Slide 16/1/2015 GLORIA™ is supported by unrestricted educational grants from.

04/18/23

GLORIA™ is supported by unrestricted educational grants from

04/18/23

GLORIA Module 3Allergic Emergencies

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Allergic Emergencies

WAO Expert Panel

Authors:Richard F Lockey, USAConnie H Katelaris, AustraliaMichael Kaliner, USA

Contributors:F.Estelle R. Simons, CanadaDaniel Vervloet, France

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Section 1: Anaphylaxis

Section 2: Upper Airway Oedema

Section 3: Severe Asthma Exacerbations

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Section 1: Anaphylaxis

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Anaphylaxis Lecture Objectives

After this lecture, participants will:

Have knowledge of the different mechanisms which cause anaphylaxis and the agents which are most likely to cause it;

Be able to recognize the signs and symptoms of anaphylaxis;

Understand how to treat anaphylaxis.

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Definition of Anaphylaxis

Anaphylaxis – a syndrome with varied mechanisms, clinical presentations, and severity.

An acute life-threatening reaction.

Usually mediated by an immunologic mechanism, allergic anaphylaxis, but not always.

Includes non-allergic anaphylaxis (formerly referred to as an anaphylactoid reaction).

Results from the release of mast-basophil mediators.

WAO Nomenclature Review Committee JACI 2004

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Gell and Coombs’ Hypersensitivity (immunopathologic reactions)

Type I Immediate Type II Cytotoxic Type III Immune Complex Type IV Delayed Hypersensitivity

Types I, II and III can result in immunologically-induced or allergic anaphylaxis

Kemp and Lockey JACI 2002

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Biochemical Mediators and Chemotactic Substances

Degranulation of mast cells and basophils. Preformed granule-associated substances, e.g.,

histamine, tryptase, chymase, heparin, histamine-releasing factor, other cytokines.

Newly generated lipid-derived mediators, e.g., prostaglandin D2, leukotriene B4, PAF, LTC4, LTD4, and LTE4.

Eosinophils may play pro-inflammatory role (release of cytotoxic granule-associated proteins) or anti-inflammatory role (e.g., metabolism of vasoactive mediators).


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Shock Organs in Anaphylaxis

Guinea pig – bronchial smooth muscle constriction. Rabbit – fatal pulmonary artery vasoconstriction

with right ventricular failure. Dog – venous system of liver contracts producing

hepatic congestion. Human – shock organs are the cardiovascular

system, respiratory tract, skin, and gastrointestinal tract. Laryngeal oedema, respiratory failure, and circulatory collapse are common.

Asthma is an important risk factor for death from anaphylaxis.

Kemp and Lockey JACI

2002 Bock, Munoz-Furlong, Sampson JACI 2001

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Incidence Analysis of published studies of most common causes 3.3 to 4 million Americans at risk. 1,433 to 1,503 at risk for fatal reaction. Neugut, Ghatak, Miller Arch Int Med 2001

Incidence Based on Epinephrine Rx for Out-of-Hospital Use From Canada and Wales. 0.95% of population in Manitoba, Canada. 0.2 per 1000 in Wales. Incidence increased in Wales between 1994 & 1999.

Simons, Peterson, Black JACI 2002

Rangaraj, Tuthill, Burr, Alfaham JACI 2002

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Incidence of Anaphylaxis to Specific Agents 1Antibiotics Most common cause of drug induced anaphylaxis.

Latex Increased incidence last decade. Population at risk includes multiple mucosal exposure to latex (catheterization & surgery) and healthcare workers.

Radiocontrast agents Introduction of lower osmolarity agents reduced reaction rate

Lieberman In: Allergy: Principles and Practice. Mosby, 2003

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Incidence of Anaphylaxis to Specific Agents 2

Hymenoptera stings Incidence ranges from 0.4% to 5% Estimated fatalities 100 per year in U.S.A.

Food Estimated 2% of US population has food allergies with up to 100 deaths per year Shellfish most common in adults; peanuts in children

Lieberman In Allergy: Principles and Practice Mosby, 2003

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Perioperative anaphylaxis Incidence ranges from 1 in 4500 to 1 in 2500 cases of general anaesthesia

Mortality rate can be as high as 3.4%

Most common agents responsible are muscle relaxants, which account for 50% to 75% of reactions.


