ENT Flashcards
Acute Otitis Media- Dr Deac
D: Acute otitis media (AOM) is defined as the presence of inflammation in the middle ear, associated with an effusion, and accompanied by the rapid onset of symptoms and signs of an ear infection that is very common in children, rarely in adults. The cause Is either viral (rhinovirus, adenovirus, enterovirus, RSV) or bacterial. In bacterial cases, the cause is usually haemophilia influenzae or streptococcus pneumoniae (but this is less common since the intro of the pneumococcus vaccination). Self limiting.
R: Most common in younger children <3. In children >3 years old, OME (otitis media with effusion) is more common. AOM is a risk factor for OME and may present as co-existing conditions.
Peak incidence between 6-18 months.
It most commonly affects children from birth to 4 years of age, especially those who are subject to passive smoking, attend daycare or nursery, are formula-fed, or have craniofacial abnormalities (such as cleft palate).Most common in winter months, due to association with URTI.
D: Other causes of middle ear inflammation or effusion include:
Otitis media with effusion (glue ear) — fluid in the middle ear without symptoms or signs of acute infection. On examination with an otoscope, an effusion and air fluid levels or bubbles are visible, with normal tympanic membrane landmarks. The most common presentation is conductive hearing loss. Chronic suppurative otitis media — persistent inflammation and perforation of the tympanic membrane with draining discharge for more than 2 weeks. Myringitis — erythema and injection of the tympanic membrane are visible on otoscopy but there are no other features of otitis media. . Earache is a common problem, and can also be caused by otitis externa. Causes of ear pain also include eustachian tube dysfunction, mastoiditis, malignancy, and referred pain.
E: male sex, Prevalence varies globally, with an average incidence rate of 3.6 new episodes per 100 people per year in central Europe compared with 43.4 for Sub-Saharan West Africa and central Africa. There is a seasonal variation in cases, with AOM occurring most commonly in the winter, and in children born in the autumn
A: Acute otitis media (AOM) can be caused by both viruses and bacteria, and commonly both are present at the same time. The most common bacterial pathogens are Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, and Streptococcus pyogenes. Viral pathogens associated with AOM include respiratory syncytial virus (RSV), rhinovirus, adenovirus, influenza virus, and parainfluenza virus. In recurrent AOM, the microbiology may be more complex, but the most common bacterial pathogens are the same as occasional episodes.
C: • In older children and adults, AOM usually presents with earache. Younger children may hold or rub their ear, or may have non-specific symptoms such as fever, crying, poor feeding, restlessness, cough, or rhinorrhoea.
• On examination the tympanic membrane is distinctly red, yellow, or cloudy and may be bulging.
• Pain and fever should be managed with paracetamol or ibuprofen
ear pain, reduced hearing in the affected ear and general symptoms of airway infection such as fever, cough, coryzal symptoms, sore throat and generally feeling unwell. It is worth noting that symptoms can be very non-specific, particularly in young children and infants. They may present with symptoms of fever, vomiting, irritability, lethargy or poor feeding. It is always worth examining the ears in unwell children. Decreased sleep.
AOM-PIMP
P: Upper respiratory tract infection, becterial or viral. This leads to inflammation and oedema of respiratory mucosa of the nose, nasopharynx and eustachian tube. There is obstruction of the eustachian tube isthmus, enlarged adenoids. Obstruction results in accumulation of secretions normally produced in middle ear. Air from middle ear is resorbed into the circulation creating negative pressure. Negative pressure in the middle ear pulls viruses and bacteria into it, infecting and inflaming the middle ear. This leads to systemic release of inflammatory cytokines, disrupting hypothalamic thermoregulation, fever. Increase pressure in middle ear stretches typanic membrane, bulging TM, otalgia. Inflammation in middle ear causes vasodilation of tympanic membrane (TM) blood vessels. Neutrophilic infiltration of middle ear to phagocytoze pathogens, creates yellow or white pus behind TM. Effusion (inflammatory fluid) behind tympanic membrane. Most (75-80%) resolve by 72 hours. If not–> compliication.
I: On otoscopic examination:
A distinctly red, yellow, or cloudy tympanic membrane.
Moderate to severe bulging of the tympanic membrane, with loss of normal landmarks and an air-fluid level behind the tympanic membrane (indicates a middle ear effusion).
