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* The [Familial association] studies have demonstrated strong heritability of CRS within immediate and secondary family members. According to a recent study by Orb, Q.et al on 496 patients with CRS, a strong genetic predisposition was involved in CRS pathogenesis, where relatives of patients with CRS had a 57.5 times higher risk of having CRS. First cousins had 9 times increased risk and second cousins had a 2.9times increased risk of pediatric CRS. Another study has suggested that this genetic predisposition may be related to the genes encoding potassium channels on the airway epithelium. These apical potassium channels mediate mucociliary clearance, air surface liquid hydration and control ion transport in epithelial cells[19*]. Other genetic diseases, like primary immunodeficiencies, primary ciliary dyskinesia (Kartagener's syndrome), and cystic fibrosis are highly associated with CRS, but their contribution to the overall prevalence is low
* The [Familial association] studies have demonstrated strong heritability of CRS within immediate and secondary family members. According to a recent study by Orb, Q.et al on 496 patients with CRS, a strong genetic predisposition was involved in CRS pathogenesis, where relatives of patients with CRS had a 57.5 times higher risk of having CRS. First cousins had 9 times increased risk and second cousins had a 2.9times increased risk of pediatric CRS. Another study has suggested that this genetic predisposition may be related to the genes encoding potassium channels on the airway epithelium. These apical potassium channels mediate mucociliary clearance, air surface liquid hydration and control ion transport in epithelial cells[19*]. Other genetic diseases, like primary immunodeficiencies, primary ciliary dyskinesia (Kartagener's syndrome), and cystic fibrosis are highly associated with CRS, but their contribution to the overall prevalence is low
* On microscopic histopathological analysis, Tissue and culture results will reveal:
* On microscopic histopathological analysis, Tissue and culture results will reveal:
Fifteen percent of aspirates contain viruses
:*Fifteen percent of aspirates contain viruses
Streptococcus pneumoniae 3%, Haemophilus influenzae 21%, anaerobes 6%, Staphylococcus aureus 4%, Streptococcus pyogenes 2%, Moraxella 2%
:*Streptococcus pneumoniae 3%, Haemophilus influenzae 21%, anaerobes 6%, Staphylococcus aureus 4%, Streptococcus pyogenes 2%, Moraxella 2%
Chronic: S. aureus 20%, anaerobes 3%, S. pneumoniae 4%, multiple organisms 16%
:*Chronic: S. aureus 20%, anaerobes 3%, S. pneumoniae 4%, multiple organisms 16%
Fungal incidence is 2% to 7%, most commonly Aspergillus and most commonly seen in immunocompromised patients.
:*Fungal incidence is 2% to 7%, most commonly Aspergillus and most commonly seen in immunocompromised patients.





Revision as of 17:40, 15 November 2020


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Template:Archana

Synonyms and keywords: Sinusitis in kids, Sinusitis in children , Pediatric rhinosinusitis, Pediatric sinusitis

