Classes of Non-Allergic Rhinitis Non-allergic rhinitis with eosinoiphilia Medication-related Hormone-related disorders:

Size: px

Start display at page:

Download "Classes of Non-Allergic Rhinitis Non-allergic rhinitis with eosinoiphilia Medication-related Hormone-related disorders:"

Aubrie Booth
5 years ago
Views:

1 Jan 10: Nasal Obstruction (updated 08/06) Preceptor: ; Vacation: Caroline and Tali 1. (Deya) Describe the treatment of allergic rhinitis. 2. (Deya) Are leukotrienes effective in allergic rhinitis? In general, three options are available for the management of allergic rhinitis: (1) avoidance & environmental controls, (2) pharmacotherapy, & (3) immunotherapy. 1. Environmental Controls depends on allergens. Avoid outdoors/close windows/use AC during relevant pollen seasons. To control dust mites, mold, & pet dander, reduce household humidity to below 50%; wash bed linens in hot water (>130 F weekly); remove carpets & pets from the most often used living areas, especially bedrooms; encase pillows, mattresses, & box springs in hypoallergenic coverings; eliminate cockroaches; use air purifiers. 2. Pharmacotherapeutic Measures selection based on symptoms, age, condition, related d/o s compliance hx, previous response to medications a. Antihistamines - antagonize the H 1 receptor mediated effects of histamine. Frequently first line. Effective in earlyphase rxn (reduce sneezing, rhinorrhea, & itching). Little effect on nasal congestion, a late-phase phenomenon. {PO: Allegra, Claritin, Clarinex, Zyrtec Nasal: Astelin} b. Decongestants - Act predominantly on α-adrenergic receptors of the mucosa of the respiratory tract producing vasoconstriction & thus reducing turbinate congestion. Do not relieve rhinorrhea, pruritus, & sneezing. Can cause rebound nasal congestion & cause dependency if used for more than 3 4 days (rhinitis medicamentosa). {Afrin} c. Intranasal & oral corticosteroids - Exert a wide range of effects on multiple cell types & mediators. Intranasal steroids may be the most effective med for overall control of allergic rhinitis sx s. Relieve sneezing, itching, rhinorrhea, & congestion. Maximal effect 1 to 2 weeks after onset of use. Effectiveness depends on regular use & proper application. Act on late phase rxn preventing influs of inflammatory cells. Minimal systemic absorption. {Nasacort, Rhinocort, Flonase, Nasonex} d. Mast cell stabilizers - Inhibit the release of mediators from mast cells. Intranasal cromolyn must be used before the onset of symptoms & must be used throughout entire exposure {Nasalcrom} e. Anticholinergic agents - Antagonize the action of acetylcholine at muscarinic receptors. Tend to control only rhinorrhea. {Atrovent} f. Leukotriene modifiers - Antagonize the action of leukotriene receptors or inhibit 5-lipoxygenase & the formation of leukotrienes. To date, clinical studies have shown its efficacy to be greater than that of placebo, but less effective than antihistamines & intranasal steroids in tx of allergic rhinitis {Singulair} 3. Immunotherapy - attempts to increase the threshold level of the appearance of symptoms after aeroallergen exposure. The exact mechanism of how immunotherapy works is still unclear; it may be the production of so-called "blocking" antibodies, as well as regulation of the immune cascade that causes allergic reactions. Indications include long-term pharmacotherapy, the inadequacy or intolerability of drug therapy, & significant allergen sensitivities. Administered through gradual increase in the dose of the antigen(s) given until either a mild systemic symptom or a large local reaction at the subcutaneous injection site occurs (optimal dose therapy). In some centers, sublingual immunotherapy is the method of choice. This is more common in Europe & tends to be easy & safe to administer at home by the patients themselves. A minimum of 2 3 years is usually given to avoid a rapid recurrence of symptoms in uncomplicated allergic rhinitis. 3. (Amy) What is non-allergic rhinitis? Elaborate on hormonal causes and therapies. Non-allergic rhinitis (NAR) refers to symptoms of rhinitis (nasal congestion, rhinorrhea, and sneezing) that are not related to an IgE mediated mechanism. Approximately 50% of patients with rhinitis have some component of NAR, with or without co-existing allergic rhinitis. Classes of Non-Allergic Rhinitis Non-allergic rhinitis with eosinoiphilia Medication-related: NSAIDS, ASA, cocaine, nasal decongestants, alpha antagonists, ACE inhibitors, beta-blockers, oral contraceptives, psychotropic agents Hormone-related disorders: hypothyroidism, acromegaly, puberty, pregnancy, postmenopausal 1/5