Perforation of the tympanic membrane and/or discharge in the external auditory canal. Note that clinical features not suggestive of AOM include a tympanic membrane which is not bulging (with or without erythema or cloudiness), and an air-fluid level without a bulging tympanic membrane.
Always examine both ears and the throat of unwell children. These are common sites of infection and can produce non-specific symptoms. Use an otoscope to visualise the tympanic membrane whilst gently pulling the pinna up and backwards. It may be difficult to visualise the tympanic membrane if there is significant discharge or wax in the ear canal.
In a normal child the tympanic membrane should be “pearly-grey”, translucent and slightly shiny. You should be able to visualise the malleolus through the membrane and a cone of light reflecting the light of the otoscope.
Otitis media will give a bulging, red, inflamed looking membrane. When there is a perforation, you may see discharge in the ear canal and a hole in the tympanic membrane.
Management: • Pain and fever should be managed with paracetamol or ibuprofen.
• Many people with AOM will not need antibiotic treatment as symptoms usually resolve spontaneously within a few days. However, antibiotics are necessary in a number of situations, including for:
o People who are systemically very unwell.
o People who have symptoms and signs of a more serious illness or condition.
o People who have a high risk of complications.
• If an antibiotic is required, a 5–7 day course of amoxicillin is recommended first-line. Clarithromycin or erythromycin are alternatives for people who are allergic to penicillin (erythromycin is preferred in pregnant women).
• The following groups of people should be admitted to hospital for immediate specialist assessment:
o People with a severe systemic infection.
o People with suspected complications of AOM, such as meningitis, mastoiditis, intracranial abscess, sinus thrombosis, or facial nerve paralysis.
o Children younger than 3 months of age with a temperature of 38°C or more.
• Management of persistent AOM involves:
o Reassessing the person.
o Considering the need for paediatric or ENT referral or admission, depending on the clinical situation.
o Considering a first-line antibiotic (if not already prescribed) or a second-line antibiotic if the initial treatment was ineffective.
• Measures to prevent recurrent AOM include:
o In children — avoiding exposure to passive smoking, use of dummies, and flat, supine feeding; and ensuring that children have had a complete course of pneumococcal vaccinations as part of the routine childhood immunization schedule.
o In adults — avoiding smoking and/or passive smoking
Most cases of otitis media will resolve without antibiotics, and NICE guidelines from 2018 highlight the importance of not providing antibiotics for otitis media. They state that most cases of otitis media will resolve within 3 days without antibiotics, but it can last for up to a week. Complications (mainly mastoiditis) are rare. Give simple analgesia to help with pain and fever.
P: Complications of AOM include recurrence of infection, hearing loss, tympanic membrane perforation, and rarely, mastoiditis, meningitis, intracranial abscess, sinus thrombosis, and facial nerve paralysis.
Choleostoma DR
D:A cholesteatoma is a skin growth that occurs in an abnormal location, the middle ear behind the eardrum. It is usually caused by repeated infection that causes an ingrowth of the skin of the eardrum. Cholesteatomas often take the form of a cyst or pouch that sheds layers of old skin that builds up inside the ear.A cholesteatoma is an abnormal sac of keratinizing squamous epithelium and accumulation of keratin within the middle ear or mastoid air cell spaces which can become infected and also erode neighbouring structures. Cholesteatomas are usually acquired, but rarely can be congenital.
R:Male sex — studies consistently identify a preponderance of male cases, with an estimated male:female ratio of 3:2.
Middle ear disease — cholesteatoma is usually preceded by a history of middle ear disease, such as otitis media.
Eustachian tube dysfunction — typically following an episode of otitis media. Eustachian tube dysfunction promotes invagination of the tympanic membrane, which is the first stage in the process of the formation of a retraction pocket.
Otological surgery or traumatic blast to ear — may result in implantation of viable keratinocytes into the middle ear cleft.
Congenital anomalies and genetic syndromes — anomalies associated with compromised eustachian tube function can increase the risk of cholesteatoma. These include cleft palate, certain craniofacial abnormalities, and Turner’s or Down’s syndrome.
Family History — occasionally, familial clusters of cholesteatoma have been observed, suggesting that genetic variants underlie the disease in rare cases.
