Allergic disorders case file

Allergic disorders case file

Eugene C. Toy MD, Donald Briscoe, MD, FA  AFP, Bruce Britton, MD, Joel J. Heidelbaugh, MD, FA  AFP, FACG

Case 6

A 35-year-old woman with a history of asthma presents to your office with symptoms of nasal itching, sneezing, and rhinorrhea. She states she feels this way most days but her symptoms are worse in the spring and fall. She has had difficulty sleeping because she is always congested. She states she has taken diphenhydramine (Benadryl) with no relief. She does not smoke cigarettes and does not have exposure to passive smoke but she does have two cats at home. On examination, she appears tired but is in no respiratory distress. Her vital signs are temperature, 98.8°F; blood pressure, 128/84 mm Hg; pulse, 88 beats/min; and respiratory rate, 18 breaths/min. The mucosa of her nasal turbinates appears swollen (boggy) and has a pale, bluish-gray color. Thin and watery secretions are seen. No abnormalities are seen on ear examination. There is no cervical lymphadenopathy noted and her lungs are clear.

⯈ What is the most likely diagnosis?

⯈ What is your next step?

⯈ What are important considerations and potential complications of management?

ANSWER TO CASE 6:

Allergic Disorders

Summary: A 35-year-old asthmatic woman complains of chronic nasal congestion that is worse in the spring and the fall.

• Most likely diagnosis: Allergic rhinitis.
• Next step in management of this patient: Treatment with antihistamines, decongestants, or intranasal steroids. These treatments can also be used in combination with each other. First-line treatment is intranasal corticosteroids for mild to moderate disease. With moderate to severe allergic rhinitis, antihistamines and decongestants should be added.
• Considerations and possible complications of therapy: Recognition and reduction of potential allergen exposure will yield more success in management than pharmacotherapy alone. Excessive use of topical decongestants can cause rebound congestion.

ANALYSIS

Objectives

1. Understand the inflammatory nature of allergic rhinitis.
2. Recognize physical examination findings consistent with allergic rhinitis.
3. Develop an approach to the management of allergic rhinitis, including the roles of pharmacotherapy and reduction of allergen exposure.
4. Recognition and management of asthma.
5. Identification of essential features and treatment of anaphylaxis.

Considerations

This patient presents with a classic history of allergic rhinitis. Her history of itchy eyes, nasal congestion and discharge, and seasonal in nature (worse in spring and fall) are all consistent with allergic rhinitis. Her examinations are also consistent with the diagnosis. The mucosa of her nasal turbinates appears swollen (boggy) and has a pale, bluish-gray color. Thin and watery secretions are seen. The best therapy for this condition is avoidance of allergens, but due to the probable allergy to pollen, this can be very difficult. Nasal corticosteroids offer the most consistent symptomatic relief.

Approach To:

Allergic Disorders

DEFINITIONS

ALLERGIC RHINITIS: Inflammation of the nasal passages caused by immunoglobulin E (IgE)-mediated response to airborne substances.

ANAPHYLAXIS: Rapidly progressing, life-threatening allergic reaction, mediated by IgE immediate hypersensitivity reaction.

CLINICAL APPROACH

Background

Rhinitis is inflammation of the nasal membranes and is characterized by any combination of the following: sneezing, nasal congestion, nasal itching, obstruction, pruritus, and rhinorrhea. The eyes, ears, sinuses, and throat can also be involved. Allergic rhinitis is the most common cause of rhinitis, occurring in up to 30% of adults and 40% of children.

Pathophysiology

Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian tubes, middle ear, sinuses, and pharynx. Inflammation of the mucous membranes is characterized by a complex interaction of inflammatory mediators but, ultimately, is triggered by an IgE-mediated response to an extrinsic protein.

In susceptible individuals, exposure to certain foreign proteins leads to allergic sensitization, which is characterized by the production of specific IgE directed against these proteins. This specific IgE coats the surface of mast cells, which are present in the nasal mucosa. When the specific allergen is inhaled into the nose, it can bind to the IgE in the mast cells, leading to the delayed release of a number of mediators.

Mediators that are immediately released include histamine, tryptase, chymase, and kinase. Mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. Symptoms can occur quickly after exposure. Mucous glands are stimulated, leading to increased secretions. Vasodilation occurs, causing congestion. Stimulation of sensory nerves leads to sneezing and itching. Other symptoms include the redness and tearing of eyes, postnasal drip, and ear pressure.

