eMedicine Specialties > Pediatrics: Surgery > Otolaryngology

Nasal Polyps: Differential Diagnoses & Workup

Author: John E McClay, MD, Associate Professor of Pediatric Otolaryngology, Department of Otolaryngology-Head and Neck Surgery, Children's Hospital of Dallas, University of Texas Southwestern Medical School
Contributor Information and Disclosures

Updated: Oct 22, 2008

Differential Diagnoses

Asthma
Cystic Fibrosis
Neuroblastoma
Neurofibromatosis
Rhabdomyosarcoma
Sinusitis

Workup

Laboratory Studies

  • Direct laboratory studies at the pathological process believed responsible for the nasal polyps.
  • Children with polyposis that is associated with allergic rhinitis should have an evaluation for their allergies; this may include a serological radioallergosorbent test (RAST) or some form of allergic skin testing. Mabry et al showed a decrease in the recurrence rate of polyps in children treated with immunotherapy directed at all antigens for which they are allergic, especially molds;4 therefore, allergy testing and treatment may be important in treating allergic fungal sinusitis (AFS).
  • Perform a sweat chloride test or genetic testing for cystic fibrosis (CF) in any child with multiple benign nasal polyps.
  • A nasal smear for eosinophils may differentiate allergic from nonallergic sinus diseases and indicate whether the child may be responsive to glucocorticoids. The presence of neutrophils may indicate chronic sinusitis.

Imaging Studies

  • The criterion standard to evaluate nasal lesions, especially nasal polyposis or sinusitis, is a thin-cut (1-3 mm) CT scan of the maxillofacial area, the sinuses axially, and the coronal plane. Perform a compatible CT scan if an intraoperative image-guided system is used. Plain film radiography has no significant value after polyps are diagnosed.
  • Also perform MRI in patients with possible intracranial involvement or extension of benign nasal polyps.
  • CT scan findings and MRI findings can help diagnose the polyp or polyps; define the extent of the lesion in the nasal cavities, sinuses, and beyond; and narrow the differential diagnosis of an unusual polyp or clinical presentation.
    • CF has a characteristic symmetrical bulging of the lateral nasal walls medially (see Media files 35-36 and Media file 40).
    • An antral-choanal polyp may show opacified maxillary sinuses with a protruding lesion heading from the maxillary antrum to the choana (see Media files 7-9).
    • A tumor, such as a rhabdomyosarcoma, may show extension of the lesion with invasion of surrounding mucosa (see Media files 19-20 and Media file 25).
    • A nasolacrimal duct cyst can show dilation of the nasolacrimal duct (see Media files 25-26).
    • An encephalocele can show expansion of the nasofrontal region (ie, foramen caecum) with herniation of brain or dura.
    • A glioma can show an isolated nasal lesion that may have a fibrous stalk to the CNS.
    • Patients with AFS exhibit heterogenous areas in the sinuses on CT and MRI scans; these areas consist of both the nasal polyposis and the allergic fungal mucin (see Media file 42 and Media file 44). This allergic fungal mucin appears black on MRI and can be confused with the absence of disease.

Procedures

  • See rigid and flexible endoscopy procedures described in Physical.

Histologic Findings

Histologically, nasal polyps are characterized by a pseudostratified ciliated columnar epithelium, thickening of the epithelial basement membrane, and few nerve endings. The stroma of nasal polyps is edematous. Vascularization is poor and lacks innervation, except at the base of the polyp. Authors report either hyperplasia of the seromucous glands or almost absent or rare glands when comparing the polyps to the inferior or middle turbinate. Hyperplasia of the gland can cause cystically dilated and degenerated glands containing inspissated mucous.

Eosinophil cells are the most commonly identified inflammatory cell, occurring in 80-90% of polyps. Eosinophils, which are found in the polyps of patients with bronchial asthma and allergy, contain granules with toxic products (eg, leukotrienes, eosinophilic cationic protein, major basophilic protein, platelet-activating factor, eosinophilic peroxidases, other vasoactive substances and chemotactic factors). These toxic factors are responsible for epithelial lysis, nerve damage, and ciliostasis. Specific granule protein, leukotriene A4, and platelet-activating factor apparently are responsible for the mucosal swelling and hyperresponsiveness.

Eosinophils in the peripheral blood and in normal nasal mucosa usually last 3 days. In a cell culture of nasal polyps, eosinophils were present at least 12 days. This delayed apoptosis of eosinophils is mediated, in part, by blockage of the Fas receptors, typically with proteases that help begin the process of cell death. Delayed apoptosis is also mediated by an increase in interleukin 5 (IL)-5, IL-3, and granulocyte-macrophage colony-stimulating factor (GM-CSF) secreted by T lymphocytes, which help sustain the eosinophil from death. Glucocorticoids seem to help reduce polyps or polypoid reactions in patients with tissue eosinophilia, possibly, in part, by inhibiting IL-5.