Social deprivation — has been inconsistently linked with cholesteatoma. A UK study using data from 2009 to 2012 found a correlation between level of social deprivation and number of mastoid operations (and therefore cholesteatoma).
Use of bisphosphonates — this has been identified as a possible risk factor for the development of cholesteatoma.
The combination of unilateral foul smelling discharge and deafness should always raise the question of a cholesteatoma. If on examination you suspect a cholesteatoma then an ENT referral is needed.
Otitis media would present with pain. Otitis externa would present with inflammation and swelling of the ear canal. Impacted wax would cause deafness but unlikely to cause a foul smelling discharge. It is unlikely for a 45-year-old woman to have a foreign body in her ear for 3 weeks.
Choleostoma-DEAC
D: The differential diagnoses of cholesteatoma include:
Otitis media with effusion — for more information see the CKS topic on Otitis media with effusion.
Otitis externa — for more information see the CKS topic on Otitis externa.
Tympanosclerosis — the white appearance of fibrotic scarring of the tympanic membrane, commonly seen after grommet insertion, can give the impression of a cholesteatoma deeper within the middle ear.
Osteonecrosis of the external auditory canal — can occur as a rare complication of bisphosphonate treatment.
Benign necrotising otitis externa — suggested by severe otalgia and a history of diabetes or immunosuppression. On otoscopy there are granulations in the ear canal but no evidence of cholesteatoma.
Myringitis — suggested by inflammation of the tympanic membrane with or without granulations, but no evidence of cholesteatoma.
Suspect cholesteatoma in a person with:
Recurrent or chronic purulent aural discharge, which may be unresponsive to antibiotic therapy. Discharge is malodorous and may be scant.
Hearing loss or tinnitus — hearing loss may go unnoticed by some people.
Less commonly, otalgia, vertigo, or facial nerve (VII) involvement (altered taste or facial weakness) may be present, often indicating more advanced disease.
E: Annual incidence ranges from 7 per 100,000 (reported in studies undertaken in Denmark and Iowa) to 13 per 100,000 (reported in studies in Scotland).
Estimates of annual surgical incidence range from 0.12 per 100,000 (Denmark) and 66 per 100,000 (Israel).
It has been estimated that a general practitioner with a list size of 2,500 patients would expect to see on average one new case of cholesteatoma every 4–5 years.
A: Disease starts in childhood. It is the sequela of acute otitis. The perforation central and becomes permanent and permits repeated infection from the external ear. Ascending infections via the eustachian tube. Infection from tonsils, adenoids and infected sinuses may be responsible for persistent or recurring otorrhoea. Persistent mucoid otorrhoea is sometimes the result of allergy to ingestaants such as milk, eggs, fish, etc. Acquired cholesteatomas are thought to most commonly arise when chronic negative middle ear pressure (due to eustachian tube dysfunction) causes an area of the tympanic membrane to be retracted inwards to form a retraction pocket. This pocket then forms a pouch with a narrow neck, which traps squamous cells with keratin accumulation and retention, these proliferate, leading to expansion and cholesteatoma formation. The outermost layer of the cholesteatoma, the basal layer of the skin, is metabolically active, producing proteolytic enzymes which are locally destructive, which can erode the adjacent bone. Initially the incus is at risk, then the stapes. With progression of the disease, the facial nerve, cochlea, semi-circular canals, mastoid bone and the roof of the middle ear can be affected.
Alternatively, an acquired cholesteatoma may arise if squamous epithelium migrates through a defect in the tympanic membrane, or due to implantation of viable keratinocytes into the middle ear cleft following otological surgery or after a traumatic blast injury.
Congenital cholesteatomas are thought to arise when squamous epithelium becomes trapped within the middle ear during embryogenesis and then gradually enlarges, causing destruction and damage to the ear and surrounding structures.
C: Cholesteatoma may be asymptomatic in its early stages.
Cholesteatoma most commonly presents with a persistent or recurrent discharge from the ear that is often foul smelling. An associated conductive hearing loss may also occur.
Rarely with progression of the disease, vertigo, sensorineural hearing loss, facial nerve palsy, meningitis, or intracranial abscess may develop.
The diagnosis requires clear visualisation of the tympanic membrane. If the tympanic membrane can be seen, a cholesteatoma should be suspected if there is:
Evidence of ear discharge.