2 Irritant: temperature, barometric changes, gustatory, chemical exposure (perfume, pollution, fumes, corrosive agents suchs as organophosphates/hydrochloric acid) Atrophic rhinitis: cocaine abuse, surgery, aging, infectious (Klebsiella) Anatomic: septal deviation, turbinate hypertrophy, nasal valve collapse, choanal atresia/stenosis, septal perforation, cleft palate Infectious: acute rhinitis (bacterial, viral), acute/chronic sinusitis, sinonasal polyposis, Samter's triad, rhinoscleroma Neoplastic: inverting papilloma, malignancy Systemic Conditions: autoimmune (SLE, Sjogren's), vasculitis (Wegener's, sarcoidosis, Churg-Strauss), ciliary dyskinesias (Kartagener's, Young's), CF, hormonal Idiopathic / Vasomotor Nasal congestion and rhinorrhea are the primary presenting symptoms in hormonal rhinits. Fluctuating serume hormone levels during menstruation and puberty can lead to rhinitis. Hypothyroidism and acromegaly also associated with nasal symptoms that result from hormone imbalances; thyrotropic hormone release results in turbinate edema. Rhinitis during pregnancy is related to increased blood volume with resultant increased nasal vascular pooling and progesterone-induced vascular smooth muscle relaxation. Estrogen, progesterone, and placental growth hormone also exert direct effects on the nasal mucosa. Estrogen also increases central parasympathetic activity and increases feedback inhibition of sympathetic neurons. Pregnancy-related rhinitis improves towards the end of pregnancy as blood is directed toward the uterus. Therapy involves treatment of underlying systemic disorder and symptomatic care with nasal saline irrigations, antihistamines, decongestants, and nasal steroids. Antihistamines should be used with caution in the first trimester; decongestants have been associated with gastroschisis in the first trimester. Topical steroids may be used without risk to the fetus. 4. (Dara) Discuss atrophic rhinitis. Am J Rhinol 2001;15: Atrophic rhinitis is characterized by progressive nasal mucosal atrophy, nasal crusting, and enlargement of the nasal space producing paradoxical complaints of nasal congestion. Primary atrophic rhinitis has decreased markedly in incidence in the last century. This probably relates to the increased use of antibiotics for chronic nasal infection. Prior to antibiotics, primary atrophic rhinitis in westernized countries was commonly associated with infection from bacteria such as Kelbsiella. Secondary atrophic rhinitis resulting from trauma, surgery, granulomatous diseases, cocaine use, and radiation exposure accounts for the majority of cases encountered by the rhinologist today. Mucosal changes (loss of mucociliary clearance and neurologic regulation) lead to decreased function, decreased ability to condition inspired air and decreased secretion production resulting in alterations of the normal pattern of airflow and sensation of nasal congestion and obstruction. The article mentioned discusses 242 patients with the diagnosis of atrophic rhinitis between 1982 and The diagnosis was confirmed by physical examination, biopsy, and imaging studies. Patients were diagnosed with primary atrophic rhinitis if their condition developed in a previously healthy nose and secondary atrophic rhinitis if their condition developed after sinonasal surgery, trauma, or chronic granulomatous disease. Treatment includes antibiotics and nasal irrigations, but is frequently unsatisfactory. Surgery to alter nasal airflow may also be considered. 5. (amy) Rhinitis medicamentosa. Describe the underlying pathophysiology. Is it reversible? How do you treat it? Rhinitis medicamentosa is rebound vasodilation and nasal congestion that results from prolonged use of topical decongestants. Alphaadrenergic agents cause relase of norepinephrine from sympathetic nerves, resulting in contraction of dilated mucosal blood vessels. After extended vasoconstriction, the mucosal receptors become downregulated, requiring more frequent and higher doses for the same effect (tachyphylaxis). This effect usually occurs after 5-7 days of use. Many theories exist for the mechanism of the rebound vasodilatation: 1) rebound swelling from longer-lasting beta effects in sympathetic amines such as phenylephrine and ephedrine. 2) prolonged vasoconstriction resulting in tissue hypoxia with reactive hyperemia and vasodilatation. 3) stimulatation of a presynaptic negative feedback loop by alpha-2 agonists, resulting in suppresion of endogenous noradrenaline and rebound congestion after withdrawal of exogenous agent. 4) medication-induced increased parasympathetic activity, resulting in vascular permeability and edema formation by altering vasomotor tone. Treatment involves topical nasal steroids and withdrawal of the decongestant spray, which can be tapered slowly by asking the patient to slowly dilute the last bottle every few days. Oral decongestants are helpful in patients with allergic rhinitis. Systemic steroids can also be used in severe cases. Patients recover with withdrawal of the offending medication. With chronic usage, rhinitis medicamentosa can lead to chronic sinusitis, atrophic rhinitis, and permanent turbinate hyperplasia; septal perforation has also been reported. 6. (Dara) Vasomotor rhinitis, medical vs. surgical therapy Vasomotor rhinitis is believed to result from disturbed regulation of the parasympathetic and sympathetic systems in which the parasympathetic system dominates, resulting in vasodilation and edema of the nasal vasculature. Resulting symptoms are rhinorrhea, sneezing, and congestion. Cold air, strong odors, stress, or inhaled irritants may exacerbate symptoms. Rates of anxiety and depression are higher in women with vasomotor rhinitis than in healthy women without rhinitis. Azelastine is a nasal antihistamine with a labeled indication for the treatment of vasomotor rhinitis. Two multicenter clinical trials showed that azelastine was more effective than placebo in patients perceptions of rhinorrhea, sneezes, nasal congestion, and postnasal drip. Before the blinding was lifted, nearly twice as many patients randomly selected to receive azelastine versus placebo 2/5