Over the next 4 to 8 hours, these mediators, through a complex interplay of events, recruit neutrophils, eosinophils, lymphocytes, and macrophages to the mucosa. These inflammatory cells cause more congestion and mucus production that may persist for hours or days. Systemic effects, including fatigue, sleepiness, and malaise, can result from the inflammatory response as well.

History

Obtaining a detailed history is important in the evaluation of allergic rhinitis, as specific triggers may be identified. Evaluation should include the nature, duration, and time course of symptoms. The recent use of medications is another important consideration as is a family history of allergic diseases, environmental exposures, and comorbid conditions.

Part of the history should include the time pattern of symptoms and whether symptoms occur at a consistent level throughout the year (perennial rhinitis), only occur in specific seasons (seasonal rhinitis), a combination of the two, or in relation to a workplace (occupational rhinitis). Trigger factors such as exposure to pollens, mold spores, specific animals, or cleaning of the house can sometimes be identified. Irritant triggers such as smoke, pollution, and strong smells can aggravate symptoms of allergic rhinitis. Response to treatment with antihistamines supports the diagnosis of allergic rhinitis.

Symptoms

Symptoms that can be associated with allergic rhinitis include sneezing, itching (of nose, eyes, or ears), rhinorrhea, postnasal drip, congestion, anosmia, headache, earache, tearing, red eyes, and drowsiness.

Physical Examination

Common findings on examination include "allergic shiners;' which are dark circles around the eyes related to vasodilation or nasal congestion. The "nasal crease" can be seen in some cases. It is a horizontal crease across the lower half of the bridge of the nose caused by repeated upward rubbing of the tip of the nose by the palm of the hand ("allergic salute").

Examination of the nose may reveal mucosa of the nasal turbinates to be swollen (boggy) and have a pale, bluish-gray color. Assessment of the character and quantity of nasal mucus may be helpful in ascertaining a diagnosis. Thin and watery secretions are frequently associated with allergic rhinitis, whereas thick and purulent secretions are usually associated with sinusitis. The characteristic of the mucous is not always diagnostic, as thick, purulent, colored mucus can also occur with allergic rhinitis.

The nasal cavity should be inspected for growths such as polyps or tumors. Polyps are firm, gray masses that are often attached by a stalk, which may not be visible. After spraying a topical decongestant, polyps do not shrink, whereas the surrounding nasal mucosa does shrink. Examine the nasal septum to look for any deviation or septa! perforation that may be present as a consequence of chronic rhinitis, granulomatous disease, cocaine abuse, prior surgery, topical decongestant abuse, or, rarely, topical steroid overuse.

Otoscopy should be performed to look for tympanic membrane retraction, air-fluid levels, or bubbles. Performing pneumatic otoscopy can be considered to look for abnormal tympanic membrane mobility. These findings can be associated with allergic rhinitis, particularly if eustachian tube dysfunction or secondary otitis media is present. Ocular examination may reveal findings of injection and swelling of the palpebral conjunctivae, with excess tear production. Dennie-Morgan lines (prominent creases below the inferior eyelid) are associated with allergic rhinitis.

"Cobblestoning" of the posterior pharynx is often observed. This is caused by the presence of streaks of lymphoid tissue on the posterior pharynx. Tonsillar hypertrophy can also be seen. The neck should be examined for the presence of lymphadenopathy. The respiratory system must be examined for findings consistent with asthma. These include wheezing, tachypnea, and a prolonged expiratory phase of respiration.

CAUSES OF ALLERGIC RHINITIS

The causes of allergic rhinitis can differ depending on whether the symptoms are seasonal, perennial, or sporadic/ episodic. Some patients are sensitive to multiple allergens and can have perennial allergic rhinitis with seasonal exacerbations. Although food allergy can cause rhinitis, particularly in children, it is rarely a cause of allergic rhinitis in the absence of gastrointestinal or skin symptoms. Seasonal allergic rhinitis is commonly caused by allergy to seasonal pollens and outdoor molds.