Presence of a deep retraction pocket, with or without granulation tissue and skin debris.
Crust or keratin in the upper part of the tympanic membrane.
The tympanic membrane may be perforated.
Congenital cholesteatoma (rare) may appear as a white mass behind an intact tympanic membrane, in a person with no prior history of ear discharge, tympanic membrane perforation, or surgical procedures on the ear.
May be asymptomatic
Painless otorrhea (scant but foul-smelling discharge from the affected ear)
Conductive hearing loss
Occurs late in primary cholesteatoma
Occurs early in secondary cholesteatoma
Choleostoma-PIMP
P: The accumulation of skin in the middle ear can cause many problems and damage nearby structures. One of the most common problems is hearing loss due to the erosion of the middle ear bones. The cholesteatoma causes an inflammatory reaction that releases lytic enzymes, growth factors, and cytokines which can recruit osteoclasts to initiate destruction of bone. Cholesteatoma, if left untreated, can also erode the bony confines of the middle ear and extend to adjacent areas such as the face, brain, and the neck. When cholesteatomas become infected, they can grow faster and cause more bony erosion. They can also cause a chronically draining ear, which is often foul smelling.
Keratinizing squamous epithelium grows from the tympanic membrane or the auditory canal into the middle ear mucosa or mastoid air cells.
Congenital cholesteatoma
Present at birth
Embryonic nests of epidermal cells that remain in the middle ear
Acquired cholesteatoma (more common)
Primary: eustachian tube dysfunction → tympanic membrane epithelium retracts inwards → retraction pocket
Secondary: epithelium migrates inwards, through a perforated tympanic membrane.
I: Otoscopic findings:
Primary acquired: retraction pocket with squamous epithelium and debris that often appears as a brown, irregular mass
Congenital and secondary acquired: white or pearly mass behind the tympanic membrane
Imaging: to assess the degree of bone destruction
X-ray of the mastoid process
CT scan of the temporal bone
MRI is only indicated if intracranial extension is suspected.
Audiometry: to assess the degree of hearing loss
M: For all people with suspected cholesteatoma, arrange semi-urgent referral to an ear, nose, and throat specialist.
Investigations carried out in secondary care will include an audiology assessment and a CT scan.
Prior to surgical treatment, aural discharge may be treated with topical antibiotics.
A commonly-employed surgical treatment for cholesteatoma is a canal wall up mastoidectomy, which allows removal of cholesteatoma but leaves the canal wall intact. This usually necessitates a second-look procedure after 9 to 12 months to examine for residual/recurrent disease.
Arrange emergency admission for people who have:
A facial nerve palsy or vertigo.
Other neurological symptoms (including pain) or signs that could be associated with the development of an intracranial abscess or meningitis.
M: Surgery is always indicated because of the risk of complications, under general anaesthetic. As well as removing the cholesteatoma, the surgeon may be able to improve your hearing. This can be done in a number of ways.
For example, a tiny artificial hearing bone (prosthesis) can be inserted to bridge the gap between your eardrum and the cochlea (hearing organ). In some cases, it may not be possible to reconstruct the hearing or a further operation may be needed.
P: Destruction of ear ossicles
Perilymph fistula
Facial nerve paralysis
Erosion of temporal bone → extradural abscess, meningitis, sigmoid sinus thrombosis. Damage to facial nerve. A cholesteatoma can come back, and you could get one in your other ear, so you’ll need to attend regular follow-up appointments to monitor this.
Sometimes a second operation is needed after about a year to check for any skin cells left behind. However, MRI scans are now often used instead of surgery to check for this.
Chronic (supprative) otitis media Dr
D: Chronic otitis media (OM) refers to a group of chronic inflammatory diseases of the middle ear, which often affects children.
R: he condition is often seen in patients with a history of acute otitis media with TM rupture. Risk factors for chronic suppurative otitis media include:
Younger age - children under five years old are most commonly affected.
Allergy/atopy.
Upper respiratory tract infection.
Acute or recurrent otitis media.
Exposure to second-hand smoke.
Social deprivation.
Snoring.
Chronic (supprative) otitis media DEAC
D: The differential diagnoses of chronic suppurative otitis media (CSOM) include:
Otitis externa — suggested by ear pain, itching, discharge, and reduced hearing. Examination may reveal an inflamed, eczematous canal without a perforation. Can also be concurrent with CSOM. See the CKS topic on Otitis externa for more information.