Overview

  • Rhinosinusitis is defined as an inflammation of the paranasal and nasal sinus mucosae. Sinusitis in children is a very common condition. It is being seen more and more by primary care physicians and pediatricians. Children average six to eight colds per year. Of those, 0.5 to 5% will develop a sinus infection. Rhinosinusitis is the inflammation of the mucous membranes of nose and paranasal sinus(es). 5–13% of upper respiratory tract infections in children complicate into acute rhinosinusitis. Though not life threatening, it profoundly affects child's school performance and sleep pattern. If untreated, it could progress to chronic rhinosinusitis (CRS). Symptoms of a cold or allergy overlap with those of rhinosinusitis in the child. Distinguishing rhinosinusitis from a cold or allergy may be challenging. It is agreed that if cold symptoms are not improving by 7 to 10 days, a sinus infection should be seriously considered. Chronic rhinosinusitis (CRS)is a common problem in the pediatric age group, and the diagnosis and treatment are challenging due to the chronicity and similarity of symptoms with allergic rhinitis and adenoid hypertrophy. Although it is less common than acute rhinosinusitis, CRS is becoming more frequent and significantly affects the quality of life in children and can substantially impair daily function. CRS is characterized by sinus symptoms lasting more than 3 months despite medical therapy. Many factors are involved in the pathogenesis of this disease and include a primary insult with a virus followed by bacterial infection and mucosal inflammation, along with predisposition to allergies. The pathogens involved in perpetuation of CRS consist of multidrug-resistant mixed microflora. CRS is challenging to manage and could further extend to cause eye or intracranial complications. In children, CRS diagnosis is often either missed or incomprehensive. Due to this, morbidity and strain on healthcare budget are tremendous. Plain radiographs can be helpful for maxillary sinusitis especially if an air-fluid level is seen; otherwise, the sensitivity and specificity of plain radiographs are poor. Computed tomography (CT) should not be used for diagnostic purposes. The role of CTis mainly in children with chronic rhinosinusitis when surgery is being considered. In cases of complicated sinusitis, a CT scan is necessary. Treatment of most rhinosinusitis cases in children is medical. Optimal management entails specific appropriate antimicrobials as well as treatment of underlying causes. The aim is to normalize sinus anatomy and physiology and regain normal mucociliary function and clearance. Medical treatment should be with an appropriate antibiotic. Adjunctive treatment with saline irrigations and topical and systemic decongestants may be helpful. The standard treatment of pediatric acute bacterial rhinosinusitis (ABRS) is nasal irrigation and antibiotic use. Medical treatment of pediatric CRS includes avoidance of allergens in allergic patients (environmental or food) and therapy with nasal irrigation, nasal corticosteroids sprays, nasal decongestants, and antibiotics directed at the most common sinonasal organisms(Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis). Surgical therapy is rarely needed after appropriate medical therapy. Surgical intervention is necessary for complicated cases and for cases that do not respond to prolonged course of medical management. Currently adenoidectomy and endoscopic sinus surgery are the most common procedures used. Flexible fiberoptic endoscopy has revolutionized management of CRS. Its utility in children is being increasingly recognized. Children needing surgical intervention are a small percentage because of the success of medical treatment. Referral to an otolaryngologist and allergy specialist is recommended in case of failure of medical treatment.

Historical Perspective

  • Rhinosinusitis was first coined by Task Force of Rhinology and Paranasal Sinus Committee, in 1997 because sinusitis is invariably accompanied by rhinitis.

Classification

  • Anatomically paranasal sinuses are classified in to [four] paired sinuses, divided into subgroups that are named according to the bones within which the sinuses lie. The paranasal air sinuses are lined with respiratory epithelium (ciliated pseudostratified columnar epithelium). Understanding the embryologic development of the paranasal sinuses is crucial for the diagnosis and treatment of pediatric rhinosinusitis. For example, treatment of CRS in children below twelve years is different than children between 13 and 18 years due to differences in sinus growth. The ethmoid and maxillary sinuses develop in the 3rd month of gestation and are usually present at birth and display early growth and reach adult size by the age of ten. The sphenoid sinuses are generally appreciable on imaging before 3 years of age, become aerated at age 5 years, and expand in size into the second or third decade of life, typically becoming fully developed by age 12–14.The frontal sinuses develop from an anterior ethmoidal air cell and are pneumatized by age 5 or 6 years. The majority of all sinuses will reach adult size by the age of 15 years with the frontal sinus, the last to develop, reaching adult size by 19 years. The outflow tract of the maxillary sinus is situated at the most superior portion of the medial wall which makes gravitational drainage difficult. There are six anatomic drainage pathways from the sinuses -- three for each side. The frontal sinus drains via the nasofrontal duct into the anterior superior nasal cavity. The maxillary and anterior ethmoid sinuses drain via a common area, the ostiomeatal unit. The sphenoid and the posterior ethmoid sinuses drain via the sphenoethmoidal recess. Obstruction of any one pathway leads to sinusitis in the respective sinus areas.
  • Maxillary Sinuses, the largest of the paranasal sinuses, are under the eyes, in the maxillary bones (open in the back of the semilunar hiatus of the nose). They are innervated by the trigeminal nerve (CN Vb)
  • Frontal Sinuses, superior to the eyes, in the frontal bone, which forms the hard part of the forehead. They are also innervated by the trigeminal nerve (CN Va)
  • Ethmoidal Sinuses, which are formed from several discrete air cells within the ethmoid bone between the nose and the eyes. They are innervated by the ethmoidal nerves, which branch from the nasociliary nerve of the trigeminal nerve (CN Va)
  • Sphenoidal Sinus, in the sphenoid bone. They are innervated by the trigeminal nerve (CN Va & Vb)
  • Sinusitis may be classified into four subtypes/groups:
  • Acute Rhinosinusitis Sudden onset, lasting less than 4 weeks with complete resolution.
  • Subacute Rhinosinusitis A continuum of acute rhinosinusitis but less than 12 weeks.
  • Recurrent Acute Rhinosinusitis Four or more episodes of acute, lasting at least 7 days each, in any 1-year period.
  • Chronic Rhinosinusitis Signs of symptoms persist 12 weeks or longer.


