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Handouts as of 9/17/18 Respiratory Allergic Rhinitis: I Can't Breathe! (CME300‐301) Asthma Updates (CME302‐303) Bronchiolitis and Respiratory Syncytial Virus (RSV) (CME304‐305) Chronic Obstructive Pulmonary Disorder (COPD): A Breath of Fresh Air (CME306‐307) Pneumonia: The Forgotten Killer (CME308‐309)

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Page 1: Respiratory Allergic Rhinitis: I Can't Breathe! (CME300 ...€¦ · using this material and for all claims that might arise out of the use of the techniques ... Determine when patients

  Handouts as of 9/17/18  

Respiratory 

 

Allergic Rhinitis: I Can't Breathe! (CME300‐301) 

Asthma Updates (CME302‐303) 

Bronchiolitis and Respiratory Syncytial Virus (RSV) (CME304‐305) 

Chronic Obstructive Pulmonary Disorder (COPD): A Breath of Fresh Air (CME306‐307) 

Pneumonia: The Forgotten Killer (CME308‐309) 

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Allergic Rhinitis: I Can’t Breathe!

Sheryl M. Beard, MD, FAAFP

ACTIVITY DISCLAIMERThe material presented here is being made available by the American Academy of Family Physicians for educational purposes only. Please note that medical information is constantly changing; the information contained in this activity was accurate at the time of publication. This material is not intended to represent the only, nor necessarily best, methods or procedures appropriate for the medical situations discussed. Rather, it is intended to present an approach, view, statement, or opinion of the faculty, which may be helpful to others who face similar situations.

The AAFP disclaims any and all liability for injury or other damages resulting to any individual using this material and for all claims that might arise out of the use of the techniques demonstrated therein by such individuals, whether these claims shall be asserted by a physician or any other person. Physicians may care to check specific details such as drug doses and contraindications, etc., in standard sources prior to clinical application. This material might contain recommendations/guidelines developed by other organizations. Please note that although these guidelines might be included, this does not necessarily imply the endorsement by the AAFP.

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DISCLOSUREIt is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflict of interest (COI), and if identified, conflicts are resolved prior to confirmation of participation. Only those participants who had no conflict of interest or who agreed to an identified resolution process prior to their participation were involved in this CME activity.

All individuals in a position to control content for this session have indicated they have no relevant financial relationships to disclose.

The content of my material/presentation in this CME activity will not include discussion of unapproved or investigational uses of products or devices.

Sheryl M. Beard, MD, FAAFPSenior Associate Program Director, Via Christi Family Medicine Residency, Wichita, Kansas; Clinical Assistant Professor, Department of Family and Community Medicine, University of Kansas (KU) School of Medicine–Wichita

Dr. Beard earned her medical degree from the KU School of Medicine–Wichita and completed her family medicine residency at the Via Christi Family Medicine Residency in Wichita. Following residency, she joined the U.S. Air Force and was stationed at McConnell Air Force Base in Wichita, Kansas. Prior to beginning her academic career, she served a brief tour in Iraq at Kirkuk Air Base in 2006 and spent a short time in private practice. Dr. Beard became a faculty member at Via Christi in 2008 and has been the Senior Associate Program Director since 2009.

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Learning Objectives1. Identify the signs and symptoms of rhinitis and use appropriate tools

to diagnose and differentiate between allergic and non-allergic rhinitis.

2. Determine when patients require referral to sub-specialists for enhanced evaluation and/or treatment of rhinitis.

3. Prepare treatment plans for rhinitis based on each patient’s specific sensitivities and symptoms and the possibility of persistent inflammation and comorbidities, and make adjustments if the patients experiences epistaxis.

4. Educate patients regarding appropriate treatment protocol for rhinitis and the responsible use of antibiotics when prescribed as necessary.

Audience Engagement SystemStep 1 Step 2 Step 3

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Practice Recommendations• Identify and treat patients for allergic rhinitis to

improve control of asthma (SOR B)

• Effectively implement correct use of intranasal steroids in patients with allergic and non-allergic rhinitis (SOR A)

• Make appropriate referrals to an allergist/immunologist for allergic rhinitis patients refractory to other treatments (SOR C)

Classification

• Temporal– Seasonal

– Perennial

– Episodic

• Frequency

• Severity-mild vs severehttps://www.freeimages.com/photo/poppies-1369329

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Definitions

• Allergic rhinitis (AR)

• Seasonal AR

• Perennial AR

• Intermittent AR

• Persistent AR

• Episodic AR

Epidemiology

• 30-60M annually

–10-30% adults

–40% children

• 2005- $11B

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Barriers to Care

• Trivial disease

• Considered educated about disease

• Untreated/undertreated3

– Asthma and allergic conjunctivitis less so

• Side effects, poor technique, cost

Chronic Comorbid Conditions• Asthma

• Atopic dermatitis

• Sleep disordered breathing

• Conjunctivitis

• Rhinosinusitis

• Otitis media

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Case #1

• 9 yo female presents with one month hxcongestion, runny nose, sneezing, and nighttime cough

• She has peanut allergy diagnosed at the age 9 months and severe eczema as a child, but is now very well controlled and intermittent

AES Question #1What percentage of patients with asthma also have allergic rhinitis?

A. 5%

B. 10%

C. 20%

D. 50%

E. 80%

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Asthma

• 80% with asthma have AR

• 40% with AR have asthma

• Children severity and duration

• “Allergic march”

Impact• 1 in 5 mod/sev impact

• > 50% impact sleep, fatigue

• 74% neg impact sleep daily activities

• Assess severity with tools

– WPAI-AS3

– Visual analog scale

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Pathogenesis

• Allergen exposure

• Presenting cells

• Invite inflammatory cells

• Release inflammatory mediatorsRhinorrhea

• Sneezing • Rhinorrhea• Congestion• Nasal obstruction• Post nasas drip • Pruritis• Asthma or sxs• Children: malaise or fatigue

History• Frequency• Duration• Environmental triggers• Seasonality• Medications• FH of atopic disease• Sxs with irritant exposure• URI sxs

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Physical Exam• Clear rhinorrhea

• Pale or bluish nasal mucosa

• Nasal congestion

• Red watery eyes

• Throat clearing

• Allergic shiners

• Nasal crease

• Absence of FB, purulence Photo used with permission

• Trees

• Grasses

• Weeds

Seasonal vs Perennial• Cats

• Dogs

• Dust mites

https://www.freeimages.com/photo/ragweed-pulled-out-1629931https://www.freeimages.com/photo/kittens-in-a-pot-3-1366163

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Case #2• 23 yo F presents with 2 week history of

worsening runny nose, also endorses congestion, post nasal drip and sneezing

• Seems to be worse in the morning, especially after drinking her morning coffee

• She takes fluticasone nasal spray daily for allergic rhinitis and it was working well until recently

AES Question #2

Which one symptom can help discern allergic vs non allergic rhinitis?A. RhinorrheaB. CongestionC. SneezingD. Post nasal drip

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Nonallergic Rhinitis• Vasomotor rhinitis• Foods• Infectious• NARES• Occupational• Hormonal• Drug induced• Atrophic

Testing

• Skin testing

• In vitro

• Diagnostic studies

• Children

https://upload.wikimedia.org/wikipedia/commons/d/d7/Allergy_skin_testing.JPG

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Imaging

• *Choosing Wisely Campaign

• “Do not routinely perform sinonasalimaging in patients with symptoms limited to a primary diagnosis of allergic rhinitis alone.”- AAO-HNSF, 2015

Treatment

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AES Question #3

Which of the following is first line treatment for allergic rhinitis?

