Asthma Hypertrophy by nikeborome


  Definitionchronic inflammatory disorder of airways that is inducible, reversible, and associated with increased
   airway inflammation, airway hyper-responsiveness resulting in bronchospasm, and increased mucus production.

  Affects 5% of population

  Strongest predisposing factor we know of is atopy (existence of allergy but may or may not have s&s)

  Pathogenesis

        o     Eroded epithelium, collagen deposition beneath basement membrane, airway edema, mast cell
              activation(releasing histamine), inflammatory cell infiltration(neutrophils, eosinophils, T-lymphocytes),
              hypertrophy, mucus plugging

  Triggers

        o     Dust mites, pets, cockroaches, pollen, fungi, exercise, cold, respiratory infections, smoking (especially
              second-hand smoke) are all common. May also occur spontaneously.

  Pathological Features

        o     Airflow obstruction/inflammation/hyperactivity

        o     Bronchoconstriction

        o     Cough

        o     Mucus hypersecretion

        o     Impaired mucus clearance

        o     Smooth muscle hypertrophy

  Before Diagnosing

        o     Establish a history of recurrent symptoms

        o     Establish reversible airflow obstruction via spirometry before and after bronchodilator given

                     Significant reversibility= increase of 12%/200mL in FEV1 or 15%/200mL increase in FVC after
                      inhaling short-acting bronchodilator

        o     Exclude alternative diagnoses

  Diagnosis

        o     Episodic/chronic symptoms of airflow obstruction (breathlessness, chest tightness, wheezing, cough)

        o     Complete/partial reversibility of airflow obstruction

        o     Symptoms freq worse @ night/early morning

        o     Prolonged expiration & diffuse wheezes on PE
       o   Limitation of airflow on PFT or positive bronchoprovocation challenge(use inhaled
           histamine/methacholine to see if it induces bronchospasm)


       o   Upper Airway

                  Vocal cord dysfunction

                  Foreign body

                  Mass/Tumor

                  Angioedema

       o   Lower Airway

                  COPD

                  Bronchiectasis

                  Cystic Fibrosis

                  Pneumonia

                  CHF, Reflux, PE

 Evaluation Tools

       o   PEfor S&S

       o   ABGseverity

       o   CBCInfection

       o   Sputum Exameosinophils, bacteria

       o   PFTs(spirometry)

                  FVCmax volume of air that can be forcibly & rapidly exhaled (measured in L)

                  FEV1Volume of air expelled in 1st second of forced expiration

                           65-75% predicted=Mild obstruction

                           40-59% predicted=Moderate obstruction

                           <40% predicted=Severe obstruction

                  FVC/FEV1Represents how much of the forced expiration was expelled in 1st second

                           Normal=80%

       o   Bronchoprovocation Challenge

       o   Skin Tests
       o   CXR

 Key Measures of Control

       o   PFTs/Peak Flows(handheld devices designed as personal monitoring tools)

       o   Rescue Meds

       o   Exacerbations

       o   Systemic Steroids

       o   ED Visits

       o   Hospitalizations

       o   Intubations

 Pharmacotherapies

       o   Long acting bronchodilators

                    Mediator inhibitorsCromolyn and Nedocromil

                             For mild persistent asthma or exercise induced asthma

                             Modulate mast cell mediator release & eosinophil recruitment, inhibit early/ late
                              asthmatic responses to allergen challenge & exercise induced bronchospasm

                    Β- Adrenergic agonistsSalmeterol and Formoterol

                             Delivered via DPI

                             Bronchodilation for up to 12 hours

                             Delayed onset so they should not be used in the Tx of acute Bronchoconstriction

                             Indicated for long term prevention, nocturnal, exercised induced

                             MUST be used w/inhaled corticosteroid in asthma (but not COPD) bc ICS only treat
                              bronchospasm not inflammation

                    Phosphodiesterase InhibitorTheophylline

                             Controlling nocturnal asthma

                             Usually adjuvant therapy in patients with moderate or severe persistent asthma

                             Serum levels must be monitored closes due to narrow therapeutic window

                              Adverse effects include GERD insomnia, dyspepsia, and urinary difficulty. Toxicities
                              include n/v, tachyarrthymias, headache, seizure, hyperglycemia, and hypokalemia

       o   Anti-inflammatories
                      Inhaled/systemic corticosteroidsmost potent & consistently effective anti-inflamm agents
                       available. May potentiate the action of β-adrenergic agonists

           o   Leukotriene modifiers

                      Zileuton5-lipoxygenase inhibitor that decreases leukotriene production

                      Zafirlukast & Montelukastleukotriene receptor antagonists

                      Leukotrienes cause:

