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URTICARIA
URTICARIA: THE BASICS
 Urticaria (hives) is a vascular reaction of the
skin characterized by wheals surrounded by
a red halo or flare (area of erythema)
 Cardinal symptom is PRURITUS (itch)
 Urticaria is caused by swelling of the upper
dermis
 Up to 20% of the population experience
urticaria at some point in their lives
ANGIOEDEMA: THE BASICS
 Angioedema can be caused by the same pathogenic
mechanisms as urticaria, but the pathology is in the
deep dermis and subcutaneous tissue and swelling is
the major manifestation
 Angioedema commonly affects the face or a portion of
an extremity
 Involvement of the lips, cheeks, and periorbital areas is
common, but angioedema also may affect the tongue,
pharynx, larynx and bowels
 May be painful or burning, but not pruritic
 May last several days
EXAMPLES OF URTICARIA
EXAMPLE OF ANGIOEDEMA
URTICARIA & ANGIOEDEMA
 Urticaria and angioedema may occur in any
location together or individually.
 Angioedema and/or urticaria may be the
cutaneous presentation of anaphylaxis, so
assessment of the respiratory and
cardiovascular systems is vital!
URTICARIA: CLINICAL FINDINGS
 Lesions typically appear over the course of
minutes, enlarge, and then disappear within hours
 Individual wheals rarely last >12hrs
 Surrounding erythema will blanch with pressure
 Urticaria may be acute or chronic
• Acute = new onset urticaria < 6 weeks
• Chronic = recurrent urticaria (most days) > 6 weeks
 Most urticaria is acute and resolves
COMMON CAUSES OF ACUTE URTICARIA
 Idiopathic
 Infection
• Upper respiratory, streptococcal infections,
helminthes
 Food reactions
• Shellfish, nuts, fruit, etc.
 Drug reactions
 IV administration
• Blood products, contrast agents
ETIOLOGY OF CHRONIC URTICARIA
 Idiopathic: over 50% of chronic urticaria
 Physical urticarias: many patients with chronic urticaria have
physical factors that contribute to their urticaria
• These factors include pressure, cold, heat, water (aquagenic),
sunlight (solar), vibration, and exercise
• Cholinergic urticaria is triggered by heat and emotion
• The diagnosis of pure physical urticaria is made when the sole
cause of a patient’s urticaria is a physical factor
 Chronic autoimmune: possibly a third or more of patients
with chronic urticaria
 Other: infections, ingestions, medications
DERMATOGRAPHISM
 Most common form of
physical urticaria
 Sharply localized
edema or wheal within
seconds to minutes
after the skin has been
rubbed
 Affects 2-5% of the
population
URTICARIA: PATHOPHYSIOLOGY
 The mast cell is the major effector cell in
urticaria
 Immunologic Urticaria: antigen binds to IgE
on the mast cell surface causing
degranulation, which results in release of
histamine
• Histamine binds to H1 and H2 receptors to
cause arteriolar dilatation, venous constriction
and increased capillary permeability.
URTICARIA: PATHOPHYSIOLOGY
 Non-Immunologic Urticaria: not dependent
on the binding of IgE receptors
• For example, aspirin may induce histamine
release through a pharmacologic mechanism
where its effect on arachidonic acid metabolism
causes a release of histamine from mast cells.
• Physical stimuli may induce histamine release
through direct mast cell degranulation
Case One
MRS. ILA COOK
CASE ONE: HISTORY
 HPI: Mrs. Cook is a 46-year-old woman with a 3-day
history of a widespread pruritic rash. Individual
lesions last approximately 8hrs. She recently started
a new laundry detergent.