A. Cromolyn

B. Avoidance

C. Nasal antihistamine (azelastine)

D. 1st gen antihistamine (diphendydramine)

E. Oral steroids

Management- Environmental

• Guidelines

• No evidence

• Dust

• Others: breastfeeding, filters, pet exposure

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Management- Education• Chronicity

• Therapy outcomes

• Implement environmental change

• Medication administration

• Benefits/side effects

• QOL

Management- Pharmacologic• Anithistamines (oral/nasal)• Decongestants (oral/nasal)• Intranasal corticosteroid (INS)• Saline• IN cromolyn• IN anticholinergics• Oral LT inhibitors• Omalizumab• Saline• Steroids

https://www.freeimages.com/photo/medicine-5-1544051

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Oral AH

• Histamine assoc sxs

• Less for congestion and ocular

• Onset fast

• Safe for children > 6 months, > 2 years

• Mild intermittent symptoms

Oral Antihistamines (AH)- 1st gen

• Adverse effects

• More lipid soluble

• Poor daily functioning

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Oral AH- 2nd gen

• Better drug profile

• Less cross BBB

• Loratadine, desloratadine, levocetirizine, fexofendine

• Except cetirizine

Intranasal Antihistamine (INA)• High concentration

• Fast action

• Azelastine, olopatadine FDA

• Conjunctival sxs, rhinitis

• Twice a day

• Cost

• Children > 5 years

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Intranasal Corticosteroids (INS)• Became OTC in 2013

• Many not aware

• Hesitant about “addiction”3

• inflammatory mediators

• Severe disease or QOL

• Children 2-6 years

INS• None superior

• Daily dosing

• Budesonide pregnancy B

• Fluticasone and triamcinolone OTC

• Adverse effects

• Carry warning about growth

• Glaucoma and cataracts

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Comparison Studies of INS

• Triamcinolone acetonide (TA), fluticasone propionate (FP), and mometasone furoate(MF)

• TA less odor, taste

• Fluticasone furoate over MF and FP

• Cost considerations

INS Demo• Correct technique

• First use prime

• Blow nose

• Nose to toes

• Angle to eye

• No snortinghttps://commons.wikimedia.org/wiki/File:Action_photo_of_nasal_spray_on_a_black_background.jpg

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AES Question #4

Which of the following factors should be considered when prescribing medications for AR?

A. DurationB. SeverityC. Quality of LifeD. AgeE. CostF. All of the above

Patient Specific Treatment

Cost Quality of Life

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Saline

• Effective for symptoms and QOL

• Alone or combo

• med use

• Inexpensive

• Second line

Decongestants• OTC

• Alpha adrenergic

• Vasoconstriction

• Side effects

• Rhinitis medicamentosa

• Not in children

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IN Cromolyn

• OTC

• Mast cell degranulation

• Dosing qid

• Children > 2 years

IN Anticholinergics

• Severe rhinorrhea

• Less than INS

• Adverse effects

• Dosing bid- tid

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LT Receptor Antagonists• D4 receptor

• Compares to oral AH

• Not as effective as INS

• Useful in asthma

• Dosing

• Children > 6 months

Combination Therapy

• Severe disease

• Multiple symptoms

• INS + Oral AH = INS

• Azelastine/fluticasone nasal spray

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Omalizumab• Approved for Asthma

• Anti-IgE antibody

• Reduce symptoms in AR

• Improve QOL

• High cost

• Not FDA approved for AR

Corticosteroids

• My yearly “allergy shot”

• Oral steroids intractable symptoms

• Parenteral steroids discouraged

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Immunotherapy (IT)• Mod to severe sxs

• Alters course of disease

• Allergic asthma

• Small amount extract sublingually (SLIT) or subcutaneously (SCIT)

• Duration 3-5 years

• Effects several years

• Effective

• Injectable

• Physicians office

• Build up phase

• 3 times a week

• Maintenance every 2-4 weeks

• Higher rates anaphylaxis

• Variety of allergens

SCIT vs. SLIT• Less effective

• Under the tongue

• Given at home

• Better compliance

• Better safety profile

• Anaphylaxis rare

• Limited number of allergens

• Cost is high

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Referral• Skin prick testing

• IgE tests

• Intolerant of medication

• Not responsive

• Children asthma + food allergy

• Uncertainty

• Immunotherapy https://commons.wikimedia.org/wiki/File:Jeremybennett-sticky-note-pad-and-pencil.svg

Surgery

• No surgical treatment for AR

• May need surgery for comorbid conditions

– Nasal septal deviation

– Inferior turbinate hypertrophy

– Adenoidal hypertrophy

– Refractory sinusitis

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Nonpharmacologic Therapies

• Acupuncture

• Herbal therapy

Summary

• Allergic rhinitis is an IgE mediated response to aeroallergens, presentation includes sneezing, rhinorrhea, congestion and itching

• Avoidance therapy should be offered to patients

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Summary

• Intranasal corticosteroids should be offered to patients with moderate to severe allergies

• Patients refractory to treatment should be referred for skin testing and potentially immunotherapy

Questions

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Contact Information

Sheryl Beard

[email protected]

References1. Seidman MD, Gurgel RK, Lin SY, et al. Clinical Practice Guideline-Allergic

Rhinitis. Otolaryngology-Head and Neck Surgery. 2015 Feb;152(1_suppl):S1-S-43

2. Wallace DV, Dykewicz mS, Berstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. The Journal of allergy and clinical immunology. 2008;122(2suppl):S1-S84

3. Carr WW, Yawn BP. Management of allergic rhinitis in the era of effective over-the-counter treatments. Postgraduate medicine. 2017

4. Sur DK, Plesa ML. Treatment of Allergic Rhinitis. American Family Physician. 2015;92(11):985-992.

5. Carr, WW, New therapeutic options for allergic rhinitis: back to the future with intranasal corticosteroid aerosols. American journal of rhinology & allergy. 2013;27(4):309-313.

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Asthma Updates

Mark Shaffer, MD, FAAFP

ACTIVITY DISCLAIMERThe material presented here is being made available by the American Academy of Family Physicians for educational purposes only. Please note that medical information is constantly changing; the information contained in this activity was accurate at the time of publication. This material is not intended to represent the only, nor necessarily best, methods or procedures appropriate for the medical situations discussed. Rather, it is intended to present an approach, view, statement, or opinion of the faculty, which may be helpful to others who face similar situations.

The AAFP disclaims any and all liability for injury or other damages resulting to any individual using this material and for all claims that might arise out of the use of the techniques demonstrated therein by such individuals, whether these claims shall be asserted by a physician or any other person. Physicians may care to check specific details such as drug doses and contraindications, etc., in standard sources prior to clinical application. This material might contain recommendations/guidelines developed by other organizations. Please note that although these guidelines might be included, this does not necessarily imply the endorsement by the AAFP.