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Non Steroidal Anti-Inflammatory Drugs (NSAIDs) Incidence varies depending on whether

asthmatic subjects are included

NSAIDs probably second most common

offending drug next to antibiotics.


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Antisera Heterologous antisera to treat snake bites (4.6%

to 10%) Immunosuppression, incidence for anti-

lymphocyte globulin as high as 2%

Idiopathic Estimated to be between 20,592 and 47,024 cases

in USA – deaths rare

Lieberman in Allergy: Principles and Practice Mosby 2003

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Allergen Immunotherapy

• Incidence of systemic reaction from 0.8% to 46.7% depending on the dose of allergen and schedule used.

Deaths occur at a rate of 1 per 2,000,000 injections.

Stewart and Lockey JACI 1992

Kemp et al In: Allergens and Allergen Immunotherapy Marcel Dekker, 2004

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Signs and Symptoms of Anaphylaxis

Diffuse erythema Diffuse pruritus Diffuse urticaria Angioedema Bronchospasm Laryngeal edema Hyperperistalsis Hypotension

Cardiac arrhythmias Nausea Vomiting Lightheadedness Headache Feeling of impending doom Unconsciousness Flushing


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Differential Diagnostic Considerations in Anaphylaxis

Vasovagal reactions Idiopathic flushing Mastocytosis Carcinoid syndrome Anxiety-induced hyperventilation Globus hystericus Serum sickness C-1 esterase inhibitor deficiency Shock-associated with myocardial infarction, blood loss, septicemia Scombroid poisoning

Montanaro and Bardana JACI 2002

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Comments About Signs and Symptoms

of Anaphylaxis Urticaria or angioedema and flush most common ( > 90%). Cutaneous manifestations may be delayed or absent Next most common manifestations are respiratory (40% to 60%). Next are dizziness, unconsciousness (30% to 35%). Gastrointestinal symptoms (20% to 30%). More rapid onset, more likely serious. Signs and symptoms within 5 to 30 minutes, but may not develop for hours.


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Agents that Cause Anaphylaxis 1Anaphylactic (IgE-Dependent) Foods (peanut, tree nuts,

and crustaceans) Milk, egg and fish also

important, especially in children

Medications (antibiotics) Venoms Latex Allergen vaccines Hormones Animal or human proteins Diagnostic allergens

Muscle relaxants Colorants (insect-derived, such as

carmine) Enzymes Polysaccharides Aspirin and other non-

steroidal anti-inflammatory drugs (probably)

Exercise (possibly, in food and medication-dependent events)

Kemp Immunol Allergy Clin N Am 2001

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Agents that Cause Anaphylaxis 2 (Allergic but not IgE Mediated)

Immune aggregates (Type II)

Intravenous immunoglobulin

Dextran (possibly)

Cytotoxic (Type III)

Transfusion reactions to cellular elements (IgG, IgM)


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Agents that Cause Anaphylaxis 3 (Non-allergic or IgE-independent)

Multimediator complement activation/activation of contact system: Radiocontrast media

Ethylene oxide gas on dialysis tubing

Protamine (possibly)

ACE-inhibitor administered during renal dialysis with sulfonated polyacrylonitrile, cuprophane, or polymethylmethacrylate dialysis membranes


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Agents that Cause Anaphylaxis 4(Non-allergic or IgE Independent)

Nonspecific degranulation of mast cellsand basophils

Opiates

Idiopathic

Physical factors:

Exercise Temperature (cold, heat)


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-Adrenergic Blockade By mouth or topically.

Paradoxical bradycardia, profound hypotension,and severe bronchospasm.

Can exacerbate disease and may impede treatment.

Selective β-blockers do not produce clinically significant adverse respiratory effects in mild-moderate asthma (including COPD). Not studied in anaphylaxis.

Toogood CMAJ 1987

Kivity and Yarchovsky JACI 1990

Salpeter, Ormiston, Salpeter Annals Int Med 2002

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Recurrent and Persistent Anaphylaxis

Recurrent or biphasic anaphylaxis occurs 8 to 12 hours in up to 20%.

Subjects with biphasic do not differ clinically but more epinephrine may be necessary for initial symptoms.

Persistent anaphylaxis may last from 5 to 32 hours.