 PMH: hip replacement 6 weeks ago
 Allergies: none
 Medications: oxycodone (for pain, s/p hip
replacement) and aspirin
 Family history: no history of atopic dermatitis or
allergies
 Social history: lives with her husband in the city
 ROS: negative
CASE ONE: EXAM
 Vital signs: afebrile,
HR 74, BP 120/70, RR
16, O2 sat 98% on RA
 Skin: diffuse
erythematous papules
coalescing into
plaques (wheals)
 No associated
bruising
CASE ONE, QUESTION 1
 What other part(s) of the exam are
essential?
a. Musculoskeletal
b. Neurologic
c. Psychiatric
d. Respiratory
e. All of the above
CASE ONE, QUESTION 1
Answer: d
 What other part(s) of the exam are
essential?
a. Musculoskeletal
b. Neurologic
c. Psychiatric
d. Respiratory
e. All of the above
CLINICAL EVALUATION
 Ask about symptoms of anaphylaxis, including: chest
tightness or difficulty breathing, hoarse voice or throat
tightness, nausea, vomiting, abdominal pain,
lightheadedness
 In addition to the skin exam, the physician should obtain a
set of vital signs and evaluate for respiratory distress
(dyspnea, wheeze, bronchospasm, stridor) and hypotension
 For acute urticaria, no lab testing is required
• Laboratory testing is generally driven by associated signs and
symptoms (e.g. C1 esterase deficiency only causes
angioedema, not hives)
CASE ONE, QUESTION 2
 What important feature(s) are revealed in
the history?
a. She recently began a new detergent
b. She recently began new medications
c. The lesions last 8hrs
d. Three-day history of rash
CASE ONE, QUESTION 2
Answer: b, c, d
 What important feature(s) are revealed in the
history?
a. She recently began a new detergent (not related)
b. She recently began new medications (likely
etiology)
c. The lesions last 8hrs (individual wheals rarely
last over 12 hrs.)
d. Three-day history of rash (this is acute
urticaria)
DIAGNOSIS: MEDICATION-INDUCED URTICARIA
 Medications are a common cause of urticaria and
angioedema
• Penicillin and related antibiotics are common via the
IgE-mediated mechanism
• Aspirin is a common cause via a non-IgE-mediated
mechanism
• 30% of chronic urticaria is exacerbated by
aspirin/NSAID use
 Many patients ask about detergent use. However, it
causes irritant or allergic contact dermatitis, not
urticaria.
Case Two
MS. SANDRA JENNINGS
CASE TWO: HISTORY
 HPI: Ms. Jennings is a 55-year-old woman who presents
to the dermatology clinic with a 6-month history of
periodic swelling on her body. The swelling started with
localized itching followed by raised lesions that disappear
within minutes to hours. She finds these lesions
embarrassing and would like treatment or a cure.
 PMH: no hospitalizations or major illnesses
 Medications: occasional NSAID, daily fish oil, Vitamin D
 Allergies: no known drug allergies
 Family history: no history of skin disease
 Social history: married, works as a nurse
 Health-related behaviors: no tobacco, alcohol or drug use
CASE TWO CONTINUED
 Further questioning reveals that Ms. Jennings’s
urticaria is worse with exercise, rubbing of the
skin, pressure (e.g. develops lesions at the site
of her purse strap on her shoulder), and
embarrassment.
 She also describes that most of the time she
does not notice an association with any
potential triggers.
 Her lesions appear 2-3x/week, often in public.
She is particularly embarrassed when lesions
appear on her face while taking care of patients
CASE TWO: SKIN EXAM
 Vital signs within normal limits
 Full skin exam reveals:
• No wheals or erythema
• Multiple benign appearing nevi on the trunk
CASE TWO, QUESTION 1
 Which of the following medications may be
contributing to her urticaria?
a. Fish oil
b. Ibuprofen
c. Vitamin D
d. All of the above
CASE TWO, QUESTION 1
Answer: b
 Which of the following medications may be
contributing to her urticaria?
a. Fish oil
b. Ibuprofen
c. Vitamin D
d. All of the above
CLINICAL EVALUATION
 Urticaria is a clinical diagnosis
 A detailed history and physical exam should be
performed
 Many times patients will not present with urticaria
during their clinic visit
• Can show patients photographs of urticaria and ask if
their lesions appear similar
• Patients can take photos of their skin lesions and bring
them to their office visit
CLINICAL EVALUATION
 In most cases of chronic urticaria, no external
cause can be identified
 If a physical urticaria is suspected, a challenge test
with the respective trigger may be performed
 Patients will often ask about food allergies
• IgE-mediated food allergy is far more likely to present
with acute urticaria
• A detailed food diary or dietary modification may reveal
foods (or additives) that cause fluctuations in symptoms
of chronic urticaria
ALLERGY TESTING
 Allergy testing is not routinely performed in
patients with chronic urticaria.