                                                Airway edema

                                                Airway smooth muscle constriction

                                                Altered airway cellular activity associated w/inflammation process

           o   Quick Relief Medications

                      Β-Adrenergic agonistsAlbuterol, Levalbuterol, Bitolterol, Pirbuterol, Terbutaline

                                Relax airway smooth muscle & cause prompt ↑ in airflow

                                Daily Albuterol Use=Poorly Controlled Asthma

Albuterol Use                                        Asthma Severity
>2 days per week but not more than once per day      Mild persistant(start with Step 2)

Daily                                          Moderate persistant(start with Step 3
Several times a day                            Severe persistant(start with Step 4 or 5)
            o AnticholinergicsIpratropium bromide

           o   Phosphodiesterase inhibitors

           o   Corticosteroids

                      Common ICS: Beclomethasone(Vanceril), Budesonide(Pulmicort), Fluticasone(Flonase),
                       Flunisolide(Aerobid), Triaminolone(Azmacort), Moemetasone (Asthmanex)

    Inhaled Delivery Devices

           o   MDImetered dose inhaler

           o   DPIdry powder inhaler

                      Diskus handled correctly more often than MDI’s due to pt failure to coordinate actuation &

           o   Spacer/Holding Chamber(with or without face mask)

           o   Nebulizer

           o   Importance of Device Handling in Asthma
                   Inhaled route of administration = best way of delivering drugs for day-to-day treatment of
                    asthma bc:

                             Allows drugs to reach high bronchial concentration

                             Minimizes systemic bioavailability

 Emergent Treatment

        o   Immediate Assessment

                   Nebulized SABA

                   IV corticosteroid

                   Nebulized anticholinergics

                   Consider Epi SQ or Terbutaline

                   Consider intubation

 Discharge Treatment

        o   Must Include:

                   Refill of any rescue medications MDI

                   Oral corticosteroids

        o   Step-up therapy to include:

                   LABA

                   ICS

                   Leukotriene inhibitor

                   MAST cell wall stabilizer

        o   Adjunctive Therapy

                   Infection

                   Antihistamine

        o   Re-evaluate after 24 hours

   11Classifications of Asthmabased on frequency/ severity of asthma symptoms, along with peak flow
                             STAGE FEV1     pH       Pa02     PaC02
                             I     50-80%   N or    N or    N or 
 Staging of Acute Asthma   II    50%      N or            

                             III   25%                      N or 

                             IV    10%                     

 6 Steps of Therapy
Intermittent                                                    Persistant
Step 1             Step 2                 Step 3                Step 4     Step 5                       Step 6
SABA as            Low-dose ICS           Low-dose ICS &        Medium-dose ICS     High-dose ICS &     High-dose ICS &
needed                                    LABA                  & LABA              LABA                LABA & oral
                   Alternative:                                                                         corticosteroid
                   Cromolyn,              OR: medium-           Alternative:        AND
                   nedocromil,            dose ICS              Medium-dose ICS &                       AND
                   leukotriene                                  either LTRA,        Consider
                   receptor antagonist,   Alternative: Low-     theophylline,       omalizumab for      Consider
                   or theophylline        dose ICS & either     zileuton            patients who have   omalizumab for
                                          LTRA, theophylline,                       allergies           patients who have
                                          or zileuton                                                   allergies
     Key Points in Determining Patient Control

               o     Frequency of rescue inhaler useshould be less than 2 times per week

               o     Last visit to ED

               o     Last course of steroidsevery month=not well controlled

               o     History of an ICU stay

               o     History of prior intubation

     Guidelines for Referral to an Asthma Specialist

               o     Pt had life-threatening asthma exacerbation

               o     Pt is not meeting goals of asthma therapy

               o     Signs/Symptoms are atypical

               o     Co-morbidity complicates asthma therapy

               o     Additional diagnostic testing is indicated

               o     Pt’s requiring Step 4 care

               o     Pt’s younger than 3 at Step 5/6

               o     Pt’s with significant psychiatric, psychosocial, or family problems

     Summary

               o     Uncontrolled asthma is a significant issue in the US

               o     Monitor control regularly regardless of reason for visit

               o     Low-dose ICS=preferred tx for mild persistant asthma

               o     Preferred tx for pt’s using daily Albuterol or uncontrolled on ICS = ICS/LABA

                             For those using Albuterol daily consider Advair Diskus 100/50
                     Advair Diskus has Tier 2 (preferred) status on more health plans than any other asthma
                      maintenance med. 7/10 pt’s pay $30 or less per month for Advair.