This CME session is supported by an educational grant from GlaxoSmithKline.

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DISCLOSUREIt is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflict of interest (COI), and if identified, conflicts are resolved prior to confirmation of participation. Only those participants who had no conflict of interest or who agreed to an identified resolution process prior to their participation were involved in this CME activity.

All individuals in a position to control content for this session have indicated they have no relevant financial relationships to disclose.

The content of my material/presentation in this CME activity will not include discussion of unapproved or investigational uses of products or devices.

Mark Shaffer, MD, FAAFPAssistant Professor, Department of Family and Preventive Medicine, University of South Carolina School of Medicine, Columbia, South Carolina; Medical Director, John A. Martin Primary Health Care Center, Winnsboro, South Carolina

Dr. Mark Shaffer has been a member of the faculty with the University of South Carolina School of Medicine’s Department of Family and Preventive Medicine since 2015. He practices and teaches full spectrum family medicine with obstetrics and is the medical director for a rural health center, which is his primary practice location. He serves as the Tanzania site director for the department’s global health fellowship. His areas of interest are childhood obesity, point-of-care ultrasound and global health. Dr. Shaffer earned his medical degree from Harvard Medical School in Boston, MA, and then completed family medicine residency at Palmetto Health Richland Hospital in Columbia, SC. After residency, he felt called to international service and became the inaugural fellow in a one year Global Health Fellows program in Mbeya, Tanzania. He remained in Tanzania as the clinical director for a large HIV/AIDS prevention and treatment program until his return to academia stateside.

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Learning Objectives1. Use evidence-based criteria to order and interpret appropriate

tests for asthma.

2. Analyze environmental triggers for asthma with patients and select factors to reasonably avoid or control them.

3. Develop system-wide interventions that promote patient adherence to long-term management of chronic asthma.

4. Collaborate with asthma patients to develop an asthma action plan that encourages adherence.

Audience Engagement SystemStep 1 Step 2 Step 3

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Key Points

• PFTs should be used as part of the diagnosis of asthma for patients over 5.

• Use of simple in-office tools can make a huge impact on patient outcomes.

• Consider vitamin D, LAMAs, SMART therapy and Biologics as effective treatment options.

Outline

• Review of Asthma Diagnosis and Evaluation

• Review of Traditional Asthma Management

• Novel Therapies

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Diagnosis and Evaluation

• Differential Diagnosis

• Role of Spirometry

• Environmental Evaluation

Diagnosing Pediatric Asthma

• 30% of Children Wheeze by Age 6

• PFTs not recommended until over age 5

• What can you do!Weiss LN. The diagnosis of wheezing in children. American family physician.2008;77(8):1109-1114.

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How do I Diagnose Asthma?To establish a diagnosis of asthma, the clinician should determine that (EPR 2 1997):• — Episodic symptoms of airflow obstruction

or airway hyper-responsiveness are present.• — Airflow obstruction is at least partially

reversible.• — Alternative diagnoses are excluded.

Guidelines for the Diagnosis and management of Asthma. Full Report 2007. National Asthma Education and Prevention Program. 2007.

Acute Pediatric Wheeze DDx

• Acute Infection– Bronchiolitis– Pneumonia– Epiglotitis

• Pulmonary Edema (CHD)

• Foreign Body

Chest X-ray indicated for acute wheezing not responsive to bronchodilators, or any recurrent wheezing

Weiss LN. The diagnosis of wheezing in children. American family physician. 2008;77(8):1109-1114.

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Chronic Pediatric Wheeze DDx

• Post Feed? -> GERD/ TE Fistula

• Positional? -> Tracheomalacia

• Recurrent Infections -> Cystic Fibrosis

Presumptive Asthma for Peds• Risk Factors/Clinical Characteristics?

– Obstructive Character– Family History of Atopy– Seasonal Pattern

• More likely alternative diagnosis?

• Clinical Response to Albuterol?– May use Peak Flow age 4+

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AES Question

To diagnose asthma by spirometry, the FEV1 must be under:A. 90% predictedB. 80% predictedC. 70% predictedD. The FEV1 may be normal

• Obstruction with significant reversal

• FEV1- Volume of Air Exhaled in 1st Second

Classic Findings

• FEV1 decreased

• FEV1 Improved with Albuterol

– Change of > 12%

Diagnosis- Spirometry

https://en.wikipedia.org/wiki/File:Spirometer_report_print.jpg Accessed 7.9.18

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Why Push PFTs?

• Poor clinical judgement of severity

• Differentiate Asthma from COPD

• Occasionally find other causes of obstruction (Vocal Cord dysfunction)

Nair et al. The influence of pulmonary function testing on the management of asthma in children. J Pediatr 2005; 147(6): 797-801

Spirometry May be Normal

• Mild Intermittent asthma

• Symptomatic only with triggers

• Recent use of bronchodilator

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Bronchoprovocation

• For high suspicion patients with normal PFTs asymptomatic at testing

• Exercise, Methacholine or Mannitol

• Watch for early drop off of FEV1

Bronchoprovication

0

20

40

60

80

100

120

0.01 0.1 1 10

%Pr

edic

ted

FEV1

Methacholine mg/mL

Asthmatic

normal

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Asthma Trigger Evaluation

• Often overlooked

• Trigger control may be best intervention

• May guide pharmacotherapy

Environmental

• Tobacco Smoke

• Allergens: dust mites, pollen, dander, insect droppings

• Odors/solvents/occupational

• Weather changes

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• Beta blockers

• NSAIDS

• Aspirin

Medications and Conditions

• GERD

• Stress/Anxiety

• Lung Disease

Exercised Induced Bronchoconstriction

• 10% general population, 90% asthmatics

• Dry, cold or toxic (pool) air part of trigger

• PFTs still indicated, usually normal

Krafczyk, M and Asplund, C. Exercise-Induced Bronchoconstriction: Diagnosis and Management. Am Fam Physician. 2011 Aug 15;84(4):427-434.

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Exercise Induced Bronchospasm

• Trigger avoidance/Awareness

• Short acting Beta Agonist pre-exercise– If asthmatic need controller agent as well

– Avoid daily use

• Leukotriene Receptor Antagonist– Up to 24 hours preventive effect

AES Question

Using a standardized office tool to assess asthma may decrease exacerbations by:A. 10-20%B. 20-30%C. 30-40%D. >40%

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• Organized approach to asthma assessment for Primary Care

• Validated with the ACT

• Studied with large multicenter randomized controlled trial

Asthma Apgar

Rank MA, Bertram S, Wollan P, Yawn RA, Yawn BP. Comparing the Asthma APGARsystem and the Asthma Control Test in a multicenter primary care sample. Mayo Clinic proceedings Mayo Clinic. 2014;89(7):917-925.

APGAR

• Activities

• Persistence

• TriGgers

• Asthma Medications

• Response to MedicationsYawn BP, Bertram S, Kurland M, et al. Protocol for the asthma tools study: a pragmatic practice-based research network trial. Pragmat Observ Res. 2013;4:1-12.