Lee and Greenes Pediatrics, 2000

Kemp and deShazo In: Allergens and Allergen Immunotherapy to Treat Allergic Diseases. Marcel Dekker, 2004

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Physician-Supervised Management of Anaphylaxis 1

I. Immediate Intervention a) Assessment of airway, breathing, circulation, and

mentation.

b) Administer EPI, 1:1000 dilution, 0.3 - 0.5 ml (0.01 mg/kg in children, max 0.3 mg dosage) IM, to

control SX and BP. Repeat, as necessary.


Simons et al JACI 1998

Simons, Gu, Simons JACI 2001

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I. Immediate Intervention continued c) IM into the anterolateral thigh (vastus lateralis)

produces higher & more rapid peak plasma level versus SQ & IM in arm. Therefore, with moderate, severe, or progressive ANA, EPI IM into anterolateral thigh. Alternatively, an EPI autoinjector given through clothing in same manner. Repeat, as necessary.


Simons et al JACI 1998

Simons, Gu, Simons JACI 2001

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I. Immediate Intervention - continued

d) Aqueous EPI 1:1000, 0.1- 0.3ml in 10ml NS (1:100,000 to 1:33,000 dilution), IV over several minutes prn.

e) For potentially moribund subjects, tubercular syringe, EPI 1:1000, 0.1 ml, insert into vein (IV), aspirate 0.9 ml of blood (1:10,000 dilution). Give as necessary for response.


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II. General measures

a) Place in recumbent position and elevate lower extremities.

b) Maintain airway (endotracheal tube or cricothyrotomy).

c) O2, 6 - 8 liters/minute.

d) NS, IV. If severe hypotension, give volume expanders (colloid solution). e) Venous tourniquet above reaction site. Question if decreases absorption of allergen.


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III. Specific Measures that Depend on Clinical Scenario

a) Aqueous EPI 1:1,000, ½ dose (0.1- 0.2 mg) at reaction site.

b) Diphenhydramine, 50 mg or more in divided doses orally or IV, maximum daily dose 200 mg (5 mg/kg) for children and 400 mg for adults.

c) Ranitidine, 50 mg in adults and 12.5 - 50 mg (1 mg/kg) in children, dilute in 5% G/W, total 20 ml,

inject IV, over 5 minutes. (Cimetidine 4 mg/kg OK for adults, not established for pediatrics).


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d) Bronchospasm, nebulized albuterol 2.5 - 5 mg in 3 ml NS or levalbuterol 0.63 - 1.25 mg

as needed.

e) Aminophylline, 5mg/kg over 30 min IV may be helpful. Adjust dose based on age, medications, disease, current use.

f) Refractory hypotension, give dopamine, 400 mg in 500 ml G/W IV 2 - 20 μg/kg/min more or less.


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g) Glucagon, 1- 5 mg (20 - 30 μg/kg [max 1 mg] in children), administered IV over 5 minutes followed with IV infusion 5-15 μg/min.

h) Methylprednisolone, 1- 2 mg/kg per 24 hr; prevents prolonged reactions and relapses.


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Vasodepressor (Vaso-Vagal) Definition

Non-allergic reaction characterized by slow pulse nausea, pallor, sweating, clammy skin, and/or hypotension.


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Vasodepressor (Vaso-Vagal)

Management

a) Place patient in supine position with elevated lower extremities.

b) For severe vasodepressor reaction ONLY (i.e., bradycardia, nausea, pallor, sweating, cool clammy skin, hypotension), atropine 0.3 - 0.5 mg (0.02 mg/kg) SQ every 10 minutes (max 2 mg/adult and 1 mg/child).

c) If hypotension persists, give IV fluids.


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Measures to Reduce the Incidence of Drug- Induced Anaphylaxis and Anaphylactic Deaths 1

General Measures Obtain thorough history for drug allergy. Avoid drugs with immunological or biochemical

cross-reactivity with any agents to which the patient is sensitive.

Administer drugs orally rather than parenterally when possible.

Check all drugs for proper labeling

Keep patients in clinic for 20 to 30 minutes after injections.

Lieberman In: Allergy: Principles and Practice Mosby, 2003

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Measures to Reduce the Incidence of Anaphylaxis and Anaphylactic Deaths 2

Measures for Patients at Risk

Avoid causative factor/s.

Have patient wear and carry warning identification.

Teach self-injection of epinephrine and caution patient to keep epinephrine kit with them.

Discontinue -adrenergic blocking agents, ACE inhibitors (controversial), monoamine oxidase inhibitors, and tricyclic antidepressants, where possible.