  DefinitionChronic obstructive pulmonary disease that shows airflow obstruction on spirometry caused by
   chronic bronchitis or emphysema.

                     Chronic Bronchitischronic cough w/expectoration that lasts at least 3 months in each of 2
                      successive years

                              ie: chronic cough w/expectoration lasting from Jan to April in 2007 followed by chronic cough
                               w/expectoration lasting from March to August in 2008

                     EmphysemaProgressive destruction of lung tissue caused by chronic irritants in the small airways

        o   Airflow limitation is not fully reversible

        o   Progressive

        o   Chronic abnormal inflamm response to: environmental pollutants, irritants, tobacco smoke

  Risk Factors

        o   Smoking80-90%

        o   Passive smoking, air pollution, hyper-responsive airways, white/male

        o   Alpha1-antitrypsin deficiency (>1%)

  Pathophysiologic Features

        o   Smooth muscle contraction

        o   ↑ cholinergic tone

        o   Loss of elastic recoil

        o   Oxidative Stress

                     ↑ neutrophils

                     ↑Macrophages

                     ↑ CD8 & lymphocytes

                     ↑ IL-8 & TNF-α

                     Protease/anti-protease imbalance

        o   Alveolar destruction

        o   Collagen deposition

        o   Glandular hypertrophy
         o    Airway fibrosis

   Clinical Features

         o    Typically smokers (mean 20 cigerettes per day x 20 years)

         o    Usually present in 5th decade of life w/productive cough or acute chest illness

         o    DOE

         o    Hx of wheezing/dyspnea may lead to erroneous dx of asthma

   Physical Exam

         o    Airflow Obstruction

                     Wheezing during auscultation

                     Prolongation of expiratory time

         o    Severe Emphysema indicated by:

                     Hyperinflation of lungs (flattens diaphragm & enlarges ribcage)

                     ↓ intensity of heart & breath sounds

         o    Severe disease indicated by:

                     Pursed-lip breathing

                     Use of accessory resp muscles

                     11Retraction of ICS

   Lab Tests

         o    Spirometrypre & post bronchodilator

                     Correlation btwn PaCO2 & FEV1:

                               ↑PaCO2=↓FEV1

         o    Chest radiography

         o    Lung volumes

         o    CO diffusing capacity

         o    ABG’s

   Classification by Severity

Stage        Characteristics                                        Tx (GOLD COPD guidelines)
0: At Risk         Normal spirometry w/chronic symptoms (cough, sputum)      Education
                                                                             Avoid risk factors (stop smoking silly! )
                                                                             Flu vaccine
I: Mild            FEV1/FVC<70% but FEV1 > 80% predicted                     Same as above plus:
                        Regardless of symptoms                              Short-acting bronchodilator(β-adrenergic) prn

                   IN ENGLISH????? the air expelled in the 1st
                   second was less than 70% of the total volume of
                   their expiration but it was better than 80% of the
                   value that was predicted for them

II: Moderate       FEV1/FVC<70% but FEV1 >30% predicted                      Regular bronchodilator + prn rehab
                        regardless of symptoms                              Consider ICS
                                                                             Flu vaccine
III: Severe        FEV1/FVC <70%                                             Same as above plus:
                         AND                                                 Long-term O2 therapy if indicated
                   FEV1<30% predicted OR FEV1<50% predicted w/resp           Surgery
                   failure or clinical Sx of R-side heart failure
          *In case anyone was actually interested in how the predicted values are obtained, here is a website w/a calculator based
          on gender, race, height, and age.