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Asthma Apgar

• More than doubled documentation of Triggers,

Med Adherence and Nighttime Symptoms

• 70% of questionnaires revealed an actionable item

• Use of APGAR reduced acute care exacerbation rate

by 50% Yawn, Bertram and Wollan. Introduction of Asthma APGAR tools improve asthma management in primary care practices. Journal of Asthma and Allergy 2008: I 1-10

Practice Recommendations

• Obtain PFTs for any patient over age 5 prior to making an asthma diagnosis.

• Use an standardized approach to asthma assessment such as the APGAR

• Consider monteleukast for frequent exercise induced bronchospasm

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Traditional Asthma Management

• Stepwise Approach

• Asthma Action Plan

• Inhaler Teaching and Use

Assessment

• Severity: How severe are symptoms when NOT on medications?

• Control: How severe are symptoms when on medications?

• Adjust medications based on assessment.

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Example Patient

Tyrone, 36 year old man with untreated asthma. • Gets winded at work 3-4 x per week• Wakes up about 1 week short of breath• Otherwise living and working well.• His PFTs showed FEV1 85% predicted,

reversible with SABA

AES QuestionIn addition to trigger control, which of the following is a recommended initial treatment for Tyrone?A. SABA PRNB. SABA+ fluticasone 110mcg BID C. SABA+ fluticasone 220mcg BIDD. SABA+

fluticasone 220mcg/Salmeterol50mcg BID

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Basic Assessment (Adults) Criteria Intermittent Mild Persistent Moderate

PersistentSevere Persistent

Nighttime Awakenings

<2/month 3-4/month > 1 weekly Nightly

Rescue Inhaler Use

≤2 days/week >2 days/week Daily >1x daily

Impairment None Minor Limitations

Some Limitations

Extremely Limited

FEV1% pred. >80% >80% 60-80% <60%

Treatment Step 1 Step 2 Step 3 +/- Pred Step 4/5 +/-pred

National Asthma Education and Prevention Program Asthma Care Quick Reference. September 2011. https://www.nhlbi.nih.gov/files/docs/guidelines/asthma_qrg.pdf accessed 7.2.18

Step by StepSTEP 1 STEP 2 STEP 3 STEP 4 STEP 5

SABA PRN Low-Dose ICS or

Low-dose ICS+ LABA or

Med Dose ICS+ LABA or

High Dose ICS+ LABA

LTRA or Medium Dose ICS or

Med-dose ICS+ LTRA, or theophylline

Consider Immunotherapy

CromolynTheophylline

Low-dose ICS+ LTRA ortheophylline

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Step Up or Down

• Uncontrolled? – Step on up!

• Controlled for 3-6 months? – Step on down!

• Assess regularly (2-4 weeks) until controlled

Asthma in Children

• Classification in general more aggressive

• Initial treatment generally more

conservative

• Diagnosis often made without PFTs

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Asthma Management

Asthma Action Plan• Part of Self Management

• Reduced Acute Care Visits

• Decreased Hospital Admission

http://www.health.state.mn.us/divs/hpcd/cdee/asthma/AAP-nonpro.html Accessed 7.9.18

Gibson PG et al. Self-management education and regular practitioner review for adults with asthma. Cochrane Database Syst Rev 2003;(1):CD001117.

Asthma Update!• Vitamin D

• LAMAs for Asthma

• SMART Asthma Management

• Biologics

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Vitamin D and Asthma

• Antimicrobrial and Antiflammatory

• Increases response to Steroids

• Common Deficiency in Asthmatic

Qiu J. Vitamin D for the Management of Asthma. American family physician.2017;96(5):290-291.

Vitamin D and Asthma

• Decreased exacerbations by 37% (absolute RR of 3.8% of hospital visit)

• No clear dosage guideline, median dose 900 IU per day range 400-4000

• No change in Asthma Quality of LifeQiu J. Vitamin D for the Management of Asthma. American family physician.2017;96(5):290-291.

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LAMAslong-acting muscarinic antagonists

• ICS+ LABA ~ ICS + LAMA

• ICS+ LABA+LAMA– No significant reduction in exacerbations or

quality of life

– Small reduction in risk of progressionSobieraj DM, Baker WL, Nguyen E, et al. Association of inhaled corticosteroids and long-acting muscarinic antagonists with asthma control in patients with uncontrolled, persistent asthma. A systematic review and meta-analysis. JAMA 2018;319(14):1473-1484.

Why Chose LAMA?

• Side effects from LABA therapy– Anxiety/Palpitations/Hypokalemia

• No concerns for anticholinergic effects– BPH, CrCl< 60, polypharmacy

• Not sure what they have…

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AES Question

Combination steroid/LABA medications may be effectively used in a PRN fashion.

A. TRUE

B. FALSE

How are you doing with those inhalers?

• “They work great doc!”

• “I take the albuterol twice a day every day”

• “…And that Advair whenever I need it.”

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SMART Asthma Therapy

• Single Maintenance and Reliever Therapy

• Reduced Exacerbations (3% absolute risk)

• Similar Quality of Life and FEV1Sobieraj DM, Weeda ER, Nguyen E, et al. Association of inhaled corticosteroids and long-acting B-agonists as controller and quick relief therapy with exacerbations and symptom control in persistent asthma. A systematic review and meta-analysis. JAMA 2018;319(14):1485-1496.

Writing SMART

• Budesonide/formoterol 80mcg/4.5mg

• 1 puff twice daily and

• As needed up to 6x more per day (8 doses total)

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SMART Prescribing

• Most studied form not available in US(Budesonide 100/Formoterol 6 dry powder)

• Part of international guidelines/off label in USA

• Salmeterol much longer onset of action-not appropriate for SMART

Global Initiative for Asthma. Global strategy for asthma management and prevention, 2017. http://ginasthma.org/2017-gina-report-global-strategy-for-asthma-management-and-prevention/. Accessed June 18, 2018.

Practice Recommendations

• Vitamin D will reduce exacerbation risk for most patients with asthma

• LAMA medications are an effective alternative to LABAs

• SMART therapy with budesonide/ formoterol may superior to traditional therapy

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Biologics

• Immunoglobin therapy to reduce inflammation underlying asthma.

• Expensive but effective

• No specific “asthma Antigen”

Who Gets Them?