Pollens (Tree, Grass, and Weed)

Tree pollens, which vary by geographic location, are typically present in high counts during the spring, although some species produce their pollens in the fall. Grass pollens also vary by geographic location. Most of the common grass species are associated with allergic rhinitis. A number of these grasses is cross-reactive, meaning that they have similar antigenic structures (ie, proteins recognized by specific IgE in allergic sensitization). Consequently, a person who is allergic to one species is also likely to be sensitive to a number of other species. The grass pollens are most prominent from the late spring through the fall, but can be present yearround in warmer climates.

Weed pollens also vary geographically. Many weeds, such as short ragweed, a common cause of allergic rhinitis in much of the United States, are most prominent in the late summer and fall. Other weed pollens are present year-round, particularly in warmer climates.

Perennial allergic rhinitis is typically caused by allergens within the home, but can also be caused by outdoor allergens that are present year-round. In warmer climates, grass pollens can be present throughout the year. In some climates, individuals may be symptomatic because of trees and grasses in the warmer months and molds and weeds in the winter.

House Dust Mites

In the United States, two major house dust mite species are associated with allergic rhinitis. These mites feed on organic material in households, particularly the skin that is shed from humans and pets. They can be found in carpets, upholstered furniture, pillows, mattresses, comforters, and stuffed toys. Exposure can be reduced by methods such as carpet removal; however, current studies have not found any benefit to using mite-proof mattresses or pillow covers.

Animals

Allergy to indoor pets is a common cause of perennial allergic rhinitis. Cat and dog allergies are encountered most commonly in clinical practice. However, allergies have been reported to occur with most of the furry animals and birds that are kept as indoor pets. Although cockroach allergy is most frequently considered to be a cause of asthma, particularly in the inner city, it can also cause perennial allergic rhinitis in infested households. Rodent infestation may also be associated with allergic sensitization.

TREATMENT

The management of allergic rhinitis consists of four major categories of treatment: patient education, allergen avoidance, pharmacologic management, and immunotherapy. All aspects of treatment are more successful when exposure to allergens is decreased. Recommendations for treatment are primarily based on symptoms and patient's age. Pharmacotherapy can involve the use of antihistamines, decongestants, intranasal corticosteroids, and, in severe cases, systemic corticosteroids.

Antihistamines competitively antagonize the receptors for histamine, which is released from mast cells. This reduces the production of symptoms mediated by the release of histamine. "First-generation" antihistamines including diphenhydramine, chlorpheniramine, and hydroxyzine are inexpensive and available over the counter. Side effects include sedation and the anticholinergic effects of dry mouth, dry eyes, blurred vision, and urinary retention; therefore, their use should be monitored in sensitive populations, such as the elderly. "Second-generation" antihistamines, including loratadine, desloratadine, fexofenadine, azelastine, and cetirizine, have a lower incidence of sedation and anticholinergic side effects, therefore are preferred over first-generation antihistamines. Caution should be used with cetirizine because sedative side effects can occur at recommended doses. Oral antihistamines begin to take effect within 15 to 30 minutes after ingestion and are best used in persons with mild and intermittent symptoms.

Corticosteroid nasal sprays are the most effective treatment and first-line therapy for the long-term management of mild to moderate persistent symptoms of allergic rhinitis. They reduce the production of inflammatory mediators and the recruitment of inflammatory cells. Systemic absorption of the steroid is relatively low, reducing the risk of complications associated with the chronic use of systemic corticosteroids. Side effects include nosebleeds, nasal irritation, and rarely nasal septum perforation. Maximal effectiveness is achieved after 2 to 4 weeks of use.

Decongestants, either given orally or intranasally, can be used to provide symptomatic relief of nasal congestion. These α-adrenergic agonist agents constrict blood vessels in the nasal mucosa and reduce the overall volume of the mucosa. Common decongestants include pseudoephedrine and phenylephrine. Oral decongestants can cause tachycardia, tremors, and insomnia. Rebound hyperemia and worsening of symptoms can occur with chronic use or upon discontinuation of nasal decongestants. Caution should be used in the elderly, young children, during the first trimester of pregnancy and individuals with cardiac arrhythmias, glaucoma, or hyperthyroidism.

Leukotriene inhibitors (zafirlukast, montelukast, zileuton) are indicated both for allergic rhinitis and for maintenance therapy for persistent asthma. They are particularly useful in patients with both asthma and allergies or in those whose asthma may be triggered by allergens. These medications can be taken alone or in combination with antihistamines.