• Skin prick testing may reveal sensitivities to a
variety of allergens that may not be relevant to
the patient’s urticaria.
• Laboratory tests may identify the 1/3 of patients
with chronic urticaria who have an autoimmune
pathogenesis. This adds additional costs and
may not change the management.
NATURAL HISTORY AND PROGNOSIS
 Symptoms of chronic urticaria can be severe
and impair the patient’s quality of life (QOL)
 In most patients, chronic urticaria is an episodic
and self-limited disorder
 Average duration of disease is two to five years
 In patients with idiopathic chronic urticaria,
there is a rate of spontaneous remission at one
year of approximately 30 to 50 percent
 However, symptoms extend beyond five years
in nearly one-fifth of patients
BACK TO MS. JENNINGS
 Ms. Jennings was recommended to avoid tight
clothing, stop ibuprofen, and start a first-
generation antihistamine (e.g. hydroxyzine).
 During a follow-up visit, Ms. Jennings reports
she stopped the hydroxyzine because it made
her too sleepy and she worried it was beginning
to affect her work performance. She became
teary-eyed and shared her frustration with her
skin condition and fear that she would not be
cur
CASE TWO: FOLLOW-UP VISIT
 Patients with chronic urticaria are often frustrated and
fearful. Validation and reassurance are important
components of successful management.
 Sharing the following information may help:
• Chronic urticaria is rarely permanent. Approximately 50 % of
patients undergo remission within one year.
• While acute urticaria and angioedema may be manifestations
of allergic reactions that can be life-threatening, chronic
urticaria is a different disorder that rarely puts the patient at
any acute risk.
• The symptoms of chronic urticaria can be successfully
managed in the majority of patients.
CASE TWO, QUESTION 2
 Which of the following treatments would you
recommend for Ms. Jennings?
a. Daily oral 2nd generation H1 antihistamine
b. Daily topical retinoid to the face
c. No need to continue with an antihistamine;
stopping the NSAID should resolve the urticaria
d. Oral 2nd generation H1 antihistamine taken when
the itching begins
CASE TWO, QUESTION 2
Answer: a
 Which of the following treatments would you
recommend for Ms. Jennings?
a. Daily oral 2nd generation H1 antihistamine
b. Daily topical retinoid to the face (not used for urticaria)
c. No need to continue with an antihistamine; stopping the
NSAID should resolve the urticaria (treatment should be
initiated in addition to removing potential triggers)
d. Oral 2nd generation H1 antihistamine taken when the
itching begins (less practical and will not help prevent
the initial lesion)
TREATMENT: ANTIHISTAMINES
 Oral H1 antihistamines are the first-line treatment for
acute and chronic urticaria
 1st-generation H1 antihistamines are less well-tolerated
due to sedation
• e.g. 10-50 mg hydroxyzine 1-2 hours before bedtime
• Can start with smaller doses (10 mg) to allow the patient to
manage the sedation effects
• Remember to warn patient not to drive a car or operate
other dangerous machines within 4-6 hours of taking this
medication
• Do not take with other sedating medications
TREATMENT: ANTIHISTAMINES
 2nd-generation H1 antihistamines (e.g. Loratadine)
are better tolerated with fewer sedative and
anticholinergic effects and may be used in patients
intolerant of or inadequately controlled by 1st-
generation agents
 Certain populations, including children, the elderly,
and patients with renal or hepatic impairment may
require dosage adjustments when using H1
antihistamines
 Also used with caution in patients with glaucoma,
prostatic hyperplasia, and respiratory disease
ANTIHISTAMINES
 The following are examples of H1 antihistamines:
• 1st Generation
• Diphenhydramine (OTC)
• Hydroxyzine (Rx, generic)
• Chlorpheniramine (OTC)
• 2nd Generation
• Cetirizine (OTC)
• Loratadine (OTC)
• Fexofenadine (OTC)
URTICARIAL LESIONS
 Not all patients with urticarial eruptions have
urticaria. Which of the following patients has
ordinary urticaria?