Uncontrolled patients with asthma with:

• Proven specific allergen sensitivity or– Anti IgE

• Eosinophilia– Anti IL5 or IL5R

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Allergen Sensitivity

Omalizumab (Xolair) anti IgE Lisc’d 2003

• Asthma not controlled by inhaled steroid

• + Allergen testing to perennial antigen

• IgE levels elevated 30-700 iu/mL)

Xolair (omalizumab) Prescribing Information. https://www.gene.com/download/pdf/xolair_prescribing.pdf. Accessed 7.7.18

Omalizumab Benefits

• Reduced Exacerbations (10 % absolute RR)

• Reduced Inhaled Steroid Use (40% wean off)

• Improved Quality of Life

Normansel et al. Omalizumab for asthma in adults and children. Cochrane Database Syst Rev. 2014

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Eosinophilia

• Anti Interleukin 5– Reduce recruitment of Eosinophils– Reslizumab(Cingair-2016) – Mepolizumab (Nucala-2015)

• Anti Interleukin 5 Receptor Alpha– Directly attack Eosinophils– Benralizumab (Fasenra-2017)

Target Population

• Severe Asthma, Uncontrolled

• Eosinophilia (>300-400/ul)

• Benefits similar to Omalizumab for IgE

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Agent ComparisonTarget Route Notable Risks Cost/Dose

Omalizumab IgE SC q 2-4 weeks 1/1000 Anaphylaxis

$1300-2600

Mepolizumab IL-5 SC q weeks Zoster $3,442

Reslizumab IL-5 IV q 4-8 weeks 3/1000 Anaphylaxis

$3,054

Benralizumab IL-5 R alpha SC q 4 weeks Helminths $5,702

Prescribing Information Benralizumab. AstraZeneca. https://www.azpicentral.com/fasenra/fasenra_pi.pdf#page=1. Accessed 7.7.18Prescribing Information Reslizumab. Teva Pharmaceautical Industries. http://cinqair.com/pdf/PrescribingInformation.pdf. Accessed 7.7.18Prescribing Information mepolizumab. GlaxoSmithKline. https://www.gsksource.com/pharma/content/dam/GlaxoSmithKline/US/en/Prescribing_Information/Nucala/pdf/NUCALA-PI-PIL.PDF. Accessed 7.7.18Lexicomp Omalizumab Drug information. Accessed 7.7.18

Practice Recommendations

• Consider IgE and Eosinophilia testing in uncontrolled patients with asthma to evaluate for immunotherapy

• Be prepared to manage anaphylaxis if overseeing immunotherapy

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Older Biologics (Herbs)

• ASHMI- Antiasthma herbal medicine intervention formulation

• Ling-Zhi, Ku-Shen and Gan-Gao• Similar efficacy to oral prednisone, less

side effects, no large trialsWen et al. Efficacy and tolerability of anti-asthma herbal medicine intervention in adult patients with moderate-severe allergic asthma. J Allergy Clin Immunol. 2005 Sep;116(3):517-24.

Key Points

• PFTs should be used as part of the diagnosis of asthma for patients over 5.

• Use of simple in-office tools can make a huge impact on patient outcomes.

• Consider vitamin D, LAMAs, SMART therapy and Biologics as effective treatment options.

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Questions

Contact Information

Mark Shaffer

[email protected]

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Bronchiolitis and Respiratory Syncytial Virus (RSV)

William R. Sonnenberg, MD, FAAFP

ACTIVITY DISCLAIMERThe material presented here is being made available by the American Academy of Family Physicians for educational purposes only. Please note that medical information is constantly changing; the information contained in this activity was accurate at the time of publication. This material is not intended to represent the only, nor necessarily best, methods or procedures appropriate for the medical situations discussed. Rather, it is intended to present an approach, view, statement, or opinion of the faculty, which may be helpful to others who face similar situations.

The AAFP disclaims any and all liability for injury or other damages resulting to any individual using this material and for all claims that might arise out of the use of the techniques demonstrated therein by such individuals, whether these claims shall be asserted by a physician or any other person. Physicians may care to check specific details such as drug doses and contraindications, etc., in standard sources prior to clinical application. This material might contain recommendations/guidelines developed by other organizations. Please note that although these guidelines might be included, this does not necessarily imply the endorsement by the AAFP.

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DISCLOSUREIt is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflict of interest (COI), and if identified, conflicts are resolved prior to confirmation of participation. Only those participants who had no conflict of interest or who agreed to an identified resolution process prior to their participation were involved in this CME activity.

All individuals in a position to control content for this session have indicated they have no relevant financial relationships to disclose.

The content of my material/presentation in this CME activity will not include discussion of unapproved or investigational uses of products or devices

William R. Sonnenberg, MD, FAAFPFamily physician, Titusville, Pennsylvania; Clinical Assistant Professor of Family and Community Medicine, Penn State College of Medicine, Hershey, Pennsylvania

Dr. Sonnenberg earned his medical degree from the University of Pittsburgh and completed his family medicine residency at McKeesport Hospital in Pennsylvania. A former president of the Pennsylvania Academy of Family Physicians, he has been in private practice in the Titusville, Pennsylvania, area since 1983. In 2017, he was a featured speaker about pneumonia and inflammatory bowel disease in three issues of the AAFP’s FP Audio™. His lectures at national meetings have been selected for publication by Audio-Digest seven times. 2018 marks his 11th time presenting at the AAFP’s annual meeting.

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Learning Objectives1. Identify the risk factors for bronchiolitis and the indications for

aggressive treatment including hospitalization.

2. Utilize comprehensive, evidence-based, and cost effective strategies for the evaluation of bronchiolitis.

3. Prescribe appropriate prevention strategies for children who are at increased risk for bronchiolitis.

4. Council patients regarding appropriate supportive care for patients who have bronchiolitis.

Audience Engagement SystemStep 1 Step 2 Step 3

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Key Guidelines from AAP and AAFP

• The diagnosis of bronchiolitis and assessment of disease severity should be based on history and physical examination. Laboratory and radiologic studies should not be routinely ordered for diagnosis.

• Risk factors for severe disease such as age < 12 weeks, premature birth, underlying cardiopulmonary disease, or immunodeficiency should be assessed when making decisions about evaluation and management of children with bronchiolitis.

• Bronchodilators (albuterol, salbutamol), epinephrine, and corticosteroids should not be administered to infants and children with the diagnosis of bronchiolitis.

• Nebulized hypertonic saline should not be administered to infants with the diagnosis of bronchiolitis in the emergency department. Nebulized hypertonic saline may be administered to infants and children hospitalized for bronchiolitis.

• Antibiotics should not be used in children with bronchiolitis unless there is a concomitant bacterial infections

• Supplemental oxygen is not necessary in children and infants with a diagnosis of bronchiolitis if SpO2 exceeds 90%.

https://www.aafp.org/patient-care/clinical-recommendations/all/bronchiolitis.html

Key Guidelines from AAP and AAFP

• Continuous pulse oximetry is optional for infants and children with bronchiolitis.

• Chest physiotherapy should not be used in the management of bronchiolitis.

• Palivizumab prophylaxis should be administered during the first year of life to infants with hemodynamically significant heart disease or chronic lung disease of prematurity (<32 weeks gestation who require >21% O2 for the first 28 days of life).

• To prevent spread of respiratory syncytial virus (RSV), hands should be decontaminated before and after direct contact with patients, after contact with inanimate objects in vicinity of patient, and after removing gloves. Alcohol rubs are the preferred method for hand decontamination. Clinicians should educate personnel and family on hand sanitation.

• Infants should not be exposed to tobacco smoke.

• Exclusive breastfeeding for at least 6 months is recommended to decrease the morbidity of respiratory infections.