Oral corticosteroids are potent inhibitors of cell-mediated immunity. The use of systemic steroids is limited by adverse effects, including suppression of the hypothalamic-pituitary-adrenal axis and hyperglycemia. Long-term use can lead to peptic ulcer formation, increased susceptibility to infection, poor wound healing, and the reduction of bone density. Because of these significant risks, systemic steroids are used only for severe allergies unresponsive to other pharmacologic modalities or a diagnosis of nasal polyposis. Oral steroids should be used in the lowest effective dose for the shortest possible time.

Desensitization therapy is frequently attempted in patients who remain symptomatic despite maximal medical therapy. Skin allergy testing is used to detect reactivity against specific antigens. The next step is to inject the patient with highly diluted concentrations of this antigen. The concentration of the antigen( s) in the injection is gradually increased, in an effort to reduce the patient's inflammatory response to the antigen(s). Injections are typically given weekly or biweekly. This process is expensive, time-consuming, and requires numerous injections. Patients and physicians must be prepared to address severe, even anaphylactic, reactions that may occur during the process.

ANAPHYLAXIS, URTICARIA, AND ANGIOEDEMA

Urticaria is characterized by large, irregularly shaped, pruritic, erythematous wheals. Angioedema is painless, deep, subcutaneous swelling that often involves the periorbital, circumoral, and facial regions. Anaphylaxis is a systemic reaction with cutaneous symptoms that is associated with dyspnea, visceral edema, and hypotension. Insect bites or stings, foods, and medications are the most common culprits of anaphylactic reactions. The manifestations of anaphylaxis include hypotension or shock from widespread vasodilation, respiratory distress from bronchospasm or laryngeal edema, gastrointestinal and uterine muscle contraction, and urticaria and angioedema.

At the first suspicion of anaphylaxis, aqueous epinephrine 1:1000, in a dose of 0.2 to 0.5 mg, is injected subcutaneously or intramuscularly. Repeated injections can be given every 5 to 15 minutes when necessary. Epinephrine administration increases peripheral resistance by causing immediate vasoconstriction. Airway obstruction and vascular collapse improve due to the inotropic properties of epinephrine on the heart and bronchodilator effects on the lungs. Rapid intravenous infusion of large volumes of fluids (saline, lactated Ringer solution, plasma or plasma expanders) is essential to replace loss of intra vascular plasma into tissues. Airway obstruction may be caused by edema of the larynx or by bronchospasm. In addition to securing the airway, oxygen therapy should be provided. Endotracheal intubation may be required. Antihistamines may be useful as adjuvant therapy for alleviating cutaneous manifestations of urticaria or angioedema and pruritus. Caution is recommended with antihistamine use given the sedative effects, which could be problematic in compromised patients. Systemic corticosteroids can be beneficial, but should not be used as first line due to its delayed onset of action. All patients with anaphylaxis should be monitored for a period of time, for example, 24 hours.

CONJUNCTIVITIS

Conjunctivitis is an infection of the palpebral and/ or bulbar conjunctiva. It is the

most common eye disease seen in community medicine. Most cases are caused by

bacterial or viral infection. Other causes include allergy and chemical irritants. The

mode of transmission of infectious conjunctivitis is usually direct contact to the

opposite eye or to other persons via fingers, towels, or handkerchiefs.

The organisms isolated most commonly in bacterial conjunctivitis are Staphylococcus, Streptococcus, Haemophilus, Moraxella, and Pseudomonas. There is no blurring of vision and only mild discomfort. In severe cases, immunocompromised patients, contact lens wearers, and those who failed initial treatment, examination of stained conjunctiva! scrapings and cultures are recommended. The disease is usually self-limited, lasting about 10 to 14 days if untreated. A sulfonamide instilled locally three times daily will usually clear the infection in 2 to 3 days.

Epidemic keratoconjunctivitis (pink eye) is highly contagious and spread by person-to-person contact or fomites. The most common cause is adenovirus. It is usually associated with pharyngitis, fever, malaise, and preauricular lymphadenopathy. Locally, the palpebral conjunctiva is red with a copious watery discharge and scanty exudates. Symptomatic treatment includes ocular decongestants, artificial tears, and cool or warm compresses to reduce the discomfort of the associated lid edema. Weak topical steroids may be necessary to treat the corneal infiltrates. The disease usually lasts at least 2 weeks.