Pathophysiology

  • Most commonly a viral upper respiratory infection causes rhinosinusitis secondary to edema and inflammation of the nasal lining and production of thick mucus that obstructs the paranasal sinuses and allows a secondary bacterial overgrowth. There are frontal, maxillary, sphenoid, and ethmoid sinuses. Allergic rhinitis can lead to sinusitis also due to ostial obstruction. Ciliary immobility can lead to increased mucus viscosity, further blocking drainage. Bacteria are introduced into the sinuses by coughing and nose blowing. Bacterial sinusitis usually occurs after a viral upper respiratory infection and worsening symptoms after 5 days, or persistent symptoms after 10 days. A key concept in understanding the pathogenesis of acute bacterial sinusitis is that the nasal and nasopharyngeal mucosae are continuous with the paranasal sinus mucosa. Any process that affects the nasal mucosa may also affect the sinus mucosa; moreover, the nasal mucosa is heavily colonized with bacteria and investigations of the sinus microbiome have shown diverse colonization of healthy paranasal sinuses by Firmicutes, Proteobacteria, and Actinobacteria in all subjects, Bacteroides spp. in 83 % of subjects and S. aureus in 68 % of subjects. The mucosa consists of mucus secreting goblet cells and pseudo-stratified ciliated columnar epithelium. The role of the mucus covering the mucosa is to catch the dust, stimulating particles and microorganisms. The drainage of mucus is by active mucociliary transport, and not by gravity. Nasal secretions originate from goblet cells, epithelial cells, epithelial cell proteins, vascular transudation and lacrimal fluid. The essential protein parts of these secretions are mucin glycoproteins composed of oligosaccharide side chains and a peptide core structure. Those glycoproteins affect the composition of the mucus and facilitate the interaction between microorganisms and host. Mucin binds surface adhesins on microorganisms therefore inhibiting their ability to colonize the epithelium. Mucociliary movement transports mucus from the paranasal sinuses to the nasal cavity and pharynx where it is swallowed. The large nasal mucosal surface consists of a mucus layer that moistens the air flowing over it and filters the air particles. In the nasal submucosa, vascular plexi swell and produce nasal congestion after exposure to certain stimuli such as noxious or allergic triggers, and temperature changes.
  • The [Familial association] studies have demonstrated strong heritability of CRS within immediate and secondary family members. According to a recent study by Orb, Q.et al on 496 patients with CRS, a strong genetic predisposition was involved in CRS pathogenesis, where relatives of patients with CRS had a 57.5 times higher risk of having CRS. First cousins had 9 times increased risk and second cousins had a 2.9times increased risk of pediatric CRS. Another study has suggested that this genetic predisposition may be related to the genes encoding potassium channels on the airway epithelium. These apical potassium channels mediate mucociliary clearance, air surface liquid hydration and control ion transport in epithelial cells[19*]. Other genetic diseases, like primary immunodeficiencies, primary ciliary dyskinesia (Kartagener's syndrome), and cystic fibrosis are highly associated with CRS, but their contribution to the overall prevalence is low
  • On microscopic histopathological analysis, Tissue and culture results will reveal:
  • Fifteen percent of aspirates contain viruses
  • Streptococcus pneumoniae 3%, Haemophilus influenzae 21%, anaerobes 6%, Staphylococcus aureus 4%, Streptococcus pyogenes 2%, Moraxella 2%
  • Chronic: S. aureus 20%, anaerobes 3%, S. pneumoniae 4%, multiple organisms 16%
  • Fungal incidence is 2% to 7%, most commonly Aspergillus and most commonly seen in immunocompromised patients.