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Bronchiolitis

Viral URI followed by increased respiratory effort and wheezing

Less than age 2

American Academy of Pediatrics, Subcommittee on Diagnosis and Management of Bronchiolitis. Pediatrics. 2006;118(4):1774–1793

Scope of Problem

• Most common lower respiratory tract infection in infants younger than age 2

• 60% of LRTI’s in first year of life

• Leading cause of hospitalization in younger than age one

• Hospitalizations have declined from 2000 to 2010

• 4500 deaths/yr 1985 to ≈ 12 deaths/yr nowShay DK et al. Infect Dis. 2001;183 :16 –22

Leader S, et al. J Pediatr. 2003;143(5 suppl) :S127 –S132The Lancet, Aug 20,2016

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Leading Cause of Infant Hospitalization

73,250

87,826

181,662

220,379

0 50,000 100,000 150,000 200,000 250,000

Dehydration

Jaundice

Bronchiolitis

RSV Bronchiolitis

Leader S, Kohlhase K. Pediatr Infect Dis J. 2002;21:629-632

Epidemiology of Bronchiolitis

Bronchiolitis Statistics

• 90% children 0-2 yrs infected with RSV

• 20% have lower respiratory infection

• 3% hospitalized

• 0.002% mortality

Age at Presentation

• Peak age 2-5 months

• Mean age 3 months

• Rare in 1st month of life

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Sex Epidemiology

• Male : Female

– Hospitalized infants 2:1

– Milder RSV disease 1:1

• Sex influences expression of illness rather than attack rate

• Preschool and daycare increases riskHall CB. RSV. Textbook of Pediatric Infectious Disease

Wikicommons

Socioeconomic Factors• Lower socioeconomic infants have

increased risk of infection

• Higher socioeconomic infants tend to be older, thus have milder disease

• More hospitalized infants are lower socioeconomic

– Daycare, crowded living quarters

Hall CB. RSV. Textbook of Pediatric Infectious Disease Wikicommons

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Risk Factors

Cigarette smoke exposureCigarette smoke exposureYounger than 6 months

Crowded conditionsLack of breast feeding

Premature before 37 weeksBirth order ≥ 2nd

Risk and Prematurity

17.3

4.7

1

0

2

4

6

8

10

12

14

16

18

20

<32 wk GA 32-35 wk GA ≥36 wk GA

Odd

s Ra

tio o

f Bro

nchi

oliti

s D

eath

Holman RC et al. Pediatric Infect Dis.

2000;22:433-439

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Premature at High Risk

• Immature lung development

– Altered airway anatomy

– Reduced lung function through early childhood

• Immature immune system

– Impaired humoral and cellular immunity

Creative Commons Attribution 2.0 Generic

Interrupted Lung Development

Medimmune

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Antibody Levels in Premature

200

320

520

1100

0

200

400

600

800

1000

1200

<28 wks GA 28-31 wks GA 32-35 wks GA Term

Seru

m Ig

G(m

g/10

0ml)

Yeung CY, Hobbs JR. Lancet. 1968;7553:1167-70

Prematurity and RSV

(Stevens TP et al. Arch Ped Adoles Med 2000)

RSV Hospitalization Rate by Gestational Age at Birth

20.6%

14.6%11.3%

6.4%

0%

5%

10%

15%

20%

25%

<= 26 wks 27-28 wks 29-30 wks 31-32 wks

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80% RSV admissions occur within 4 months discharge from

NICU

Wikicommons

NICU Discharge and RSV Admissions

42.0%

27.0%

16.0%

41.0%

0%

10%

20%

30%

40%

50%

Jan Feb-Apr May-Aug Sept-Dec

Respiratory Illness Hospitalization Rate by Month of Discharge from NICU in Infants <= 32 Weeks

GA

(Cunningham CK, McMillan JA, Gross SJ Pediatrics 1991

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Honeymoon Period

• 0-4 weeks of age

• Transplacental maternal antibody gives partial immunity

• Preterm infants may miss IgG transfer at full term

N Engl J Med 2016; 374:62-72Creative Commons

Elective Caesarean Section

• 11% increase in hospital admissions for bronchiolitis

– Records of 212,068 babies over a 10-year period

• No increase in pneumonia admissions

Creative Commons Attribution-Share Alike 2.5 Generic

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“Mandatory” Vitamin D Slide

• Prospective study on healthy term neonates

• Mean 25-OHD 82 nmol/L

• <50 nmol/L had 6 times risk of RSV LRTI in first year of life compared to those ≥ 75 nmol/L

Belderbos M et al. Pediatrics, May 9 2011, onlineCreative Commons

Maternal Asthma and Smoking

Carroll, K. N. et al. Pediatrics 2007;119:1104-1112

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Maternal Smoking and Bronchiolitis

• United Kingdom prospective cohort study, 378 infants

• Doubles need for oxygen

• Five times risk of ventilator care

• Infants should not be exposed to cigarette smoke

Malcolm G. Semple, David C. Taylor-Robinson, Steven Lane, Rosalind L. Smyth.. PLoS ONE, 2011; 6 (7): e22425 Creative Commons

Breast Feeding and Bronchiolitis

• Not breast feeding in first 4 months of life more than triples risk for hospitalization

• Exclusive breastfeeding for first 14 days protects against hospitalization (OR=0.21)

• Exclusive breastfeeding for at least 6 months is recommended to decrease the morbidity of respiratory infections

Bachrach VR et al. Arch Pediatric Adolescent Med. 2003 Mar;157(3):237-43Von Linstow ML et al. Eur J Pediatrics. Oct;167(10):1125-33 CDC

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The Season for Wheezin?

• Generally November through April

• Parts of Florida, early as July 1

Hall CB et al. N Engl J Med. 2009;360(6):588–598 CDC

Pathology of Bronchiolitis

Creative Commons

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Pathogenesis

Incubation

2-8 days

Nose + lower resp tract

1-3 days

Worsening lower airway

disease

3-5 days

Some repair

Next 2 weeks

Complete repair

4-8 weeks

Associated Conditions with RSV

Hall CB, NEJM 2001;344:1917-1927

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Clinical Findings

Cough 98%

Fever 75%

Rhinorrhea, Wheezing 65-78%

Labored Respirations 73-95%

Hypoxia Occasionally

Hall CB et al. N Engl J Med. 2009;360(6):588–598

Fever

• Most have low grade fever lasting 2-4 days

• Height and duration does not correlate with disease severity

• Tends to disappear with progression to lower respiratory tract

Wikicommons

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Clinical Course of BronchiolitisP

erc

en

t

Days of symptoms

0

20

40

60

80

100

0 5 10 15 20 25 30 35Swingler et al. 2000

Pathology• Bronchiolar mucosal inflammation

• Submucosa & adventitia edema

• Sloughed, necrotic epithelium and fibrin plug airway

• Airway trapping

• Atelectasis – lack collateral channels

• Little smooth-muscle constrictionThis file is licensed under the Creative CommonsAttribution-Share Alike 2.0 Generic license.

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Airway Debris

www.flickr.com/photos

Airway Plugging

Wikicommons

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Histopathology

• Marked transmural cellular infiltrate

• Metaplastic changes

• Ulcerative changes

(Image courtesy of T. Colby, MD, Mayo Clinic, Scottsdale, Ariz.)

Apnea and RSV

• 20% of hospitalized infants with RSV previously

• 2.7%

• Risk factors for apnea

– History of apnea

– < one month of age

– Post conception age of 48 weeks for prematureFrederic W. Bruhn (J. Pediatr. 1977;90:382-6Ralston S et al. J Pediatr. 2009;155(5):728–73

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Bronchiolitis and Asthma?