URTICARIAL LESIONS
Urticarial
Vasculitis
Ordinary
Urticaria
Bullous
Pemphigoi
d
BEYOND ORDINARY URTICARIA
 The appearance of the hives does not tell
you the underlying cause
 The presence of systemic symptoms should
signal the possibility that an urticarial rash is
not ordinary urticaria but rather a systemic
syndrome with urticaria-like skin lesions
REFERRAL TO DERMATOLOGY
 Referral to a dermatologist and biopsy should be
performed in patients with one or more of the
following features:
• Individual lesions that persist beyond 48 hours, are
painful rather than pruritic, or have accompanying
petechial characteristics
• Systemic symptoms
• Lack of response to antihistamines
• Lesions that leave pigmentation changes upon
resolution
Case Three
MRS. JULIE WALKER
CASE THREE: HISTORY
 HPI: Mrs. Walker is a 25-year-old woman who was
brought to the emergency department by her husband
after she began feeling short of breath with a new and
expanding rash
 PMH: asthma, no history of intubations
 Allergies: aspirin (causes a rash) & shellfish (reaction at a
young age of facial swelling)
 Medications: occasional use of albuterol
 Family history: noncontributory
 Social history: recently started cooking school
 ROS: short of breath, anxious
CASE THREE: EXAM
 Vitals: T 98.6F, HR 110,
BP 90/50, RR 34
 General: anxious-
appearing woman sitting
upright with difficulty
breathing, unable to
speak in full sentences
 Respiratory: tachypneic,
using accessory
muscles, bilateral
rhonchi
 Skin: periorbital edema,
scattered erythematous
wheals on the trunk
CASE THREE, QUESTION 1
 What is the next course of action in this
patient?
a. Administer IV metoprolol
b. Assess ABC’s (airway, breathing, circulation)
c. Give systemic corticosteroids
d. Make a food diary
CASE THREE, QUESTION 1
Answer: b
 What is the next course of action in this
patient?
a. Administer IV metoprolol
b. Assess ABC’s (airway, breathing,
circulation)
c. Give systemic corticosteroids
d. Make a food diary
ANAPHYLAXIS
 Anaphylaxis is a serious allergic reaction that is rapid in
onset and may cause death
 Patients with anaphylaxis may have no skin lesions,
lesions of angioedema, and/or typical urticarial wheals
 Morphology of the skin lesion does not matter
• Patients with angioedema are not more likely to have
anaphylaxis compared to patients with urticaria
 ABC’s first!
 Recruit more help. May need to triage to higher level of
care (in clinic this means calling 911).
ANAPHYLAXIS: TREATMENT
 First-line therapy for anaphylaxis includes
epinephrine, IV fluids and oxygen
 Administer 0.3-0.5ml in 1:1000 epinephrine
dilution IM repeating every 10-20min as
necessary
 Make sure airway is patent or else intubation
may be emergently necessary
 Patients who have severe reactions requiring
epinephrine should be monitored in the hospital
SYNOPSIS
 Urticaria (hives) is a vascular reaction of the skin
characterized by wheals surrounded by a red halo or
flare.
 Urticaria is classified as acute or chronic. Acute urticaria
is defined as periodic outbreaks of urticarial lesions that
resolve within six weeks.
 Over 50% of chronic urticaria is idiopathic.
 Oral H1 antihistamines are first-line treatment for acute
and chronic urticaria.
 1st generation H1 antihistamines can cause sedation.
 The presence of systemic symptoms should signal the
possibility that an urticarial rash is not ordinary urtica
SYNOPSIS
 Anaphylaxis is a serious allergic reaction that is
rapid in onset and may cause death.
 Remember to ask about symptoms of
anaphylaxis, including: chest tightness or
difficulty breathing, hoarse voice or throat
tightness, nausea, vomiting, abdominal pain,
lightheadedness.
 The 1st step in management of a patient with
signs and symptoms of anaphylaxis is to assess
airway, breathing, circulation, and adequacy of
mentation.
