Croup”. BMJ Clin Evid. 2009. PMC 2907784. PMID 19445760.
  2. ↑ 2.0 2.1 Klassen TP (1999). “Croup. A current perspective”. Pediatr. Clin. North Am. 46 (6): 1167–78. PMID 10629679.


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Differentiating Croup from other Diseases

Differentiating Croup from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Croup must be differentiated from other upper respiratory diseases and conditions that cause airway obstruction around the larynx, as well as those that present similar symptoms to influenza.

Differentiating Croup from Other Diseases

Croup must be differentiated from other upper respiratory diseases and conditions that cause airway obstruction around the larynx:[1][2]

The tables below summarize the differences between croup and other upper respiratory conditions with similar symptoms:

Disease Findings
Epiglottitis Typically presents with fever, difficulty swallowing, dysphonia, drooling, and stridor. Can rapidly progress to include cyanosis and asphyxiation and is much more severe than croup; it is often an emergency requiring intubation.[3]
Subglottic stenosis Presents with stridor and difficulty breathing; can be a life-threatening emergency requiring intubation to remove the airway obstruction.[4]
Bacterial tracheitis Presents with barking cough, stridor, fever, chest pain, ear pain, difficulty breathing, headache, dizziness. Symptoms, particularly fever, are more severe than croup. Requires antibiotic treatment.[5]
Retropharyngeal abscess Presents with neck pain, stiff neck, torticollis and may include enlarged cervical lymph nodes, fever, malaise, stridor, and barking cough. Requires tonsillectomy and use of antibiotics.[6]
Angioneurotic edema Presents with swelling of the dermis, subcutaneous, mucosa and submucosal tissues. Can occur in the upper respiratory system and result in stridor and respiratory arrest, requiring emergency treatment. Acquired angioneurotic edema results from an allergic reaction and be treated with epinephrine.[7]



Variable Croup Epiglottitis Pharyngitis Bacterial tracheitis Tonsilitis Retropharyngeal abscess Subglottic stenosis
Presentation Cough ✔ — Sore throat, pain on swallowing, fever, headache, abdominal pain, nausea and vomiting Barking cough, stridor,

fever, chest pain,

ear pain, difficulty breathing, headache, dizziness.

Sore throat, pain on swallowing, fever, headache, cough Neck pain, stiff neck, torticollis

fever, malaise, stridor, and barking cough

Depends on severity. May have respiratory distress at birth, exercise-induced dyspnea, intermittent wheezing. Inspiratory stridor. [8]
Stridor ✔ ✔
Drooling — ✔
Others are Hoarseness, Difficulty breathing, symptoms of the common cold, Runny nose, Fever Other symptoms include difficulty breathing, fever, chills, difficulty swallowing, hoarseness of voice
Causes Parainfluenza virus H. influenza type b, beta-hemolytic streptococci, Staphylococcus aureus, fungi and viruses. Group A beta-hemolytic streptococcus. Staphylococcus aureus Most common cause is viral including adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. Second most common causes are bacterial; Group A streptococcal bacteria,[9]  Polymicrobial infection. Mostly; Streptococcus pyogenes, Staphylococcus aureus and respiratory anaerobes (example; Fusobacteria, Prevotella, and Veillonella species)[10][11][12][13][14][15] Congenital, trauma
Physical exams findings Suprasternal and intercostal indrawing,[16] Inspiratory stridor[17], expiratory wheezing,[17] Sternal wall retractions[18] Cyanosis, Cervical lymphadenopathy, Inflammed epiglottis Inflammed pharynx with or without exudate Subglottic narrowing with purulent secretions in the trachea[19][20] Fever, especially 100°F or higher.[21][22]Erythema, edema and Exudate of the tonsils.[23] cervical lymphadenopathy, Dysphonia.[24] Child may be unable to open the mouth widely. May have enlarged

cervical lymph nodes and neck mass.