• Retrospective study 90,341 children

– 18% had bronchiolitis visit

– 31% of those had childhood asthma dx

– Adjusted odds ratio 1.86

• No clear answer – does bronchiolitis alter airways or are infants born predisposed to asthma and wheezing?

• Maybe rhinovirus more likely to result in asthmaCarroll KN et al. J Allergy Clin Immunol. 2009 May;123(5):1055-61

http://news.vanderbilt.edu/2011/02/bronchiolitis-asthma-allergies/

Creative Commons

The Viral Pathogens

Creative Commons

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Viral Causes of Bronchiolitis76%

7% 2% 1% 0.60% 0.60% 0.20%0%

10%20%30%40%50%60%70%80%

Miron D et al. Pediatr Infect Dis J. 2010:29(1):e7-e10

Respiratory Syncytial Virus

• RNA virus

• Subtype A & B

• A more severe

• Strains shift each year

• Hardy virus

• Inhibits detoxifying enzymes that lessens oxidative stress

CDC

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What Does Syncytial Mean?

• Surface F protein causes cells to merge call a Syncytium

• Fusion allows cell-to-cell viral spread

CDC

RSV Pathogenesis

• RSV damages airway epithelium

• RSV fuses to cell membrane and forms Syncytia, multinucleated cells

• Resistant to host defense mechanisms

• Syncytia eventually slough into airway lumen

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RSV Transmission

• Direct inoculation of contagious secretions from the hands

• Large-particle aerosols into eyes and nose

• Rarely by mouth

• Cuddling transmits but not sitting nearby

Hall CB, Douglas RG. Modes of transmission of respiratory syncytial virus. J Pediatr 1981;99:100-103

RSV TransmissionPercent Infected

Nursing students sitting 6 feet from a child with bronchiolitis for 8 hours 0%

Nurses holding an infant with RSV in their arms intermittently 70%

Subjects touching bed clothes after an infant with RSV was removed from the room 78%

Hall, Ped Research : 1978

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Human Metapneumovirus

• Same viral family as RSV

• Bronchiolitis, sometimes pneumonia

• 8% of LRTI’s

• Peaks December to March, every other year

• Alternates with RSV

• Virtually all children exposed by age 5 Flickr.com

Creative Commons

Bocavirus

• Parvovirus, identified 2005

• Wheezing in infants, asthma exacerbations in general

• Winter months

• Maybe GI symptoms

• High rate (20%-50%) of coinfection with other respiratory viruses

AJ CannCreative Commons

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Viral Coinfection

• 67% chance of RSV sole pathogen

• 30% of hospitalized children with bronchiolitis had coinfection

• Adenovirus usually had another virus

• Coinfection does not increase ICU admission but prolongs stay

– RSV and HRV prolong stay 33%

Mansbach, ACEP News, Aug 2011

Diagnosis of Bronchiolitis

Creative Commons

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Diagnostic Testing

• Dx Based on H&P, no routinely ordered tests

• Rapid antigen testing

– Does not change management

– 90% sensitive (best antigen test)

– 96% specific

• Chest X-ray

• WBC – normal or slightly elevated AAFP, 2014

Chest X-Ray?

• Study of 265 cases, 0.75% of CXR’s showed lobar consolidation– Low yield if O2 saturation > 92%

• Of value when:– Temp >38.4° in ED

– Hypoxia < 90%

– Previous cardiopulmonary disease

– ICU or ventilator need

– Atypical cases Schuh S et al. J Pediatr 150. (4): 429-433.2007; Mahabee-Gittens E.M et al. Clin Pediatr 38. (7): 395-399.1999

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Chest X-Ray

Flattened diaphragm

Bilateral atelectasis

WikiCommonshttp://en.wikipedia.org/wiki/File:Bronchiolitis_chest_X-ray.jpg

Usual RSV X-Ray Findings

• Diffuse interstitial pneumonitis most common in all lobes

• Hyperaeration > 50%

• Peribronchial thickening

• Lobar or segmental consolidation 20-50%

• RUL, RML most common

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Bilateral Perihilar Fullness

http://commons.wikimedia.org/wiki/File:RSV.PNG

Hyperinflation

http://openi.nlm.nih.gov/detailedresult.php?img=3529428_CCRP2012-861867.002&req=4

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Hyperinflated

Flattened diaphragm

Wikipedia Commons

Immunity

• Natural immunity neither complete nor durable

• Mucosally restricted

• Recurrent infections common

Caroline Breese Hall, M.D. NEJM 2001; 344:1917-1928CDC

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Prevention of RSV

Creative Commons

Prevention• Frequent hand washing – alcohol wipes

preferred

• Keep sick school-age children away from younger siblings (under 2 years of age)

• Minimize visitors with an infant

• Avoid crowded places

– Malls, grocery stores

• If possible, avoid daycare during RSV season

wikicommons

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RSV Viability

• Hard surfaces 6 hours

• Rubber gloves 90 minutes

• Skin 20 minutes

Breast Feeding – Always the Right Answer

• Hazard ratio for no breast feeding 1.57 at 12 months

• Risk for exclusive breast feeding similar to breastfed with formula

Lanari M et al. Early Hum Dev. 2013 Jun;89 Suppl 1:S51-7

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Palivizumab

• Administer in first year of life

– Hemodynamically heart disease

– Chronic lung disease of prematurity

• <32 weeks gestation who require >21% O2 for the first 28 days of life

Pediatrics November 2014, VOLUME 134 / ISSUE 5From the American Academy of Pediatrics Clinical Practice Guideline

Palivizumab

• Monoclonal antibody to F protein of RSV

– 55% ↓ hospitalizations for preterm/chronic lung disease

– 45% ↓ hospitalizations for congenital heart disease

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Cost-Effectiveness

• Kansas Medicaid Study

– Reduced hospitalization – 0.47 odds

– Shorter length of stay - 74%

– Less inpatient costs - $703

– No deaths in either group

• Costs 6.67 times as much as no treatment

• About $6,000 per seasonArch Pediatr Adolesc Med. 2002 Dec;156(12):1251-5

Palivizumab and Wheezing in Healthy Preterm Infants

• Preterm 33 – 35 weeks,

• All otherwise healthy

• ≤ 6 months at start of RSV season

• Outcome: Wheezing in first year of life

• Relative reduction 61% wheezing days

• Respiratory episodes same, less coinfectionsMaarten O. et al. NEJM 2013; 368:1791-1799

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Palivizumab and Wheezing in Healthy Preterm Infants

Maarten O. et al. NEJM 2013; 368:1791-1799

Palivizumab: Wheezing 6 years Follow-up

• ≥ 3 doses of palivizumab

– 15.3% treated v. 31.6% untreated wheezing

• No prevention of atopic asthma

• Nonrandomized

• Untreated group

– More likely to have smoker in household

– More family hx of asthma

Hiroyuki Mochizuki ; Satoshi Kusuda ; Kenji Okada ; Shigemi Yoshihara ; Hiroyuki Furuya ; Eric A. F. Simões. Palivizumab Prophylaxis in Preterm Infants and Subsequent Recurrent Wheezing. American Journal of Respiratory and Critical Care Medicine, February 2017

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Does Palivizumab Prevent Asthma?