 Call for help if you suspect a patient has
anaphylaxis
The End
Yours Sincerely: Group 90 (Class of 2016)

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Urticaria

  • 2. URTICARIA: THE BASICS  Urticaria (hives) is a vascular reaction of the skin characterized by wheals surrounded by a red halo or flare (area of erythema)  Cardinal symptom is PRURITUS (itch)  Urticaria is caused by swelling of the upper dermis  Up to 20% of the population experience urticaria at some point in their lives
  • 3. ANGIOEDEMA: THE BASICS  Angioedema can be caused by the same pathogenic mechanisms as urticaria, but the pathology is in the deep dermis and subcutaneous tissue and swelling is the major manifestation  Angioedema commonly affects the face or a portion of an extremity  Involvement of the lips, cheeks, and periorbital areas is common, but angioedema also may affect the tongue, pharynx, larynx and bowels  May be painful or burning, but not pruritic  May last several days
  • 6. URTICARIA & ANGIOEDEMA  Urticaria and angioedema may occur in any location together or individually.  Angioedema and/or urticaria may be the cutaneous presentation of anaphylaxis, so assessment of the respiratory and cardiovascular systems is vital!
  • 7. URTICARIA: CLINICAL FINDINGS  Lesions typically appear over the course of minutes, enlarge, and then disappear within hours  Individual wheals rarely last >12hrs  Surrounding erythema will blanch with pressure  Urticaria may be acute or chronic • Acute = new onset urticaria < 6 weeks • Chronic = recurrent urticaria (most days) > 6 weeks  Most urticaria is acute and resolves
  • 8. COMMON CAUSES OF ACUTE URTICARIA  Idiopathic  Infection • Upper respiratory, streptococcal infections, helminthes  Food reactions • Shellfish, nuts, fruit, etc.  Drug reactions  IV administration • Blood products, contrast agents
  • 9. ETIOLOGY OF CHRONIC URTICARIA  Idiopathic: over 50% of chronic urticaria  Physical urticarias: many patients with chronic urticaria have physical factors that contribute to their urticaria • These factors include pressure, cold, heat, water (aquagenic), sunlight (solar), vibration, and exercise • Cholinergic urticaria is triggered by heat and emotion • The diagnosis of pure physical urticaria is made when the sole cause of a patient’s urticaria is a physical factor  Chronic autoimmune: possibly a third or more of patients with chronic urticaria  Other: infections, ingestions, medications
  • 10. DERMATOGRAPHISM  Most common form of physical urticaria  Sharply localized edema or wheal within seconds to minutes after the skin has been rubbed  Affects 2-5% of the population
  • 11. URTICARIA: PATHOPHYSIOLOGY  The mast cell is the major effector cell in urticaria  Immunologic Urticaria: antigen binds to IgE on the mast cell surface causing degranulation, which results in release of histamine • Histamine binds to H1 and H2 receptors to cause arteriolar dilatation, venous constriction and increased capillary permeability.
  • 12. URTICARIA: PATHOPHYSIOLOGY  Non-Immunologic Urticaria: not dependent on the binding of IgE receptors • For example, aspirin may induce histamine release through a pharmacologic mechanism where its effect on arachidonic acid metabolism causes a release of histamine from mast cells. • Physical stimuli may induce histamine release through direct mast cell degranulation
  • 14. CASE ONE: HISTORY  HPI: Mrs. Cook is a 46-year-old woman with a 3-day history of a widespread pruritic rash. Individual lesions last approximately 8hrs. She recently started a new laundry detergent.  PMH: hip replacement 6 weeks ago  Allergies: none  Medications: oxycodone (for pain, s/p hip replacement) and aspirin  Family history: no history of atopic dermatitis or allergies  Social history: lives with her husband in the city  ROS: negative
  • 15. CASE ONE: EXAM  Vital signs: afebrile, HR 74, BP 120/70, RR 16, O2 sat 98% on RA  Skin: diffuse erythematous papules coalescing into plaques (wheals)  No associated bruising
  • 16. CASE ONE, QUESTION 1  What other part(s) of the exam are essential? a. Musculoskeletal b. Neurologic c. Psychiatric d. Respiratory e. All of the above
  • 17. CASE ONE, QUESTION 1 Answer: d  What other part(s) of the exam are essential? a. Musculoskeletal b. Neurologic c. Psychiatric d. Respiratory e. All of the above