Signs of respiratory distress, intermittent wheezing. Inspiratory stridor. [8]
Age commonly affected Mainly 6 months and 3 years old

rarely, adolescents and adults[25]

Used to be mostly found in

pediatric age group between 3 to 5 years,

however, recent trend favors adults

as most commonly affected individuals[26]

with a mean age of 44.94 years.

Mostly in children and young adults,

with 50% of cases identified

between the ages of 5 to 24 years.[27]

Mostly during the first six years of life Primarily affects children

between 5 and 15 years old.[28]

Mostly between 2-4 years, but can occur in other age groups.[6][29] May be congenital congenital or acquired. Mean age in acquired is 54.1 years[30]
Imaging finding Steeple sign on neck X-ray Thumbprint sign on neck x-ray — Lateral neck xray shows intraluminal membranes and tracheal wall irregularity. Intraoral or transcutaneous USG may show an abscess making CT scan unnecessary.[31][32][33] On CT scan, a mass impinging on the posterior pharyngeal wall with rim enhancement is seen[34][35] Bronchoscopy reveals subglottic stenosis. Computed tomography may reveal a concentric stenotic tracheal segment.[36]
Treatment Dexamethasone and nebulised epinephrine Airway maintenance, parenteral Cefotaxime or Ceftriaxone in combination with Vancomycin. Adjuvant therapy includes corticosteroids and racemic Epinephrine.[37][38] Antimicrobial therapy mainly penicillin-based and analgesics. Airway maintenance and antibiotics Antimicrobial therapy mainly penicillin-based and analgesics with tonsilectomy in selected cases. Immediate surgical drainage and antimicrobial therapy. emperic therapy involves; ampicillin-sulbactam or clindamycin. Endoscopic balloon dilation for patients with low-grade subglottic stenosis,[39] glucocorticoid injections, and resection.[40]