Acute suppurative otitis media (ASOM) — suggested by ear pain, fever, vomiting in children, reduced hearing, and discharge if the eardrum perforates (or examination may reveal pus in the middle ear). Most cases resolve spontaneously within a few days. See the CKS topic on Otitis media - acute for more information.
Otitis media with effusion (OME) — suggested by fluid in the middle ear without acute signs or symptoms. See the CKS topic on Otitis media with effusion for more information.
A foreign body.
Impacted ear wax.
A cholesteatoma — suggested by chronic smelly ear discharge, and the presence of squamous epithelium and keratin in the middle ear. See the CKS topic on Cholesteatoma for more information.
Neoplasm — suggested by an ear canal swelling that bleeds on contact.
Osteonecrosis of the external auditory canal — consider in people receiving denosumab who present with chronic ear infection or suspected cholesteatoma.
E: most common in children and adolescents > 15 years old
A: bacterial infection following perforation of the tympanic membrane due to
(Recurrent) acute otitis media
Placement of ventilation tube
Trauma.
C: Painless, recurrent otorrhea (usually odorless; mucoid or serous )
Conductive hearing loss → Weber test lateralizes to the affected ear
Possibly development of concurrent cholesteatoma
Fever is not typical and indicative of complications if it occurs.
Suspect chronic suppurative otitis media (CSOM) in a person with:
Ear discharge persisting for more than 2 weeks, without ear pain or fever.
Hearing loss in the affected ear.
A history of acute otitis media (AOM), ear trauma, or glue ear and grommet insertion. See the CKS topics on Otitis media - acute and Otitis media with effusion for more information.
A history of allergy, atopy, and/or upper respiratory tract infection.
Tinnitus and/or a sensation of pressure in the ear may also be present.
Chronic (supprative) otitis media -pimp
P: infection secondary to translocation of bacteria of the external ear canal into the middle ear through the perforated tympanic membrane
I: Clinical diagnosis
Otoscopy: visible defect of the tympanic membrane → confirmation of diagnosis
Cranial CT or MRI: if complications are suspected (see below)
M: Goal: restore integrity of the tympanic membrane , prevent permanent hearing loss
Conservative treatment: rinsing of the ear; topical antibiotic (e.g., ciprofloxacin) and steroid drops (e.g., dexamethasone)
Surgical treatment: tympanoplasty with insertion of a graft
P/C: Complications
Possibly life-threatening spread of infection (e.g., meningitis, intracranial abscess, facial paralysis); rarely occurs with adequate treatment
Tympanosclerosis
Scarring of the tympanic membrane due to recurrent ear infections or otitis media with effusion
May be asymptomatic or lead to conductive hearing loss
White calcified plaques in the tympanic membrane seen on otoscopy
Prognosis: usually good with adequate treatment; conductive hearing loss can often be improved, but may not be fully recovered
Earache (otalgia)-dr
D: earache. Otalgia is defined as ear pain. Two separate and distinct types of otalgia exist. Pain that originates within the ear is primary otalgia; pain that originates outside the ear is referred otalgia. [1, 2]
Typical sources of primary otalgia are external otitis, otitis media, mastoiditis, and auricular infections. Most physicians are well trained in the diagnosis of these conditions
R:
earache: deac
Differential diagnosis:
E: Otalgia is very common, especially in children, and most cases are transient[1].
A: Primary causes are those that originate in the ear and are a direct cause of pain through stimulation of nociceptor fibres. Secondary causes are those that the patient feels have originated from the ear, but in fact are referred from other sources and require a higher index of suspicion to determine the precise aeitiology. Additionally, primary otalgia seems to be more common in children and secondary otalgia more common in adults.
Primary causes: infection, trauma and foreign bodies, impacted cerumen, otalgic neoplasms.
Secondary: dental inflammation and infection, temporomandibular joint disorders, trigeminal neuralgia, head and neck cancer, eagle’s syndrome, temporal arteritis.
C: earache. History - especially pertaining to onset, and precipitating factors - eg, noise, duration, discharge, fever, swallowing disorder, dental history.
Examination - auroscopy looking for causes - eg, otitis media, cerumen.