3 stated that they would continue taking the study medication. Whether this efficacy is specific to azelastine or whether it can be applied to the entire class of antihistamines is not clear. Large clinical trials and trials to evaluate the role of azelastine on a cellular level relative to other antihistamines would be helpful if conducted. The theory is that it is the general anti-inflammatory effect, rather than the H1-receptor antagonism that allows azelastine to treat vasomotor rhinitis. Ipratropium bromide, a topical anticholinergic, acts locally and blocks parasympathetic input to the nasal mucosa only and systemic side effects are uncommon, though epistaxis and nasal dryness may occur. Initially, 2 sprays are prescribed TID. Symptoms control should be apparent after one week, at which time dosing can be lowered to one spray TID. One spray BID is the lowest recommended maintenance dose. In refractory cases, endoscopic vidian neurectomy has been effective in treating vasomotor rhinitis, having gained popularity in the early 1990s. The vidian nerve contains contributions from the greater and deep petrosal nerves and supplies autonomic input to nasal mucosa. Electrical stimulation of the vidian nerve leads to nasal vasodilation and increased secretions. This procedure has been used to manage severe vasomotor rhinitis secondary to medical management. As medical therapy has improved over the past 2 decades, use of this procedure has declined. However, its efficacy is not in question. Transnasal bilateral vidian neurectomy was performed in 271 patients at an institution over 8 years in the late 1980s; in 88%, symptoms ceased. 7. (Josh) Discuss the role of ipratropium bromide in rhinitis. Ipratropium bromide is a congener of atropine available in a 0.03 percent nasal spray, which can reduce rhinorrhea. It may act by decreasing the release of substance P. It is less effective than INGCs for sneezing, pruritus, or nasal obstruction. Ipratropium is not recommended as a first-line drug in allergic rhinitis. It is sometimes useful in children or adults who have profuse rhinorrhea not otherwise controlled with topical nasal steroids, a complaint most commonly observed in adult patients with concomitant allergic and nonallergic (or vasomotor) rhinitis. When rhinorrhea is the dominant symptom or the only symptom, as in gustatory rhinitis, ipratropium bromide (0.03 percent) nasal spray is recommended. Ipratropium bromide is usually employed at a dose of two sprays to each nostril three times a day. Alternatively, it can also be used as needed, or prior to exposures that cause rhinorrhea, such as cold air, or before eating. This medication is also available in a concentration of 0.06 percent, although this strength is intended for short term use only (eg, treatment of rhinorrhea associated with the common cold). Two multicenter, placebo-controlled trials demonstrated the effectiveness of ipratropium bromide to control rhinorrhea. The administration of ipratropium bromide nasal spray (0.03 percent) for one year among 285 patients with nonallergic perennial rhinitis resulted in significant improvement in rhinorrhea as well as a decreased need for additional medications to control symptoms. In a study of 253 patients with perennial nonallergic rhinitis, ipratropium nasal spray significantly reduced rhinorrhea versus that observed with placebo. 8. (Dave) What is the empty nose syndrome? Do turbinate implants have a role in the management of this condition? Empty nose syndrome is a name given in the 1990's by E.B. Kern at Mayo Clinic to the collection of symptoms experienced by patients who have undergone total inferior turbinectomies. These patients may experience persistent nasal obstruction and shortness of breath despite a completely patent nasal airway. Due to the lack of turbinate tissue in the nasal cavities, laminar airflow becomes compromised, and the resulting turbulent air is not conducted as efficiently to the lungs. Other contributing factors include: loss of trigeminal stimulation leading to perception of nasal obstruction, loss of humidification and warming of air leading to decreased efficiency of gas exchange in alveoli, loss of nasal resistance to lungs leading to decreased lung expansion, and constant dryness and atrophy of nasal mucosa leading to rhinitis sicca, and potentially atrophic rhinitis and ozena. Houser in 2007 published case series of 8 patients who underwent submucosal implantation of Alloderm to simulate missing turbinate tissue. Reported significant improvement in SNOT-20 scores. 3/5