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Measures to Reduce the Incidence of Anaphylaxis and Anaphylactic Deaths 3

Measures for Patients at Risk

Use preventive techniques when patient is required to undergo a procedure or take an agent which places them at risk. Such techniques include:

Pretreatment Provocative challenge

Desensitization


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Summary

Prognosis

Factor Poor Good

Dose of antigen (allergen) Large Small

Onset of symptoms Early Late

Initiation of treatment LateEarly

Route of exposure ParenteralOral*

β-adrenergic blocker use Yes No

Presence of underlying disease Yes No

* True for drugs, not foods

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Section 2: Upper Airway Oedema

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Upper Airway Oedema Lecture Objectives

To understand the causes of angioedema;

To review the spectrum and management of hereditary angioedema;

To review Angiotensin Converting Enzyme (ACE) inhibitor related angioedema.

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Outline of Lecture Clinical description

Classification

Examples of life-threatening oedema:

Hereditary angioedema Acquired oedema Angiotensin enzyme inhibitor-induced oedema

Clinical description Pathophysiology Management

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Angioedema First described by Quincke in

1882 Well-demarcated non-pitting

oedema Caused by same pathological

factors that cause urticaria Reaction occurs deeper in

dermis and subcutaneous tissues

Face, tongue, lips, eyelids most commonly affected

May cause life-threatening respiratory distress if larynx involved

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Classification of Angioedema 1

Hereditary Type 1: C1 esterase inhibitor deficiency Type 2: functional abnormality of C1 esterase

inhibitor

Acquired Idiopathic IgE-mediated Non-IgE-mediated Systemic disease Physical causes Other

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IgE-mediated Drugs Foods Stings Infections (eg viral, helminthic)

Non-IgE-mediated Cyclooxygenase inhibition (ASA and other

NSAIDS) Angiotensin converting enzyme inhibition

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Systemic diseases

Systemic lupus erythematosis

Hypereosinophilia

Lymphoma: abnormal antibodies activate complement

system

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Physical causes Cold Cholinergic Solar Vibratory

Other Some contact reactions Autoantibodies to C1-esterase inhibitor Unopposed complement activation

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Incidence

Chronic idiopathic urticaria/angioedema occurs in 0.1% population

65% remit within 3 years85% remit within 5 years95% remit within 10 years

Angioedema occurs most commonly with urticaria (40% cases)

May occur in isolation (10% cases)

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Hereditary Angioedema (HAE)

1888 - family described by William Osler

1963 - Donaldson and Evans described the biochemical defect responsible - absence of C1

inhibitor

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Subtypes

Type 1*

Autosomal dominant Markedly suppressed C1 esterase

inhibitor protein levels

* Accounts for 85% cases

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Subtypes

Type 2*

Autosomal dominant, with a point mutation leading to synthesis of a dysfunctional protein

Functional assay required for diagnosis as level may be normal

* Accounts for 15% cases

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Epidemiology 1:10,000 - 1:150,000 with no racial or gender predilection

Clinical manifestations Usually manifests in 2nd decade May be seen in young children Oedema may develop in one or several organs Presentation depends upon site of swelling Attacks last 2- 5 days before spontaneous resolution

Nzeako Arch Intern Med, 2001

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Clinical Manifestations 1

Angioedema may develop in subcutaneous tissues of extremities, genitalia, face, trunk.

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Oedema of wall of intestine may present as an acute abdominal emergency.

Submucosal oedema of larynx or pharynx may cause asphyxiation – this may occur on first presentation.

Bork Mayo Clin Proc 2000

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Laryngeal oedema

Commonest cause of mortality in HAE Time from onset of swelling to death 1- 14 hours

(mean 7 hours) May be presenting feature Death may occur in those with no previous

laryngeal oedema episodes Increased risk within certain families Early symptoms - lump in throat, tightness in throat Hoarseness, dysphagia, progressive dyspnoea

Bork Mayo Clin Proc 2000

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Diagnosis

Clinical presentation For screening - quantitative and functional

assays of C1 inhibitor C4 and C2 levels reduced in acute attack C4 persistently low in most patients

Nzeako Arch Intern Med 2001

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Hereditary Angioedema (HAE)Pathophysiology 1