If auroscopy is unremarkable, consider referred causes of pain and examine the cranial nerves, especially V, IX and X. Also examine - the nose, sinuses, oropharynx and nasopharynx (occult carcinoma often presents with otalgia), TMJ , parotid glands, larynx, and trachea.
earache/otalgia pimp
p- the most common causes are otitis media and otitis externa.
i-Examination - auroscopy looking for causes - eg, otitis media, cerumen.
If auroscopy is unremarkable, consider referred causes of pain and examine the cranial nerves, especially V, IX and X.
M-Analgesia.
Treat the underlying cause.
If no cause is found, consider re-reviewing the patient in a few days.
If pain continues and still the cause is unclear, consider referral to specialist to exclude a sinister cause of otalgia.
P-Almost 50% of patients will have spontaneous resolution of otalgia with no underlying cause detectable
Rhinitis, Dr
D: Rhinitis usually refers to inflammation of the nasal mucosa as a result of a type 1 hypersensitivity reaction (allergic rhinitis) and/or upper respiratory tract infection (infectious rhinitis). Allergic rhinitis: an IgE-mediated process
Non-allergic rhinitis: not the result of an IgE-mediated process
Infectious rhinitis
Vasomotor rhinitis
R: Colds and allergies such as atopy, asthma, eczema and other allergic diseases.
Rhinitis -DEAC
D:
Nasal polyps
Deviated nasal septum
Adenoid hypertrophy (in case of children)
Foreign nasal body
Epidemiology: mostly young children (2–5 years)
Etiology: organic (e.g., food items) or inorganic objects (e.g., pearls, stones, small toys) are inserted into the nose
Clinical features
Unilateral, foul smelling, purulent rhinorrhea
Nasal obstruction
Epistaxis
Diagnostics
Headlight or otoscope
Flexible fiberoptic endoscopy
Treatment: removal through positive pressure techniques ; if this fails, extraction via endoscopy and anesthesia
Infective rhinitis
There is an acute onset of symptoms of one week or less, with typical features of an associated viral upper respiratory tract infection, such as cough, fever, or lymphadenopathy. If nasal discharge is clear, infection is less likely. See the CKS topic on Common cold for more information.
Non-allergic rhinitis
Autonomic or irritant rhinitis
Symptoms typically follow a known physical exposure (changes in temperature or humidity, or with exercise) or chemical irritant exposure (volatile chemicals such as perfumes, tobacco smoke, and odours). These triggers cause nasal airway hyper-reactivity through a non-IgE mediated pathway.
Drugs
A number of drugs may cause or aggravate rhinitis symptoms, such as alpha-blockers, angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, chlorpromazine, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and cocaine.
Rebound symptoms and a paradoxical increase in nasal congestion may occur when stopping prolonged treatment with intranasal decongestants due to rebound vasodilatation (so-called ‘rhinitis medicamentosa’). See the section on Intranasal decongestants in Prescribing information for more information.
Endocrine
Hormonal rhinitis should be considered when symptoms coincide with pregnancy, starting the oral contraceptive pill, hormone replacement therapy (HRT), or hypothyroidism. See the CKS topics on Contraception - combined hormonal methods and Hypothyroidism for more information.
Food and drink
Alcohol, sulphites, and spicy foods may cause rhinorrhoea and facial flushing.
Non-allergic rhinitis with eosinophilia syndrome (NARES)
This rare condition is a diagnosis of exclusion characterized by nasal eosinophils in people with perennial symptoms, and occasionally reduced sense of smell.
50% of people develop aspirin-sensitive disease with asthma and nasal polyposis later in life.
Systemic
May be caused by primary defects in mucus production (for example, cystic fibrosis), primary ciliary dyskinesia (Kartagener syndrome), and granulomatous disease (for example, Wegener’s granulomatosis and sarcoidosis).
Structural
Typically caused by deviated nasal septum, nasal polyps, hypertrophic turbinates, adenoidal hypertrophy, foreign body, or cerebrospinal fluid (CSF) leak (rare), for example.
Sinonasal tumour (rare) should be excluded if there are unilateral symptoms, recurrent bloody nasal discharge or nosebleeds, nasal pain, anosmia, or visual disturbance. See the CKS topic on Epistaxis (nosebleeds) for more information.