4 9. (Dave) Discuss the surgical management of hypertophic inferior turbinates. Which do you think has better success rates? Any data to support your thoughts? Adapted from Jackson and Koch, PRS Jan Technique Advantages Disadvantages Injection procedures Corticosteroid injection Destructive procedures Electrocautery Cryosurgery Laser reduction Turbinate s Partial turbinate Total turbinate Submucous turbinate Nerve s Vidian neurectomy Minimally invasive Not technically difficult Can be done under local anesthesia Not technically difficult Can be performed under local anesthesia Effective in controlling severe rhinorrhea in vasomotor rhinitis Can be performed under local anesthesia Excellent intraoperative hemostasis Relatively stable prolonged symptomatic relief of nasal obstruction for at least 2 years Easiest among procedures High degree of symptomatic relief of nasal obstruction, with prolonged results reported for as long as 16 years Amount resected can be altered according to symptoms Stable symptomatic relief of nasal obstruction, with prolonged results for as long as 15 years More subjective symptomatic improvement of nasal obstruction than partial turbinate Improved smell acuity Preserves turbinate mucosal function Minimal crusting Decreases incidence of hemorrhage among turbinate procedures Effective against bony sources of nasal obstruction Low potential for rhinitis sicca syndrome and atrophic rhinitis Effective against significant rhinorrhea High degree of symptomatic relief of nasal obstruction for at least 5 years 4/5 Symptomatic relief of nasal obstruction is brief (3-6 weeks) Rare reports of visual loss Symptomatic relief of nasal obstruction is of short duration (months to years) Postoperative crusting Adhesions in 20-30% of cases Delayed hemorrhage Generally described decline of symptomatic relief of nasal obstruction after 1 year Postoperative hemorrhage, but does not routinely require nasal packing for control Postoperative eschar formation Postoperative crusting for 6-8 weeks Ineffective against bony sources of nasal obstruction Laser equipment and expertise required Synechiae formation Prolonged crusting Perioperative hemorrhage potentially severe Possibilities of rhinitis sicca syndrome and atrophic rhinitis Synechiae formation Prolonged crusting Increased incidence of postoperative hemorrhage compared with PRIT Potentially increases incidence of rhinitis sicca syndrome and atrophic rhinitis compared with partial turbinate Over not reversible Difficult to perform Preserves potentially hypertrophied turbinate mucosa Higher incidence of recurrence of symptoms of nasal obstruction among turbinate procedures Persistent rhinorrhea Dry eyes Temporary headache and facial pain Transient numbness of palate, teeth, and cheek Rarely ophthalmoplegia and cranial neuralgias