References

  1. ↑ Everard ML (2009). “Acute bronchiolitis and croup”. Pediatr. Clin. North Am. 56 (1): 119–33, x–xi. doi:10.1016/j.pcl.2008.10.007. PMID 19135584.
  2. ↑ Cherry JD (2008). “Clinical practice. Croup”. N. Engl. J. Med. 358 (4): 384–91. doi:10.1056/NEJMcp072022. PMID 18216359.
  3. ↑ de Vries CJ, de Jongh E, Zwart S, van den Akker EH, Opstelten W (2015). “[Epiglottitis in adults in general practice: difficult to recognise and life-threatening]”. Ned Tijdschr Geneeskd (in Dutch; Flemish). 159: A9061. PMID 26332815.
  4. ↑ “Subglottic Stenosis | Otolaryngology – Head and Neck Surgery | Baylor College of Medicine | Houston, Texas”.
  5. ↑ Al-Mutairi B, Kirk V (2004). “Bacterial tracheitis in children: Approach to diagnosis and treatment”. Paediatr Child Health. 9 (1): 25–30. PMC 2719512. PMID 19654977.
  6. ↑ 6.0 6.1 Craig FW, Schunk JE (2003). “Retropharyngeal abscess in children: clinical presentation, utility of imaging, and current management”. Pediatrics. 111 (6 Pt 1): 1394–8. PMID 12777558.
  7. ↑ Cicardi M, Zanichelli A (2010). “Acquired angioedema”. Allergy Asthma Clin Immunol. 6 (1): 14. doi:10.1186/1710-1492-6-14. PMC 2925362. PMID 20667117.
  8. ↑ 8.0 8.1 Nussbaumer-Ochsner Y, Thurnheer R (2015). “IMAGES IN CLINICAL MEDICINE. Subglottic Stenosis”. N Engl J Med. 373 (1): 73. doi:10.1056/NEJMicm1404785. PMID 26132943.
  9. ↑ Putto A (1987). “Febrile exudative tonsillitis: viral or streptococcal?”. Pediatrics. 80 (1): 6–12. PMID 3601520.
  10. ↑ Cheng J, Elden L (2013). “Children with deep space neck infections: our experience with 178 children”. Otolaryngol Head Neck Surg. 148 (6): 1037–42. doi:10.1177/0194599813482292. PMID 23520072.
  11. ↑ Abdel-Haq N, Quezada M, Asmar BI (2012). “Retropharyngeal abscess in children: the rising incidence of methicillin-resistant Staphylococcus aureus”. Pediatr Infect Dis J. 31 (7): 696–9. doi:10.1097/INF.0b013e318256fff0. PMID 22481424.
  12. ↑ Inman JC, Rowe M, Ghostine M, Fleck T (2008). “Pediatric neck abscesses: changing organisms and empiric therapies”. Laryngoscope. 118 (12): 2111–4. doi:10.1097/MLG.0b013e318182a4fb. PMID 18948832.
  13. ↑ Brook I (2004). “Microbiology and management of peritonsillar, retropharyngeal, and parapharyngeal abscesses”. J Oral Maxillofac Surg. 62 (12): 1545–50. PMID 15573356.
  14. ↑ Wright CT, Stocks RM, Armstrong DL, Arnold SR, Gould HJ (2008). “Pediatric mediastinitis as a complication of methicillin-resistant Staphylococcus aureus retropharyngeal abscess”. Arch Otolaryngol Head Neck Surg. 134 (4): 408–13. doi:10.1001/archotol.134.4.408. PMID 18427007.
  15. ↑ Asmar BI (1990). “Bacteriology of retropharyngeal abscess in children”. Pediatr Infect Dis J. 9 (8): 595–7. PMID 2235179.
  16. ↑ Johnson D (2009). “Croup”. BMJ Clin Evid. 2009. PMC 2907784. PMID 19445760.
  17. ↑ 17.0 17.1 Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
  18. ↑ Johnson D (2009). “Croup”. BMJ Clin Evid. 2009. PMC 2907784. PMID 19445760.
  19. ↑ Liston SL, Gehrz RC, Siegel LG, Tilelli J (1983). “Bacterial tracheitis”. Am J Dis Child. 137 (8): 764–7. PMID 6869336.
  20. ↑ Liston SL, Gehrz RC, Jarvis CW (1981). “Bacterial tracheitis”. Arch Otolaryngol. 107 (9): 561–4. PMID 7271556.
  21. ↑ Tonsillitis. Medline Plus. https://www.nlm.nih.gov/medlineplus/ency/article/001043.htm. Accessed May 2nd, 2016.
  22. ↑ “Tonsillitis – NHS Choices”.
  23. ↑ Stelter K (2014). “Tonsillitis and sore throat in children”. GMS Curr Top Otorhinolaryngol Head Neck Surg. 13: Doc07. doi:10.3205/cto000110. PMC 4273168. PMID 25587367.