C1 inhibitor

Single chain glycoprotein; molecular weight 104,000; serine protease family

Important regulatory protein of complement cascade

Inactivates C1 esterase complex Regulates coagulation, fibrinolytic, kinin,

complement systems

Nielson Immunopharmacology 1996

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Hereditary Angioedema (HAE) Pathophysiology 2

Lack of C1 inhibitor leads to abnormal activation of complement pathway, reduced C2 and C4 levels

Hageman factor induces formation of kallikrein from prekallikrein

Bradykinin is released from high molecular weight kininogen

All these mediators increase capillary permeability and are responsible for attacks of angioedema

Kaplan JACI 2002

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Genetics

Autosomal dominant; all patients heterozygous

25% no prior family history - spontaneous mutations

More than 100 different mutations reported

Varied clinical pattern may be explained by variable effect of mutations on C1 inhibitor synthesis

Agostini Medicine (Baltimore) 1992

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Hereditary Angioedema (HAE)Management

Principles

Action plan for acute episodes

Strategy for long term prophylaxis

Short term prophylaxis for high risk procedures

Regular follow up for education and monitoring side effects of therapy

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Management 1

Acute attacks

Treatment of choice is C1 inhibitor concentrate, 500 - 1,000U intravenous infusion Safe and effective - no long term side effects reported Excellent and prompt response in most patients Not available in USA, but in clinical trials

Bork Arch Intern Med 2001

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Management 2

Acute attacks when C1 inhibitor concentrate notavailable

Intubation and respiratory support may be necessary when laryngeal oedema present

Fresh frozen plasma (FFP) has been used successfully for acute attacks. Exacerbation of symptoms by supplying more kallikrein substrate is a theoretical consideration but is rarely seen

Bork Arch Intern Med 2001

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Management 3

Long term – adults

Attenuated androgens (stanozolol, danazol, oxandrin) can prevent attacks

Increase levels of C1 inhibitor, C4 and C2

Titrate to lowest effective dose to control attacks - for danazol may be able to reduce to 200 mg/d every second day

Regular monitoring necessary


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Management 4

Long term – children

Antifibrinolytic agents have been used as first line prophylaxis

Low dose danazol


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Management 5

Short term prophylaxis

Necessary for high risk interventions, eg, dental procedures, tonsillectomy

C1 inhibitor concentrate, where available, given before procedure

Increasing dose of attenuated androgen for a few days beforehand

Fresh frozen plasma

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Management 6

Other

Avoid oral contraceptive pill, ACE inhibitor medication Premedicate before procedures requiring

radiocontrast media or streptokinase as they may decrease C1 inhibitor levels

Reassurance; address issues such as ongoing stress Treat infections promptly Genetic counseling and screening

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Acquired Angioedema (AAE) 1

Type 1 Associated with rheumatologic diseases, B cell

lymphoproliferative disorders

Activation of complement by complexes of anti-idiotypic antibodies and surface immunoglobulins consumes C1 inhibitor so levels decline

Type 2 Development of autoantibodies against C1 inhibitor

Autoantibodies bind at active site on molecule leading to inactivation

Markovic Ann Int Med 2000

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Acquired Angioedema (AAE) 2 Decreased C1q levels distinguish AAE from HAE where

C1q is usually normal

Treatment of underlying condition may result in resolution

For acute attacks, C1 inhibitor concentrate, where available should be used

Attenuated androgen may be useful in Type 1

Immunosuppressive therapy for Type 2

Laurent Clin Rev Allergy Immunol 1999

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Angiotensin Converting Enzyme (ACE) Inhibitors and Angioedema 1

Angioedema develops in 0.1% to 0.5% of those receiving the drug

Onset from 1st week of use to 2 - 3 years of use Symptoms resolve within 24 - 48 hours of cessation of

drug Most commonly seen with captopril and enalopril but

described with all in class Genetic factors may be important Subjects with a history of angioedema from other

causes are more susceptible to ACE-induced angioedema

Slater JAMA 1988

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Face and lips most commonly involvedbut laryngeal oedema reported

Risk factors include obesity, prior endotracheal intubation and face and neck surgery

ACE inhibitors will trigger attacks in those with HAE so avoid in these patients

Jain Chest 1992

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Pathophysiology

ACE inhibitors may cause bradykinin accumulation resulting in vasodilatation, capillary leakage and angioedema

Patients may have a congenital or acquired impairment of kininase 1 which degrades bradykinin leading to bradykinin accumulation once ACE is blocked