     Bronchodilators

               o    Ipratropium bromideanticholinergic. Preferred over short acting β-2 agonists as 1st line agent bc of its
                    longer duration of action & absence of sympathomimetic side effects. (Sympathomimetic drugs are
                    substances that mimic the effects of the catecholamines, epinephrine (adrenaline), norepinephrine
                    (noradrenaline), and/or dopamine.)

               o    Tiotropiumanticholinergic. QD dosing.

               o    Albuterol2.5-5.0 mg every 20 min

                            Adverse effects: tachycardia, tremors, vomiting

               o    Levalbuterol(Xopenex) less side effects.

               o    ICS Regular Tx for symptomatic COPD pt’s w/documented spirometry or FEV1 <50% predicted &
                    repeated exacerbations requiring Tx w/abx or oral glucocorticosteroids

                            CorticosteroidsControversial. Oral cs cause large losses in bone mineral density as early as 1st
                             6 months of therapy.

               o    Aminophyllinefor acute setting, controversial, many side effects, narrow therapeutic window

               o    Magnesiuminhibits Ca+ induced bronchoconstriction

               o    Broad Spectrum abxbc most episodes are triggered by infxn

     Indications for ICU Admission

               o    Severe dyspnea w/poor response to Tx

               o    Confusion, lethargy, or resp muscle fatigue

               o    Severe resp acidosis(< 7.2)
          o   Assisted ventilation

   Indications for hospitalizationinadequate home care, deteriorating level of activity, altered mental status,
    new/worsening hypercapnia, new resp acidosis, worsening hypoxemia, increased comorbidity

   Cor PulmonaleHeart failure caused by chronic hypoxia & ↓ CO secondary to pulm HTN. Usually from COPD.

          o   Sx: inaudible breath sounds, JVD, peripheral edema

   Emergent Tx

          o   O2, bronchodilators, anticholinergics, corticosteroids, aminophylline, magnesium

Occupational Lung Disorders & Lung Tumors
   Smoke Inhalation

          o   30% pt’s w/smoke inhalation are admitted to burn units

          o   Leading COD in structural fires…not burning!

          o   Hxsuspect if close-spaced smoke and/or fire exposure until proven otherwise

          o   3 Primary Processes:

                      Thermal Injury (heat exposure)heated gases, mucosal injury, impaired ability to clear
                       secretions(retrograde alveolar flooding), resp distress (swelling, inflamm)

          o   PE

                      Facial burns, soot in mucosal areas, cyanosis/cherry red, edema

                      Stridorobvious sign of trouble-high pitched breathing

          o   Evaluation

                      ABC’s

                      SpO2, CBC, CMP, ABG

                      CarboxyHgb & methemoglobin levels in pt’s w/↓BP & mental status changes

                               Can be elevated in smokers/firefighters

          o   Tx

                      O2, suctioning, general support (IV fluids, cardiac monitoring etc), abx (prevent topical infxn),
                       bronchodilators, hyperbaric tx or intubation w/PEEP (positive end expiratory pressure)

   Chemical Injury

          o   Toxic gases

          o   Vocal cord dysfunction, reactive laryngeal dysfunction, etc
       o   Due to product of combustion or toxin

       o   Damage due totime, type, intensity

       o   TxSupportive, O2, steroids

       o   Complications

                  ARDSadult resp distress syndrome. Pathologic hallmark=diffuse alveolar damage

                  Pneumonia

 Pneumoconioseschronic fibrotic interstitial lung diseases

       o   Inhalation of certain dusts

       o   Workplace exposure m/c (environmental rare)

       o   Examples:

                  Siderosismetal dusts, iron salts (mining, welding etc)

                  Coal Workers Pneumoconiosiscoal dust

                  Silicosisrock mining, stone cutting, sandblasting, pottery

                  Asbestosisconstruction, insulation

                  Other occupational disorders: asthma, bronchitis, toxic injuries, lung injury from radiation tx

 Lung Cancer

       o   Many occupational carcinogens identified

       o   Smoking

       o   Vapors/feul

       o   Neoplasms of the Lung200,000 new cases of lung ca annually

                  >120,000 die within 1 year of dx

                  Leading COD from ca in both genders

                  6th decade of life m/c87% from smoking

                  Types of tumors

                            Solitary pulmonary nodules on CXRCoin Lesions

                            Pathologic diff may determine outcome/Tx

                  Clinical Presentationcough that doesn’t subside, weight loss, hemoptysis, smoking, chest pain,
                   fatigue, loss of appetite, SOB

       o   Mesotheliomaappear in pleura, peritoneum, or pericardium
          80% localize in the pleura (m/c)

          Asbestos m/c

          Smoking/environmental irritants can predispose

          Onset @ age 60. Slow growing (over 20-40 years)

          ¾ are malignant due to stage @ dx

          Dxbiopsy. CT aids in extra-pleural.