Another inflammatory cell, the neutrophil, occurs in 7% of polyp cases. This type of polyp occurs in association with CF, primary ciliary dyskinesia syndrome, or Young syndrome. These polyps do not respond well to corticosteroids because they lack corticosteroid-sensitive eosinophils. Degranulated mast cells are present. Degranulation presumably occurs in a nonimmunoglobulin E–mediated fashion. Increased numbers of plasma cells, lymphocytes, and myofibroblasts also occur.

Chemical mediators

The stroma of nasal polyps have numerous mediators, including cytokines, growth factors, adhesion molecules, and immunoglobulins; polyps also contain vasoactive amines, serotonin, prostaglandins, leukotrienes, norepinephrine, kinins, esterases, heparin, and histamine. The level of histamine in nasal polyps is 100-1000 times the level found in the blood stream.

  • Cytokines present in polyps
    • IL-1 - Found regularly
    • IL-3 - Varies, based on study, from absent to intermittent at low levels to regularly present
    • IL-4 - Inconsistently detected
    • IL-5 - Found regularly; IL-5 is essential for proliferation and differentiation of eosinophils. IL-5 is chemotactic to eosinophils, promotes the migration of eosinophils from the systemic circulation to the polyps, and inhibits eosinophil cell death.
    • IL-6 - Same as in controls (no increase)
    • IL-8 - Varies, based on study, from undetected to regularly detected; may cause sustained recruitment of leukocytes into nasal polyps and may decrease fibroblastic proliferation
    • IL-10 - Same as in controls; no increase regulated on activation, normal T cell expressed and secreted (RANTES); varies, based on study, from same as controls to regularly detected to increased levels interferon gamma; increases in eosinophils, seromucous glands, and epithelium of nasal polyps
  • Growth factors found in nasal polyps
    • Tumor necrosis factor (TNF) alpha and beta - Varies, based on study, from same as controls to regularly detected; believed to be from eosinophils
    • GM-CSF - mRNA and protein amount varies, based on study, from never to intermittent to present
    • Platelet derived growth factor - Present
    • Vascular permeable factors (VPFs) - Present
    • Vascular endothelial growth factors (VEGFs) - Present
    • Insulinlike growth factor I - Present
    • Stem cell factor - Present
  • Adhesion molecules
    • Vascular adhesion molecule 1 (VCAM-1) - Present
    • E and P selectin - Present
  • Immunoglobulins (Ig)
    • IgG - No increase; same levels as in the middle and inferior turbinate mucosa
    • IgA - More in polyps than in the middle and inferior turbinate mucosa, especially IgA1 over IgA2
    • IgM - No increase, same as in the middle and inferior turbinate mucosa
    • IgD - No increase, same as in the middle and inferior turbinate mucosa
    • IgE - Increased levels compared with the middle and inferior turbinate mucosa; same level in patients without allergy as in those with allergy

Staging

Polyposis has no uniform staging system.

More on Nasal Polyps

Overview: Nasal Polyps
Differential Diagnoses & Workup: Nasal Polyps
Treatment & Medication: Nasal Polyps
Follow-up: Nasal Polyps
Multimedia: Nasal Polyps
References

References

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Further Reading

Contributor Information and Disclosures

Author

John E McClay, MD, Associate Professor of Pediatric Otolaryngology, Department of Otolaryngology-Head and Neck Surgery, Children's Hospital of Dallas, University of Texas Southwestern Medical School
John E McClay, MD is a member of the following medical societies: American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Orval Brown, MD, Director of Otolaryngology Clinic, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center at Dallas
Orval Brown, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American Bronchoesophagological Association, American College of Surgeons, American Medical Association, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in Children, and Society of University Otolaryngologists-Head and Neck Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Alan D Murray, MD, Pediatric Otolaryngologist, ENT for Children; Full-Time Staff, Medical City Dallas Children's Hospital; Consulting Staff, Department of Otolaryngology, Medical Center of Lewisville, Children's Medical Center at Dallas, Cook Children's Medical Center; Full-Time Staff, Texas Pediatric Surgery Center, The Pediatric Surgery Center
Alan D Murray, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American College of Surgeons, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in Children, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Glenn C Isaacson, MD, FACS, FAAP, Professor of Otolaryngology-Head and Neck Surgery and Pediatrics, Temple University School of Medicine
Glenn C Isaacson, MD, FACS, FAAP is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American Bronchoesophagological Association, American College of Surgeons, American Laryngological Rhinological and Otological Society, American Society of Pediatric Otolaryngology, and Society of University Otolaryngologists-Head and Neck Surgeons
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