Causes

  • Sinusitis predisposed by a number of local and systemic factors. Any local condition that interferes with normal sinus drainage predisposes to the development of infection. Obstruction of the sinus outflow tract may be due to mucosal swelling (allergic rhinitis, viral URI) or mechanical obstruction (nasal polyp, foreign body, tumor, anatomic abnormality). The obstruction will decrease oxygen supply to the sinus that in turn will result in 1) vasodilation of local vasculature, 2) ciliary dysfunction, and 3) mucus gland dysfunction. These events conspire to cause transudation and stagnation of the viscid fluid thus leading to acute rhinosinusitis with retained thick secretions. Instrumentation (with nasotracheal, nasogastric, orotracheal, or orogastric tubes) is an essential risk factor for ABRS. In fact, in a study of pediatric intensive care unit (PICU) patients, Moore et al found that almost 50% of PICU patients who underwent imaging for reasons other than assessment for sinus abnormality had evidence of sinusitis. This finding raised the concern that sinusitis in PICU patients is frequent and should be considered in the differential diagnosis of fever in PICU patients.
  • Other risk factors for sinusitis include:

Anatomic defects such as septal deviations, polyps, conchae bullosa, other trauma and fractures involving the sinuses or the facial area surrounding them Impaired mucous transport from diseases such as cystic fibrosis, ciliary dyskinesia Immunodeficiency from chemotherapy, HIV, diabetes mellitus, etc. Body positioning, intensive care unit (ICU) patients due to prolonged supine positioning that compromises mucociliary clearance. Rhinitis medicamentosa, toxic rhinitis, nasal cocaine abuse, barotrauma, foreign bodies Prolonged oxygen use due to drying of mucosal lining Patients with nasogastric or nasotracheal tube


Differentiating [disease name] from other Diseases

For further information about the differential diagnosis, click here.

Epidemiology and Demographics

There are higher rates of sinusitis in the South, Midwest, and among women.

  • The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
  • In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].

Age

  • Patients of all age groups may develop sinusitis but more commonly observed among children younger than 15 years of age and adults aged 25 to 64 years.


Gender

  • Women are more commonly affected with sinusitis than men.


Race

  • There is no racial predilection for sinusitis.
  • [Disease name] usually affects individuals of the [race 1] race.
  • [Race 2] individuals are less likely to develop [disease name].

Risk Factors

  • Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].


Natural History, Complications and Prognosis

  • The majority of patients with [disease name] remain asymptomatic for [duration/years].
  • Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
  • If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
  • Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
  • Prognosis is generally [excellent/good/poor], and the [1/5/10­year mortality/survival rate] of patients with [disease name] is approximately [#%].

Diagnosis

Diagnostic Criteria

  • The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
  • [criterion 1]
  • [criterion 2]
  • [criterion 3]
  • [criterion 4]

Symptoms

  • [Disease name] is usually asymptomatic.
  • Symptoms of [disease name] may include the following:
  • [symptom 1]
  • [symptom 2]
  • [symptom 3]
  • [symptom 4]
  • [symptom 5]
  • [symptom 6]

Physical Examination

  • Patients with [disease name] usually appear [general appearance].
  • Physical examination may be remarkable for:
  • [finding 1]
  • [finding 2]
  • [finding 3]
  • [finding 4]
  • [finding 5]
  • [finding 6]

Laboratory Findings

  • There are no specific laboratory findings associated with [disease name].
  • A [positive/negative] [test name] is diagnostic of [disease name].
  • An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
  • Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

Electrocardiogram

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

X-ray

There are no x-ray findings associated with [disease name].

OR

An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Echocardiography or Ultrasound

There are no echocardiography/ultrasound findings associated with [disease name].

OR

Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

CT scan

There are no CT scan findings associated with [disease name].

OR

[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

MRI

There are no MRI findings associated with [disease name].

OR

[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Other Imaging Findings

There are no other imaging findings associated with [disease name].

OR

[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

  • [Disease name] may also be diagnosed using [diagnostic study name].
  • Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

  • There is no treatment for [disease name]; the mainstay of therapy is supportive care.
  • The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
  • [Medical therapy 1] acts by [mechanism of action 1].
  • Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Surgery

  • Surgery is the mainstay of therapy for [disease name].
  • [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
  • [Surgical procedure] can only be performed for patients with [disease stage] [disease name].

Prevention

  • There are no primary preventive measures available for [disease name].
  • Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
  • Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].

References