          TxSurgery, radiation, Chemotherapy (Cisplatin, Alimtra)

          Poor outcomes25% survive post 1 year

o   Adenocarcinoma

          Non-small cell75% of lung tumors (m/c), usually found in periphery

          Epithelial tumor m/c types are Acinar, papillary, & bronchoalveolar

                     Pathologic features: histochemical stains used to ID intracellular mucin

                     Most are poorly differentiated

          Women>Men

o   Squamous Cell Carcinoma

          Non-small cell2nd m/c (25-35% of tumors)

          Women=Men

          PF: keratinization, cellular stratification, intracellular bridges

          Slow growing, late mets

o   Small Cell Carcinoma

          Oat Cell

          15-25% of lung ca

          Highly malignant, early mets

          PF: small round nuclei w/nuclear chromatin & cytoplasm, polygonal spindles or oval cells

o   Large Cell Carcinoma

          Rare 7-8% of tumors

          Highly malignant, rapid growth

o   Bronchial adenomaCarcinoid
          2-3% of tumors

          Mucous glands=truly benign (good prognosis)

          Associated serotonin activity

          PF: Kulchitsky type cells centrally located

          Malignant, slow growing, slow mets

          Clinical Presentation related to: severity/intensity/time of tumor

o   Pulmonary Symptoms:

                  Intra-thoraciccoughing, hemoptysis, wheezing, pneumonia, hoarseness(recurrent
                   laryngeal nerve), bloody sputum, Vena Cava syndrome (R atrial compression, edema),
                   diaphragmatic paralysis due to phrenic nerve impingement, pleural/pericardial
                   effusions, Pancoast’s Syndrome (brachial plexus & symp ganglia involvement-squam cell
                   mostly. m/c=lung apex), Horner’s Syndrome (ptosis, miosis, enopthalmos, ipsilateral
                   ↓sweating. Interruption of symp nerve to eye)

                  Extra-thoracicCaused by both metastatic (liver, adrenals, brain, bone)& non-
                   metastatic(paraneoplastic syndromes)

o   Paraneoplastic SyndromesNon-metastatic extrapulmonary manifestations due to hormone-like subst
    elaborated by tumor.

          Metabolic

                  Cushing’s SyndromeMoon face, weight gain m/c, “buffalo hump”, striae, slow healing

                  Ectopic ACTH Syndromepit tumor from ↑ ADH, ↑cortisol levels, hypercalcemia

                  IDDM, HTN, meds (ie long term steroids)

          Neuromuscularmyopathy, neuropathy

                  Eaton-Lambert Myasthenic Syndromeimpaired release of Ach, prox muscle weakness,
                   DTR’s, may resemble MG

          Derm

                  Dermatomyositispatchy bluish rash on flex surfaces

                  Acanthosis nigricansdark, velvety skin markings. Obesity, endocrine disorders.

                  SclerodermaAbn growth of CT. Raynaud’s Phen.

          Hematologicanemia, purpura, leukocytosis, polycythemia

          PTH activity hypercalcemia (squam cell)

o   How to Evaluate pt w/suspected Lung Ca
                      Hx, PE, Dx tests, radiology

                      DxCXR, CT/MRI, bronchoscopy (hilar tumors), Wedge Biopsy, mediastinoscopy (nodes), PET
                       scan, bone scan, thoracentesis

                      ManagementCure requires surgery. Must eval for:

                              Mets, spread beyond thorax(staging), type of ca, if pt can tolerate surgery

                      StagingTNM. X=poorly differentiated

                              TPrimary tumor x-4

                              NRegional lymph nodes x-3

                              Mdistant mets x-1

                              Example: T3 N2 M0large tumor, spread to nearby lymph nodes, but no mets

                      Radiation Therapyfor both resectable & non-resectable tumors

                              Pre-op radiation: small cell, Pancoast tumors

                              Palliation, reduces recurrence

                      Chemotherapymany types. Difficult to tolerate. No good specific agents.

Allergy & Clinical Immunology
   Allergy/Atopy35% of population suffers from allergic sx. 70% risk if both parents have allergic sx.

          o   May begin as childhood disease but exposure driven.