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Management

Stop drug and use other classes of antihypertensive agents

ALL ACE inhibitors are to be avoided Management of angioedema depends on site of

involvement - securing the airway by intubation may be necessary

ACE receptor antagonists are generally considered to be safe

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Angioedema - Conclusions

Most often occurs in association with urticaria When angioedema occurs alone, consider HAE,

AAE HAE is a rare disease but must be identified as it

can be life-threatening Refer to appropriate specialist for ongoing

management ACE-inhibitor induced angioedema is an

important cause in older people

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Section 3: Severe Asthma Exacerbations

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Lecture Objectives

At the end of this lecture participants will be able to:

Understand the risk factors for asthma exacerbations;

Identify the signs and symptoms of acute asthma;

Outline appropriate treatment strategies.

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Features of a Severe Asthma Exacerbation

One or more present:

Use of accessory muscles of respiration Pulsus paradoxicus >25 mm Hg Pulse > 110 BPM Inability to speak sentences Respiratory rate >25 - 30 breaths/min PEFR or FEV1 < 50% predicted SaO2 <91- 92%

McFadden Am J Respir Crit Care Med 2003

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Risk Factors for Fatal or Near-Fatal Asthma Attacks

Previous episode of near-fatal asthma Multiple prior ER visits or hospitalizations Poor compliance with medical treatments Adolescents or inner city asthmatics (USA) African-Americans>Hispanics>Caucasians Allergy to Alternaria Recent use of oral CCS Inadequate therapy:

Excessive use of β-agonists No inhaled CCS Concomitant β-blockers

Ramirez and Lockey In: Asthma, American College of Physicians, 2002

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Physical Findings in Severe Asthma Exacerbations

Tachypnea Tachycardia Wheeze Hyperinflation Accessory muscle use Pulsus paradoxicus Diaphoresis Cyanosis Sweating Obtundation

Brenner, Tyndall and Crain In: Emergency Asthma. Marcel Dekker 1999

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Causes of Asthma Exacerbations

Lower or upper respiratory infections Cessation or reduction of medication Concomitant medication, e.g. β-blocker Allergen or pollutant exposure

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Differential Diagnosis

COPD Bronchitis Bronchiectasis Endobronchial

diseases Foreign bodies Extra- or intra-thoracic

tracheal obstruction Cardiogenic

pulmonary edema

Non-cardiogenic pulmonary edema

Pneumonia Pulmonary emboli Chemical pneumonitis Hyperventilation

syndrome Pulmonary embolus Carcinoid syndrome

Brenner, Tyndall, Crain In: Emergency Asthma. Marcel Dekker, 1999

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Peak Flow Meters Use peak flow meters to monitor asthma and prevent exacerbations: Inexpensive Easy to use Accurate Provide “real life” measurements at worst and best times of the day Provide objective measurement of pulmonary function Detect early changes of asthma worsening

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Patient “Self Management”

If personal best peak flow measurements: Fall 10+%, double dose of inhaled CCS Fall 20+%, use short-acting bronchodilator Q4

-6 hour, plus 2 x inhaled CCS Call office, try to determine if infection is

present Fall 40 - 50%, add oral CCS Fall greater than 50%, urgent visit to either

Outpatient office Emergency room

Kaliner In: Current Review of Asthma. Curent Medicine, 2003

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Stages of Asthma Exacerbations Stage 1:

Symptoms Somewhat short of breath Can lie down and sleep through the night Cannot perform full physical activities without shortness of

breath

Signs Some wheezes on examination Respiratory rate, 15 (normal <12) Pulse 100 Peak flows and spirometry reduced by 10%

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Symptoms Less able to do physical activity due to shortness of

breath Dyspnea on walking stairs May wake up at night short of breath Uncomfortable on lying down Some use of accessory muscles of respiration

Signs Wheezing Respiratory rate 18 Pulse 111 Peak flows and spirometry reduced by 20+%

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Symptoms Unable to perform physical activity without

shortness of breath Cannot lie down without dyspnea Speaks in short sentences Using accessory musclesSigns Wheezing Respiratory rate 19 - 20 Pulse 120 Peak flows and spirometry reduced by 30+%

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Symptoms Sitting bent forward Unable to ambulate without shortness of breath Single word sentences Mentally-oriented and alert Use of accessory muscles