  24. ↑ “Tonsillitis – Symptoms – NHS Choices”.
  25. ↑ Tong MC, Chu MC, Leighton SE, van Hasselt CA (1996). “Adult croup”. Chest. 109 (6): 1659–62. PMID 8769531.
  26. ↑ Lichtor JL, Roche Rodriguez M, Aaronson NL, Spock T, Goodman TR, Baum ED (2016). “Epiglottitis: It Hasn’t Gone Away”. Anesthesiology. 124 (6): 1404–7. doi:10.1097/ALN.0000000000001125. PMID 27031010.
  27. ↑ Bennett, John (2015). Mandell, Douglas, and Bennett’s principles and practice of infectious diseases. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455748013.
  28. ↑ Sharav, Yair; Benoliel, Rafael (2008). Orofacial Pain and Headache. Elsevier. ISBN 0723434123.
  29. ↑ Coulthard M, Isaacs D (1991). “Neonatal retropharyngeal abscess”. Pediatr Infect Dis J. 10 (7): 547–9. PMID 1876473.
  30. ↑ Nicolli EA, Carey RM, Farquhar D, Haft S, Alfonso KP, Mirza N (2017). “Risk factors for adult acquired subglottic stenosis”. J Laryngol Otol. 131 (3): 264–267. doi:10.1017/S0022215116009798. PMID 28007041.
  31. ↑ Kawabata M, Umakoshi M, Makise T, Miyashita K, Harada M, Nagano H; et al. (2016). “Clinical classification of peritonsillar abscess based on CT and indications for immediate abscess tonsillectomy”. Auris Nasus Larynx. 43 (2): 182–6. doi:10.1016/j.anl.2015.09.014. PMID 26527518.
  32. ↑ Nogan S, Jandali D, Cipolla M, DeSilva B (2015). “The use of ultrasound imaging in evaluation of peritonsillar infections”. Laryngoscope. 125 (11): 2604–7. doi:10.1002/lary.25313. PMID 25946659.
  33. ↑ Fordham MT, Rock AN, Bandarkar A, Preciado D, Levy M, Cohen J; et al. (2015). “Transcervical ultrasonography in the diagnosis of pediatric peritonsillar abscess”. Laryngoscope. 125 (12): 2799–804. doi:10.1002/lary.25354. PMID 25945805.
  34. ↑ Philpott CM, Selvadurai D, Banerjee AR (2004). “Paediatric retropharyngeal abscess”. J Laryngol Otol. 118 (12): 919–26. PMID 15667676.
  35. ↑ Vural C, Gungor A, Comerci S (2003). “Accuracy of computerized tomography in deep neck infections in the pediatric population”. Am J Otolaryngol. 24 (3): 143–8. PMID 12761699.
  36. ↑ Nussbaumer-Ochsner Y, Thurnheer R (2015). “IMAGES IN CLINICAL MEDICINE. Subglottic Stenosis”. N Engl J Med. 373 (1): 73. doi:10.1056/NEJMicm1404785. PMID 26132943.
  37. ↑ Nickas BJ (2005). “A 60-year-old man with stridor, drooling, and “tripoding” following a nasal polypectomy”. J Emerg Nurs. 31 (3): 234–5, quiz 321. doi:10.1016/j.jen.2004.10.015. PMID 15983574.
  38. ↑ Wick F, Ballmer PE, Haller A (2002). “Acute epiglottis in adults”. Swiss Med Wkly. 132 (37–38): 541–7. PMID 12557859.
  39. ↑ Cui PC, Luo JS, Zhao DQ, Guo ZH, Ma RN (2016). “[Management of subglottic stenosis in children with endoscopic balloon dilation]”. Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 51 (4): 286–8. doi:10.3760/cma.j.issn.1673-0860.2016.04.009. PMID 27095722.
  40. ↑ Nussbaumer-Ochsner Y, Thurnheer R (2015). “IMAGES IN CLINICAL MEDICINE. Subglottic Stenosis”. N Engl J Med. 373 (1): 73. doi:10.1056/NEJMicm1404785. PMID 26132943.
Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Annually, the incidence of croup is approximately 532/100,000 individuals, peaking in the fall of each year. Croup is primarily found in children between 6 months and 6 years of age, but rare cases have been reported in children as young as 3 months and as old as 15 years. Males are 1.5 times more likely to develop croup. Croup is found more often in developing countries due to the larger proportion of children in the populations, as well as the higher proportion of malnutrition and vitamin deficiency.