   Atopyallergic constitution. Ability to mount specific IgE ab to 1 or more allergens.

          o   Atopic-related diseases: Asthma (60% adults, 90% children w/allergic triggers), rhinitis (50% allergic),
              OM, atopic eczema/dermatitis, URI’s, LRI’s etc

   Allergyreaction &/or symptoms to those specific allergens

          o   Type I IgE-mediated hypersensitivity

   Sensitizationdown-regulation of immune system & recruit/activation of inflamm cells

   Immunoglobulinsglycoprotein molecules produced by plasma cells in response to an immunogen

          o   Function as ab, migrate w globular proteins

          o   IgG=major component in serum (75%)

          o   IgE=allergic response

   Hypersensitivity

          o   Type I IgE mediated. Immediate response to allergen. Mast cell degranulation
       o   Type IIIgG/IgM mediated. Ab reacts to ag on cell surface activating complement. Ex: hemolyt anemia

       o   Type IIIIgG mediated. Compliment reacts w ag=granulocyte accum resulting in localized tissue
           damage(Arthur’s Rxn). Serum sickness: foreign protein=formation of IgG ab (constitutional sx)

       o   Type IVCaused by lymphocytes, not ab. Delayed hypersensitivity (12-48 hrs after exposure) ie PPD

 PE

       o   Allergic vs Nonallergicsimilar overall appearance. Need to encompass exam, hx, testing, specific IgE

       o   Tx depends onallergic vs nonallergic, severity, compliance, comorbidities (HTN), affordability

       o   Testingatopic vs nonatopic. Identifying triggers(allergic, irritant, neurogenic, anatomical). Evidence-
           based decision making(appropriate referrals:allergist vs ENT etc)

 NIH 2007 Asthma Guidelines”For at least those pts w persistent asthma on daily meds, the clinician should
  eval role of allergens, particularly indoor inhalants” in vitro or in vivo

 Tests:

                  In vivoskin testing

                          m/c done in allergist office

                          physical rxn to allergen based on histamine response

                          highly sensitive-few false negatives. Must be off meds 5-7 days prior. Risk of anaphylaxis

                          Result=right away

                  In vitroblood testing

                          Any clinician may do

                          Measure of serum circulating IgE

                          Highly specific-few false positives. No need to be off meds. No risk of anaphylaxis

                          Result=2-3 days

       o   RASTRadioAllergoSorbentTest

                  2-D paper disc, little binding site for IgE ab/ag complex, qualitative, minimal accuracy

       o   ImmunoCAPmeasure of circulating specific IgE

                  3-D sponge-like sphere, much greater binding site, interchangeable w skin prick, accurate @ 3
                   mo age & up, high PPV/NPV (pos/neg predictive value)

 Tx

       o   Antihistaminescompete for H1/H2 receptors to block receptor sites on mast cells

                  H1 blockerm/c. Allergic response
                          Loratidine, cetirizine, fexofenadine, diphenhydramine

                  H2 blockerGI

                          Cimetidine, ranitidine

                  Combo works best

       o   Leukotriene ModifiersAR/asthma. Prevent leukotriene release from mast cells.

                  Montelukast, zileuton, zafirlukast

       o   Nasal AntihistaminesAzelastine, olopatadine

       o   Nasal steroidslocalized anti-inflamm

                  Triamcinolone, fluticasone, mometasone, budesonide, ciclesonide

       o   Topicalcorticosteroids, immune modulators(suppress T-cell activity. Pimecrolimus, tacrolimus),

       o   Asthmasee pg 2-3

       o   Immunotherapyprocess of desensitization by giving SQ doses of allergen

                  Pt must be able to come in weekly for 5-6 months & wait 30 min post injection, afford co-pays

 Anaphylaxissystem allergic response; ag triggers mast cell degran but systemically overreacts. Triphasic rxn.

       o   SxSOB, h/a, urticaria, hypotension, abd pain, dysphagia, angioedema, anxiety, etc

       o   M/C foods, IT, drug, venoms, latex

       o   Txemergent! Check for changes in skin color/pruritis, uvular edema etc

       o   Office protocolEpinephrine , diphenhydramine, IM steroid, vitals q15 min x 1hr minimum, send home
           w/course of PO steroids (for late phase rxn)

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