E: Estimates of the prevalence of allergic rhinitis range from as low as 9% to as high as 42%. Although the prevalence of nonallergic rhinitis has not been studied definitively, it appears to be very common with an estimated prevalence in the United States of approximately 19 million
A: Allergic rhinitis: Etiology
Type I hypersensitivity reaction
Genetic predisposition to atopy
Most often idiopathic
Drug-induced rhinitis is caused by one of the following drugs:
Antihypertensives (e.g., ACE inhibitors, propanolol)
NSAIDs
Rhinitis medicamentosa: rebound nasal congestion that is seen upon discontinuing intranasal sympathomimetics (e.g., xylometazoline)
Gustatory rhinitis: rhinitis that is associated with spicy food and/or alcohol
Emotional stimuli (e.g., anxiety, excitement)
Irritant odors (e.g., cigarette smoke, perfumes, car exhaust)
Weather patterns (e.g. cold and dry air, changes in temperature and humidity)
Honeymoon rhinitis: rhinitis associated with sexual activity
Hormonal rhinitis
Rhinitis associated with pregnancy and the use of oral contraceptive pills
Rhinitis associated with hypothyroidism.
C: Recurrent episodes of sneezing, nasal congestion, rhinorrhea, and post-nasal drip
Itchy nose and throat
Pale, boggy nasal mucosa with hypertrophic turbinates, and/or nasal polyps may be seen in long-standing cases of allergic rhinitis.
Cobblestone appearance of the posterior pharyngeal wall
Associated allergic conditions
Allergic conjunctivitis
Atopic dermatitis and/or bronchial asthma
Long-standing allergic rhinitis can predispose the patient to recurrent sinusitis and/or otitis media. Suspect a diagnosis of allergic rhinitis if alternative causes for rhinitis have been excluded, and a person presents with typical clinical features:
Classic symptoms of sneezing, nasal itching, nasal discharge (rhinorrhoea), and nasal congestion — bilateral symptoms typically develop within minutes following allergen exposure.
Additional symptoms such as postnasal drip, itching of the palate, and cough; and features suggestive of chronic nasal congestion, such as snoring, mouth breathing, and halitosis.
Associated eye symptoms such as bilateral itching, redness, and tearing. See the CKS topic on Conjunctivititis - allergic for more information.
A personal or family history of atopy (asthma, eczema, or allergic rhinitis). See the CKS topics on Asthma and Eczema - atopic for more information.
Symptoms which occur following exposure to a known causative allergen, such as:
Tree pollens — intermittent or chronic symptoms occur from early to late spring.
Grass pollens — intermittent or chronic symptoms occur from late spring to early summer. Can be occupational: symptoms improve on holidays, away from work, weekends. Hypertrophic turbinates may be seen in long-standing cases of vasomotor rhinitis.
Rhinitis -PIMP
P: Genetic, environmental. Antigen presenting cells (APCs), such as dendritic cells in the mucosal surface, process allergens and present some peptides from allergens on the major histocompatibility complex (MHC) class II molecule.10 This MHC class II molecule and antigen complex take a role as the ligand of T-cell receptors on Naive CD4+ T cells, which result in differentiation of Naive CD4+ T cells to allergen-specific Th2 cell. Activated Th2 cells secret several cytokines, which induce isotype switching of B cells to produce specific IgE and proliferation of eosinophils, mast cells and neutrophils (Fig. 1).11 Produced antigen-specific IgE binds to high-affinity IgE receptors on mast cells or basophils. When AR patients are exposed to allergens, allergic reactions develop in 2 different patterns according to time sequence. One is the early reaction, in which sneezing and rhinorrhea develops in 30 minutes and disappears. The other is the late reaction, which shows nasal obstruction approximately 6 hours after exposure to allergens and subsides slowly. The early reaction is the response of mast cells to offending allergens (type I hypersensitivity). Stimulated mast cells induce nasal symptoms by secreting chemical mediators such as histamine, prostaglandins and leukotrienes.12 In contrast to the early reaction, eosinophil chemotaxis is the main mechanism in the late reaction, which is caused by chemical mediators produced in the early reaction. Several inflammatory cells, eosinophils, mast cells and T cells migrate to nasal mucosa, break up and remodel normal nasal tissue,13 and these processes result in nasal obstruction which is the main symptom of AR patients.