  • 18. CLINICAL EVALUATION  Ask about symptoms of anaphylaxis, including: chest tightness or difficulty breathing, hoarse voice or throat tightness, nausea, vomiting, abdominal pain, lightheadedness  In addition to the skin exam, the physician should obtain a set of vital signs and evaluate for respiratory distress (dyspnea, wheeze, bronchospasm, stridor) and hypotension  For acute urticaria, no lab testing is required • Laboratory testing is generally driven by associated signs and symptoms (e.g. C1 esterase deficiency only causes angioedema, not hives)
  • 19. CASE ONE, QUESTION 2  What important feature(s) are revealed in the history? a. She recently began a new detergent b. She recently began new medications c. The lesions last 8hrs d. Three-day history of rash
  • 20. CASE ONE, QUESTION 2 Answer: b, c, d  What important feature(s) are revealed in the history? a. She recently began a new detergent (not related) b. She recently began new medications (likely etiology) c. The lesions last 8hrs (individual wheals rarely last over 12 hrs.) d. Three-day history of rash (this is acute urticaria)
  • 21. DIAGNOSIS: MEDICATION-INDUCED URTICARIA  Medications are a common cause of urticaria and angioedema • Penicillin and related antibiotics are common via the IgE-mediated mechanism • Aspirin is a common cause via a non-IgE-mediated mechanism • 30% of chronic urticaria is exacerbated by aspirin/NSAID use  Many patients ask about detergent use. However, it causes irritant or allergic contact dermatitis, not urticaria.
  • 23. CASE TWO: HISTORY  HPI: Ms. Jennings is a 55-year-old woman who presents to the dermatology clinic with a 6-month history of periodic swelling on her body. The swelling started with localized itching followed by raised lesions that disappear within minutes to hours. She finds these lesions embarrassing and would like treatment or a cure.  PMH: no hospitalizations or major illnesses  Medications: occasional NSAID, daily fish oil, Vitamin D  Allergies: no known drug allergies  Family history: no history of skin disease  Social history: married, works as a nurse  Health-related behaviors: no tobacco, alcohol or drug use
  • 24. CASE TWO CONTINUED  Further questioning reveals that Ms. Jennings’s urticaria is worse with exercise, rubbing of the skin, pressure (e.g. develops lesions at the site of her purse strap on her shoulder), and embarrassment.  She also describes that most of the time she does not notice an association with any potential triggers.  Her lesions appear 2-3x/week, often in public. She is particularly embarrassed when lesions appear on her face while taking care of patients
  • 25. CASE TWO: SKIN EXAM  Vital signs within normal limits  Full skin exam reveals: • No wheals or erythema • Multiple benign appearing nevi on the trunk
  • 26. CASE TWO, QUESTION 1  Which of the following medications may be contributing to her urticaria? a. Fish oil b. Ibuprofen c. Vitamin D d. All of the above
  • 27. CASE TWO, QUESTION 1 Answer: b  Which of the following medications may be contributing to her urticaria? a. Fish oil b. Ibuprofen c. Vitamin D d. All of the above
  • 28. CLINICAL EVALUATION  Urticaria is a clinical diagnosis  A detailed history and physical exam should be performed  Many times patients will not present with urticaria during their clinic visit • Can show patients photographs of urticaria and ask if their lesions appear similar • Patients can take photos of their skin lesions and bring them to their office visit
  • 29. CLINICAL EVALUATION  In most cases of chronic urticaria, no external cause can be identified  If a physical urticaria is suspected, a challenge test with the respective trigger may be performed  Patients will often ask about food allergies • IgE-mediated food allergy is far more likely to present with acute urticaria • A detailed food diary or dietary modification may reveal foods (or additives) that cause fluctuations in symptoms of chronic urticaria
  • 30. ALLERGY TESTING  Allergy testing is not routinely performed in patients with chronic urticaria. • Skin prick testing may reveal sensitivities to a variety of allergens that may not be relevant to the patient’s urticaria. • Laboratory tests may identify the 1/3 of patients with chronic urticaria who have an autoimmune pathogenesis. This adds additional costs and may not change the management.