Epidemiology and Demographics

Incidence

Age

  • Croup is primarily found in children between the ages of 6 months and 6 years.[4]
    • Croup accounts for approximately 5% of hospital admissions of children within that age range.[1]
  • Rare cases may occur in children as young as 3 months and as old as 15 years.[1]

Gender

  • Males are affected by croup more frequently than females, at a ratio of 1.5 to 1.[4]

Race

  • There is no racial predilection to croup.

Developing countries

  • Croup is more common in developing countries due to the following:[5]
    • Larger proportion of children between 6 months and 6 years old in populations.
    • Larger proportion of malnutrition and vitamin deficiency.

References

  1. ↑ 1.0 1.1 1.2 Johnson D (2009). “Croup”. BMJ Clin Evid. 2009. PMC 2907784. PMID 19445760.
  2. ↑ “The World Factbook”.
  3. ↑ “Human Parainfluenza Viruses | HPIV Seasons | CDC”.
  4. ↑ 4.0 4.1 Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
  5. ↑ Berman S (1991). “Epidemiology of acute respiratory infections in children of developing countries”. Rev. Infect. Dis. 13 Suppl 6: S454–62. PMID 1862276.


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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Risk factors for croup include being male and between 6 months and 6 years old, family history of the disease, living in a densely populated region, traveling to or from developing countries, and lacking an influenza vaccine.

Risk Factors

  • Being between 6 months and 6 years old.
  • Having a family history of croup.[1]
  • Being male.[2]
  • Living in a densely populated region.[3]
  • Traveling to or from developing countries.[2]

References

  1. ↑ Pruikkonen H, Dunder T, Renko M, Pokka T, Uhari M (2009). “Risk factors for croup in children with recurrent respiratory infections: a case-control study”. Paediatr Perinat Epidemiol. 23 (2): 153–9. doi:10.1111/j.1365-3016.2008.00986.x. PMID 19159401.
  2. ↑ 2.0 2.1 Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
  3. ↑ Berman S (1991). “Epidemiology of acute respiratory infections in children of developing countries”. Rev. Infect. Dis. 13 Suppl 6: S454–62. PMID 1862276.
  4. ↑ Cherry JD (2008). “Clinical practice. Croup”. N. Engl. J. Med. 358 (4): 384–91. doi:10.1056/NEJMcp072022. PMID 18216359.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Croup symptoms typically manifest after 2-7 days of human parainfluenza virus infection. Symptoms will typically last between 24-48 hours; very rarely they will last up to 7 days. They will typically resolve without treatment, excepting the most severe cases that pose the threat of respiratory failure. Prognosis is good in mild and moderate croup with and without treatment. Severe croup and impending respiratory failure classifications have poor prognosis, if left untreated, due to life-threatening airway obstruction. With treatment, all manifestations of croup have a good prognosis. Complications of croup stem from airway obstruction, including respiratory failure and respiratory distress. They also stem from infections due to immunocompromise from the causative human parainfluenza virus and corticosteroid therapy; these include bacterial tracheitis, atelectasis, pneumonia, pulmonary edema, and epiglottitis.

Natural History

  • The incubation period for human parainfluenza virus (HPIV), causing croup, is typically 2 to 7 days upon infection.[1]
  • Croup symptoms will usually develop abruptly post-incubation, often overnight, including simultaneous manifestation of barking cough, stridor, hoarseness, and difficulty breathing.[2]
  • Without treatment, mild and moderate croup symptoms will usually resolve within 1 to 2 days of manifestation.[3]
    • 50% of childrens’ symptoms resolve within 24 hours.
    • 80% of childrens’ symptoms resolve within 48 hours.
  • Croup is self-limited and usually does not require treatment for symptom resolution.

Complications

Prognosis

  • Croup is self-limiting and prognosis for croup is usually good, but can vary due to severity of symptoms and complications.

Mild and Moderate Croup

  • Symptoms are not life threatening and will resolve without treatment.[2]
    • Treatment can shorten the duration of croup and lower the severity of symptoms.[4]

Severe Croup and Impending Respiratory Failure

  • The mortality rate for croup is very low at <1 per 100,000 individuals.[2]

References

  1. ↑ “Human Parainfluenza Viruses | Symptoms and HPIV Illnesses | CDC”.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Johnson D (2009). “Croup”. BMJ Clin Evid. 2009. PMC 2907784. PMID 19445760.
  3. ↑ Thompson M, Vodicka TA, Blair PS, Buckley DI, Heneghan C, Hay AD (2013). “Duration of symptoms of respiratory tract infections in children: systematic review”. BMJ. 347: f7027. PMC 3898587. PMID 24335668.
  4. ↑ 4.0 4.1 Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | X Ray | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

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