5 10. (Kathy) When comparing different surgical techniques to treat nasal obstruction secondary to inferior turbinate hypertrophy, what is the effect on nasal mucociliary function? Laryngoscope 2003;113: Prospective, randomized clinical trial comparing nasal function after treatment with: 1) radiofrequency tissue ablation (RFA); 2) laser ablation (LA); and 3) partial turbinectomy (PT); using rhinomanometry and isotopic study of nasal mucociliary transport time to assess treatment outcomes. METHODS: N= 45 adult patients with symptoms and signs of nasal obstruction and stuffiness related to enlarged turbinates. Patients divided into three groups: o Group A- Laser ablation was applied to inferior turbinate on one side; partial turbinectomy to inferior turbinate on other side. o Group B- Radiofrequency tissue ablation was applied to the inferior turbinate on one side and partial turbinectomy to the inferior turbinate on the other side. o Group C- Untreated patients constituted control group. RESULTS: At 12 weeks after surgery, the nasal mucociliary transport times were averaged with these results: Laser ablation minutes. Partial turbinectomy and minutes. Radiofrequency ablation minutes. Rhinomanometric measurements demonstrated a significant decrease in nasal resistances in both treatment groups. CONCLUSIONS: All methods were effective in improving nasal obstruction, however, laser ablation of the turbinate disturbs mucociliary function significantly. With the partial turbinectomy technique, results obtained were similar to the results with the radiofrequency tissue ablation technique. 11. (Scott) Describe surgical management of septal perforation. Any contraindications to repair? Central concepts in septal perforation, repair include wide elevation, tension-free suture lines, multilayer closure, and humidification. Often needed in a nose that has already undergone surgery and has limited tissue and a compromised blood supply. The size of the perforation is important to the success of closure. The height of the perforation correlates closely with the degree of difficulty of the repair. Larger perforations require greater tissue mobilization and can result in greater tension on the closure. Success typically 64% to 95%. The primary problem with septal perforation is turbulent airflow. Disruption of normal laminar airflow results in the formation of crusts at the edges of the perforation, leading to bleeding, malodor, further enlargement of septal perforation. Medically, one can improve things with humidification and/or providing laminar airflow with a silastic button placement. Principles of surgical repair: 1) Aggressive mucosal mobilization; 2) Multilayer closure with interposition graft; 3) Tension-free closure of at least one mucosal flap; 4) Application of postoperative silastic sheeting; 5) Aggressive postoperative humidification: saline irrigations and emollients. One can approach the surgical repair via a closed approach (Killian or hemitransfixion), an open rhinoplasty approach (better exposure). Tissue expanders have been used to expand the inferior flap for better tension-free closure. Also, pedicled flap and/or free flaps have been described for better closure if there is a significant gap in the mucosal flap closure. Contraindications to repair: current cocaine use, Neoplastic etiologies, Infectious and inflammatory etiologies, (including tuberculosis, syphilis, Wegener granulomatosis, and sarcoidosis), poor anesthestic risk. 5/5

Introduction. Allergic Rhinitis. Seventh Pediatric Asthma Education Conference 5/9/2018

Introduction. Allergic Rhinitis. Seventh Pediatric Asthma Education Conference 5/9/2018 It Is All One Airway Or How Allergic Rhinitis and Its Management can Affect Asthmatic Patients Stacy Dorris, MD Allergy/Immunology Vanderbilt Medical Center May 9, 2018 Introduction Allergic Rhinitis Allergic