Signs Wheezing less pronounced than anticipated Respiratory rate 20 - 25 Pulse 125+ Peak flows and spirometry reduced by 40+% SaO2 91- 92%

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Symptoms Reduced consciousness Dyspnea Silent chest – no wheezing

Signs Fast, superficial respiration Respiratory rate >25 Unable to perform peak flows or spirometry Pulse 130 - 150+ SAO2 <90

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Severity of Asthma as Graded by % Predicted FEV1

FEV% predicted Severity 70 - 100 Mild 60 - 69 Moderate 50 - 59 Moderately severe 35 - 49 Severe < 35 Very severe

(life-threatening)

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Treatment of Asthma Exacerbations 1

Preferred treatment choices β2-agonists

Inhaled by MDI or nebulizer Injected

Anticholinergics Inhaled by MDI or nebulizer

Corticosteroids Parenteral, oral or inhaled

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Treatment of Asthma Exacerbations 2

Secondary treatment choices Aminophylline or theophylline (oral,

parenteral) Leukotriene receptor antagonists (oral) Oxygen Magnesium sulfate

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Treatment of Asthma Exacerbations 3Beta Agonists

Inhaled is preferred route

MDI plus spacer, 4 - 8 puffs Q 20 min x 3 Nebulizer, 2.5 - 5 mg albuterol Q 20 min x 3 Epinephrine SQ, 0.3 - 0.5ml (0.01 ml/kg children) Levalbuterol, 0.63 - 1.25 mg Q 4 - 8 hours (if

available)

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Treatment of Asthma Exacerbations 4Anticholinergics

Ipratropium

Preferred use: combined with beta agonist MDI plus spacer, 2 - 4 puffs Q 20 min x 3 Nebulizer, 500 μg Q 20 min x 3

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Treatment of Asthma Exacerbations 5Corticosteroids

No immediate effect Earliest effects 6 hours after high dose Oral is as effective as parenteral Prednisone (equivalent), 45 - 60 mg Higher doses have increased side effects and no

appreciable increased therapeutic benefit Methylprednisolone, 1 – 2 mg/kg/24 hours No substantial data for usefulness in acute

setting

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Treatment of Asthma Exacerbations 6 Aminophylline and Theophylline

Controversial: Added no benefit to inhaled beta agonists Increased complications

Loading dose for aminophylline: 5 – 6 mg/kg over 20 - 30 min

Maintenance dose: 0.4 mg/kg/hr (adjust for heart and liver disease)

Try to achieve 5 - 15 μg/ml, monitor plasma levels to adjust dose

Doses for theophylline similar but slightly less

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Treatment of Asthma Exacerbations 7 Leukotriene Modifiers

Few studies Suggest usefulness in reducing hospitalizations Montelukast, 10 mg orally Zafirlukast, 20 mg orally

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Treatment of Asthma Exacerbations 8 Magnesium Sulfate

Controversial: Inconsistent data

Used in very severe asthma in emergency settings:

FEV1 < 25% predicted Other signs of severe disease

1.2 - 2 gm IV over 10 - 20 min in 50 ml saline Minor side effects

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Preventing Exacerbations 1Oral Corticosteroids

Oral corticosteroids are the most powerful medications available to reduce airway inflammation

Use until attack completely abated: PEFR and FEV1 at baseline levels Symptoms gone

Taper to QOD and determine if patient can remain well if corticosteroids are withdrawn completely

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Preventing Exacerbations 2 Inhaled Corticosteroids

Place patient on high dose inhaled corticosteroids Fluticasone, 880 - 1760 μg Budesonide, 800 - 1600 μg

Once oral corticosteroids are withdrawn, reduce the inhaled dose incrementally, while maintaining PEFR at personal best level

Consider combination of long acting β2-agonist and inhaled corticosteroid in order to achieve the lowest dose of corticosteroid possible

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Preventing Exacerbations 3Underlying Causes and Patient Education

Evaluate patient for: Allergy Infection Compliance Inappropriate concomitant medications Social factors Tobacco, drugs, irritants, fumes Psychiatric disorders

Patient education www.anafylaxis.nl

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World Allergy Organization (WAO)

For more information on the World Allergy Organization (WAO), please visit www.worldallery.org or contact the:

WAO Secretariat555 East Wells Street, Suite 1100

Milwaukee, WI 53202United States

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Email: [email protected]

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