Noninfectious causes of conjunctivitis include allergic and chemical irritants. Symptoms of allergic conjunctivitis include itching, tearing, redness, stringy discharge, and sometimes photophobia. In addition to avoiding the irritant, treatment can include the use of oral antihistamines or topical antihistamine or anti inflammatory eye drops.

COMPREHENSION QUESTIONS

6.1 A 30-year-old man has both mild persistent asthma and chronic environmental allergies. Which of the following medications is indicated for the management of this patient's conditions?

A. Inhaled albuterol (short-acting β-adrenergic agonist)

B. Intranasal fluticasone (corticosteroid)

C. Oral montelukast (leukotriene modifier)

D. Oral cetirizine (second-generation antihistamine)

6.2 A 12-year-old boy presents with eye itching and redness. He has clear drainage from his eyes but no crusting. Examination today is normal except for mildly injected conjunctiva bilaterally. Which of the following is the most appropriate treatment?

A. Antibiotic eye drops

B. Ophthalmology consultation

C. Anti-inflammatory eye drops

D. Oral leukotriene inhibitor

6.3 A 56-year-old man presents to his physician with symptoms consistent with allergic rhinitis. His past medical history is positive for benign prostatic hyperplasia. He continues to work in a warehouse as a forklift operator. Which of the following medications should be used to treat this patient?

A. Diphenhydramine

B. Hydroxyzine

C. Chlorpheniramine

D. Fexofenadine

ANSWERS

6.1 C. Montelukast is indicated for both the management of persistent asthma and chronic allergies. Nasal steroids and oral antihistamines are indicated only for allergies.

6.2 C. This patient has allergic conjunctivitis. Topical anti-inflammatory drops are appropriate therapy. Other options would include topical or oral antihistamines. The other therapies listed are not appropriate in this condition.

6.3 D. The second-generation antihistamines, such as fexofenadine, are less sedating and have fewer anticholinergic side effects than the first-generation antihistamines. They would be a better choice for someone who operates heavy machinery and has benign prostatic hyperplasia. However, they are no more effective at symptom relief than the first-generation antihistamines listed earlier.

CLINICAL PEARLS

⯈ The management of allergic rhinitis consists of four major categories of treatment: patient education, allergen avoidance, pharmacologic management, and immunotherapy.

⯈ At the first suspicion of anaphylaxis, aqueous epinephrine 1:1000 in a dose of 0.2 to 0.5 ml (0.2-0.5 mg) is injected subcutaneously or intramuscularly. The airway should always be assessed and patient intubated if necessary to secure breathing.

REFERENCES

American Academy of Allergy Asthma & Immunology. Allergy testing: tips to remember. Available at: http:/ I www.aaaai.org/ conditions-and-treatments/library I at-a-glance/ allergy-testing.aspx. Accessed May 24, 2015. 

Arnold JJ, Williams PM. Anaphylaxis: recognition and management. Am Fam Physician. 2011 Nov 15;84(10):1111-1118. 

Barnes PJ. Asthma. In: Kasper D, Fauci A, Hauser S, et al, eds. Harrison's Principles of Internal Medicine. 19th ed. New York, NY : McGraw-Hill Education; 2015. Available at: http://accessmedicine. mhmedical.com/. Accessed May 24, 2015. 

Boyce AJ, Austen KF. Allergies, anaphylaxis and systemic mastocytosis. In: Kasper D, Fauci A, Hauser S, et al, eds. Harrison's Principles of Internal Medicine.19th ed. New York, NY: McGraw-Hill Education; 2015. Available at: http://accessmedicine.mhmedical.com. Accessed May 24, 2015. 

Cronau H, Kankanala RR, Mauger T. Diagnosis and management of red eye in primary care. Am Fam Physician. 2010 Jan 15;81(2):1137-1441. 

Lambert M. Practice parameters for for allergic rhinitis. Am Fam Physician. 2009 Jul 1;80(1):79-85. 

Quillen DM, Feller DB. Diagnosing rhinitis: allergic vs. non-allergic.Am Fam Physician. 2006;73(9):1583- 1590. 

Scow OT, Luttermoser GK, Dickerson KS. Leukotriene inhibitor in the treatment of allergy and asthma. Am Fam Physician. 2007;75(1):65-70. 

Sur DK, Scandale S. Treatment of allergic rhinitis. Am Fam Physician. 2010;81(12):1440-1446.

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