  • 31. NATURAL HISTORY AND PROGNOSIS  Symptoms of chronic urticaria can be severe and impair the patient’s quality of life (QOL)  In most patients, chronic urticaria is an episodic and self-limited disorder  Average duration of disease is two to five years  In patients with idiopathic chronic urticaria, there is a rate of spontaneous remission at one year of approximately 30 to 50 percent  However, symptoms extend beyond five years in nearly one-fifth of patients
  • 32. BACK TO MS. JENNINGS  Ms. Jennings was recommended to avoid tight clothing, stop ibuprofen, and start a first- generation antihistamine (e.g. hydroxyzine).  During a follow-up visit, Ms. Jennings reports she stopped the hydroxyzine because it made her too sleepy and she worried it was beginning to affect her work performance. She became teary-eyed and shared her frustration with her skin condition and fear that she would not be cur
  • 33. CASE TWO: FOLLOW-UP VISIT  Patients with chronic urticaria are often frustrated and fearful. Validation and reassurance are important components of successful management.  Sharing the following information may help: • Chronic urticaria is rarely permanent. Approximately 50 % of patients undergo remission within one year. • While acute urticaria and angioedema may be manifestations of allergic reactions that can be life-threatening, chronic urticaria is a different disorder that rarely puts the patient at any acute risk. • The symptoms of chronic urticaria can be successfully managed in the majority of patients.
  • 34. CASE TWO, QUESTION 2  Which of the following treatments would you recommend for Ms. Jennings? a. Daily oral 2nd generation H1 antihistamine b. Daily topical retinoid to the face c. No need to continue with an antihistamine; stopping the NSAID should resolve the urticaria d. Oral 2nd generation H1 antihistamine taken when the itching begins
  • 35. CASE TWO, QUESTION 2 Answer: a  Which of the following treatments would you recommend for Ms. Jennings? a. Daily oral 2nd generation H1 antihistamine b. Daily topical retinoid to the face (not used for urticaria) c. No need to continue with an antihistamine; stopping the NSAID should resolve the urticaria (treatment should be initiated in addition to removing potential triggers) d. Oral 2nd generation H1 antihistamine taken when the itching begins (less practical and will not help prevent the initial lesion)
  • 36. TREATMENT: ANTIHISTAMINES  Oral H1 antihistamines are the first-line treatment for acute and chronic urticaria  1st-generation H1 antihistamines are less well-tolerated due to sedation • e.g. 10-50 mg hydroxyzine 1-2 hours before bedtime • Can start with smaller doses (10 mg) to allow the patient to manage the sedation effects • Remember to warn patient not to drive a car or operate other dangerous machines within 4-6 hours of taking this medication • Do not take with other sedating medications
  • 37. TREATMENT: ANTIHISTAMINES  2nd-generation H1 antihistamines (e.g. Loratadine) are better tolerated with fewer sedative and anticholinergic effects and may be used in patients intolerant of or inadequately controlled by 1st- generation agents  Certain populations, including children, the elderly, and patients with renal or hepatic impairment may require dosage adjustments when using H1 antihistamines  Also used with caution in patients with glaucoma, prostatic hyperplasia, and respiratory disease
  • 38. ANTIHISTAMINES  The following are examples of H1 antihistamines: • 1st Generation • Diphenhydramine (OTC) • Hydroxyzine (Rx, generic) • Chlorpheniramine (OTC) • 2nd Generation • Cetirizine (OTC) • Loratadine (OTC) • Fexofenadine (OTC)
  • 39. URTICARIAL LESIONS  Not all patients with urticarial eruptions have urticaria. Which of the following patients has ordinary urticaria?