House dust mites
These feed on shed human skin flakes which are particularly abundant in mattresses, bed bases, pillows, carpets, upholstered furniture, and furry toys.
Their growth is maximal at temperatures above 20°C and when humidity is above 80%. When humidity falls below 50%, they die.
They are present all year-round, but their numbers tend to peak in the spring and autumn.
Grass, tree, and weed pollens
The length, duration, and intensity of the pollinating season varies from year to year, which can complicate identification of the responsible allergen.
Trees generally pollinate in the spring.
Grasses pollinate at the end of spring and beginning of summer.
Weeds may pollinate from early spring to late autumn.
Moulds
Indoor moulds such as Alternaria, Cladosporium, and Aspergillus may be associated with damp environments.
Animal dander
Cat and dog hair are the most common animal allergens, which cause perennial symptoms.
Less commonly, dander from horses, cattle, rabbits, and rodents (such as guinea pigs, hamsters, and rats) may cause allergic rhinitis.
Occupational
The incidence of allergic rhinitis is increased in certain occupations, such as working with latex gloves, chlorine, flour, wood dust, or laboratory animals.
Typically, there is a defined latency period of months to years, during which sensitization to a causal agent occurs.
I: RAST (radioallergosorbent test): measures serum concentrations of IgE antibodies against a specific allergen
Prick and intradermal tests to identify the allergen
M:
Avoid the trigger. Hoovering and changing pillows regularly and allowing good ventilation of the home can help with house dust mite allergy. Staying indoors during high pollen counts can help with hay fever symptoms. Minimise contact with pets that are known to trigger allergies.
Oral antihistamines are taken prior to exposure to reduce allergic symptoms:
Non-sedating antihistamines include cetirizine, loratadine and fexofenadine
Sedating antihistamines include chlorphenamine (Piriton) and promethazine
Nasal corticosteroid sprays such as fluticasone and mometasone can be taken regularly to suppress local allergic symptoms.
Nasal antihistamines may be a good option for rapid onset symptoms in response to a trigger.
Referral to an immunologist may be necessary if symptoms are still unmanageable.
Avoid exposure to the putative allergen (e.g., allergen, dust).
1st line: use one or more of the following drugs
Intranasal sprays
Antihistamines (e.g., azelastine)
Decongestants (α1-sympathicomimetics such as phenylephrine, oxymetazoline, xylometazoline)
Corticosteroids (e.g., budesonide, fluticasone)
Sodium cromoglycate
Ipratropium bromide
Oral drugs
Antihistamines (e.g., cetirizine, levocetirizine, loratadine)
Decongestants (α1-sympathicomimetics such as phenylephrine and pseudoephedrine)
Leukotriene receptor antagonists (e.g., monteleukast)
2nd line: controlled exposure to gradually increasing doses of the allergen in order to hyposensitize the IgE response (imunotherapy)
3rd line: resection of hypertrophic nasal turbinates to relieve nasal obstrubenign lesions of the nasal mucosa or paranasal sinuses due to chronic mucosal inflammatiotion
P: The 2016 revision of the Allergic Rhinitis and its Impact on Asthma (ARIA) international guideline notes that it is a condition that usually persists throughout life.
Nasal Polyps -Dr
D: benign lesions of the nasal mucosa or paranasal sinuses due to chronic mucosal inflammation. Nasal polyps are painless soft growths inside your nose. They’re not usually serious, but they can keep growing and block your nose if not treated.
Benign lesions of the nasal mucosa or paranasal sinuses due to chronic mucosal inflammation. Typically present with postnasal drip, bilateral nasal obstruction, and impaired olfactory function (from hyposmia to anosmia). Nasal polyps do not decrease in size following therapy with nasal decongestants.
R: Chronic rhinosinusitis
Cystic fibrosis (CF)
Aspirin exacerbated respiratory disease (AERD; aspirin or NSAID induced): triad of asthma, chronic sinusitis with polyps, and bronchospasm .They commonly occur in more general diseases such as late onset asthma in an adult patient, aspirin intolerance or cystic fibrosis. Late onset asthma rather than childhood asthma is associated with nasal polyps. RF also include frequent sinus infections, aspirin sensitivity or allergy, hay fever, cystic fibrosis, Chur-Strauss syndrome.