  • 41. BEYOND ORDINARY URTICARIA  The appearance of the hives does not tell you the underlying cause  The presence of systemic symptoms should signal the possibility that an urticarial rash is not ordinary urticaria but rather a systemic syndrome with urticaria-like skin lesions
  • 42. REFERRAL TO DERMATOLOGY  Referral to a dermatologist and biopsy should be performed in patients with one or more of the following features: • Individual lesions that persist beyond 48 hours, are painful rather than pruritic, or have accompanying petechial characteristics • Systemic symptoms • Lack of response to antihistamines • Lesions that leave pigmentation changes upon resolution
  • 44. CASE THREE: HISTORY  HPI: Mrs. Walker is a 25-year-old woman who was brought to the emergency department by her husband after she began feeling short of breath with a new and expanding rash  PMH: asthma, no history of intubations  Allergies: aspirin (causes a rash) & shellfish (reaction at a young age of facial swelling)  Medications: occasional use of albuterol  Family history: noncontributory  Social history: recently started cooking school  ROS: short of breath, anxious
  • 45. CASE THREE: EXAM  Vitals: T 98.6F, HR 110, BP 90/50, RR 34  General: anxious- appearing woman sitting upright with difficulty breathing, unable to speak in full sentences  Respiratory: tachypneic, using accessory muscles, bilateral rhonchi  Skin: periorbital edema, scattered erythematous wheals on the trunk
  • 46. CASE THREE, QUESTION 1  What is the next course of action in this patient? a. Administer IV metoprolol b. Assess ABC’s (airway, breathing, circulation) c. Give systemic corticosteroids d. Make a food diary
  • 47. CASE THREE, QUESTION 1 Answer: b  What is the next course of action in this patient? a. Administer IV metoprolol b. Assess ABC’s (airway, breathing, circulation) c. Give systemic corticosteroids d. Make a food diary
  • 48. ANAPHYLAXIS  Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death  Patients with anaphylaxis may have no skin lesions, lesions of angioedema, and/or typical urticarial wheals  Morphology of the skin lesion does not matter • Patients with angioedema are not more likely to have anaphylaxis compared to patients with urticaria  ABC’s first!  Recruit more help. May need to triage to higher level of care (in clinic this means calling 911).
  • 49. ANAPHYLAXIS: TREATMENT  First-line therapy for anaphylaxis includes epinephrine, IV fluids and oxygen  Administer 0.3-0.5ml in 1:1000 epinephrine dilution IM repeating every 10-20min as necessary  Make sure airway is patent or else intubation may be emergently necessary  Patients who have severe reactions requiring epinephrine should be monitored in the hospital
  • 50. SYNOPSIS  Urticaria (hives) is a vascular reaction of the skin characterized by wheals surrounded by a red halo or flare.  Urticaria is classified as acute or chronic. Acute urticaria is defined as periodic outbreaks of urticarial lesions that resolve within six weeks.  Over 50% of chronic urticaria is idiopathic.  Oral H1 antihistamines are first-line treatment for acute and chronic urticaria.  1st generation H1 antihistamines can cause sedation.  The presence of systemic symptoms should signal the possibility that an urticarial rash is not ordinary urtica
  • 51. SYNOPSIS  Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death.  Remember to ask about symptoms of anaphylaxis, including: chest tightness or difficulty breathing, hoarse voice or throat tightness, nausea, vomiting, abdominal pain, lightheadedness.  The 1st step in management of a patient with signs and symptoms of anaphylaxis is to assess airway, breathing, circulation, and adequacy of mentation.  Call for help if you suspect a patient has anaphylaxis
  • 52. The End Yours Sincerely: Group 90 (Class of 2016)

Notas do Editor

  1. 2nd generation H1 antihistamine Eg: Loratadine, Astemizole, Rupatadine & Bilastine
  2. Some Things To Consider in Differential Diagnosis: i)Bullous pemphigoid is an acute or chronic autoimmune skin disease, involving the formation of blisters, more appropriately known as bullae, at the space between the skin layers epidermisand dermis. It is classified as a type II hypersensitivity (cytotoxic) reaction. ii) Urticarial Vasculitis is a rare autoimmune disease characterised by recurrent urticaria (nettle rash). There is no defined paradigm for the syndrome aetiology and severity. Diagnosis is confirmed with the identification of at least two conditions: venulitis on skin biopsy, arthritis, ocular inflammation, abdominal pain or positive C1q antibodies to immune complexes. It is the anti-C1q antibodies, that all HUV (Hypocomplementemic urticarial vasculitis syndrome) patients test positive for.