• 429 infants, GA 32-35 weeks randomized to prophylaxis or placebo

• No major effect on asthma or lung function at 6 years

– 10.3% placebo v. 9.9% treated.

Scheltema N et al. Lancet, Respiratory April 2018. p 257-264

Palivizumab Points

• Does not prevent RSV infection but prevents LRI

• Can’t treat existing infection

• Reduces subsequent wheezing but not asthma

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RSV Vaccination?

• Failed vaccine trial in 1968

– Vaccinated:

• 12/15 hospitalized, 2 deaths

– Unvaccinated:

• 1/19 hospitalized, no deaths

• Exaggerated immune response

Caroline Breese Hall, M.D. NEJM 2001; 344:1917-1928Wikicommons

Future Vaccine Strategies

• Overcoming RSV genetic variation

– F component of RSV/A2 strain

– Conserved region of the G protein BBG2Na

• Cold live, attenuated RSV

• Maternal immunization in third trimester

• 15 in development

Karron, R, Lancet 6:1. p 85 Wikicommons

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Outpatient Treatment

Risk Factors for Severe Disease

• Age < 12 weeks

• Premature birth

• Underlying cardiopulmonary disease

• Immunodeficiency

Diagnosis and Management of Bronchiolitis, was developed by the American

Academy of Pediatrics and endorsed by the American Academy of Family Physicians.

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Signs of Worsening

• More than 60 breaths/minute

• Labored breathing

– Accessory muscles, retractions, cyanosis, flared nostrils

• Fewer wet diapers

• Worsening appearance

• Lethargy or toxic appearing

• Bronchodilator

– Albuterol

– Salbutamol

• Epinephrine

Don’t Use These

• Corticosteroids

• Chest physiotherapy

• Antibiotics

Pediatrics November 2014, VOLUME 134 / ISSUE 5From the American Academy of Pediatrics Clinical Practice Guideline

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Supportive Care

• Saline nose drops, bulb suctioning

• Frequent hand washing

• Limit visitors

• No cigarette exposure

• No antibiotics, antihistamines, decongestants, nasal vasoconstrictors

Presenter’s toolbox – royalty freeWikicommons

Inpatient Treatment

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Hospitalization Rates

• 1-2% of all USA infants hospitalized with RSV

• 20-30% of premature infants are hospitalized with RSV disease

Hall CB. RSV. Textbook of Pediatric Infectious Disease

Indications for Hospitalization

• Age less than 3 months

• Gestational age less than 34 weeks

• Cardiopulmonary disease or immunodeficiency

• Respiratory rate higher the 70 breaths/min

• Wheezing and respiratory distress with O2saturations below 92% on room air

• Hypercarbia

• Atelectasis or consolidation on CXR

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Predictors of Severity

Increased Severity• Younger age

• Dehydration

• Work of breathing (retractions)

• Tachycardia (HR > 97% for age)

Mild Disease• Adequate oral intake

• Age ≥ 2 months

• Hx of eczema

• Initial O2 sat of at least 94%

• Lower respiratory rate

• No Hx of intubation

• No or mild retractionsWalsh P, Rothenberg SJ, O'Doherty S, Hoey H, Healy R. Eur J Emerg Med. 2004;11(5):265–272.Mansbach JM, Clark S, Christopher NC, et al. Pediatrics. 2008;121(4):680–688.

• Bronchodilator

– Albuterol

– Salbutamol

• Epinephrine

Don’t Use These

• Corticosteroids

• Chest physiotherapy

• Antibiotics

Pediatrics November 2014, VOLUME 134 / ISSUE 5From the American Academy of Pediatrics Clinical Practice Guideline

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Clearly Effective Treatments

• Supportive care

• Hydration

• Supplemental oxygen

Turner T., et al. Aust Fam Physician 37. (6): 6-13.2008

Supportive

• Nasal suctioning to clear upper airway

• Monitor for apnea, hypoxemia, and impending respiratory failure

• Normalize body temperature

• Rehydrate with oral or intravenous fluids

• Monitor hydration status

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IV Fluids

• Severe respiratory difficulties

• Respiratory rate greater than 80 beats per minute

• Fatigue during feeding

Fitzgerald DA et al. Med J Aust. 2004;180(8):399–404 Purchased Clip Art

Oxygen

• Supplemental oxygen is not necessary if SpO2 exceeds 90%

• Continuous pulse oximetry optional

– Headbox or tent

• Mechanical ventilation if

– PaCO2 ≥ 55 mmHg

– PaO2 ≤ 70 on 60% O2Pediatrics November 2014, VOLUME 134 / ISSUE 5

From the American Academy of Pediatrics Clinical Practice Guideline

Presenters toolbox – royalty free

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High Flow Oxygen?

Standard Flow High-Flow

Up to 2 L/min 2 L/min/Kg for FIO2 of 92% to 98%

Escalation of care 23% Escalation of care 12%

Same LOS, stay in ICU, or duration of oxygen therapy

Franklin D et al. NEJM 2018; 378:1121-1131

How Much O2 and How Long?

• O2 saturations improve 66 hours after other problems resolve

• Continuous oximetry reveals characteristic transient dips

• AAP suggest less intense oximetry as infants improve otherwise

• Home 02 being studiedPediatrics Vol. 125 No. 2 February 1, 2010 pp. 342 -349

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Choosing Wisely Campaign for Hospitalized Infants

• No CXR’s in childhood asthma or bronchiolitis– Radiation and false positives

• No bronchodilators in bronchiolitis– Minimal or no benefit

• No systemic steroids in children under 2 – harmful and no benefit

• No continuous pulse oximetry unless on O2

– Over diagnosis hypoxemia

Nebulized 3% Hypertonic Saline

• Improve mucociliary transit time in cystic fibrosis

• Osmotic hydration

• Double blind study of 127 patients showed no difference in LOS between 3% and saline

• Don’t use in ER, may use inpatient

– Better with longer LOS

Montefiore Medical Center. "Common treatment for bronchiolitis ineffective at reducing length of hospital stay, study suggests." ScienceDaily. ScienceDaily, 6 May 2013

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Antibiotics

• Frequently used because of fever, young age, concerns over secondary bacterial infection

• Secondary infection uncommon (0%-3.7%)

• Given to 50-80% of hospitalized infants

• Most common secondary infection is UTI

• Antibiotics should not be used in children with bronchiolitis unless there is a concomitant bacterial infection

PEDIATRICS Vol. 118 No. 4 October 2006, pp. 1774-1793Caroline Breese Hall, M.D. N Engl J Med 2007; 357:402-404

Take Home Points

• Avoid daycare, older siblings, cigarettes, formula, poverty, prematurity, and crowds to lessen risk of bronchiolitis

• Transmission is mostly direct contact

• Most treatment is supportive; supportive, hydration and oxygen

• Palivizumab is indicated for certain premature infants during RSV season

Creative Commons

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Questions

William R. Sonnenberg, [email protected]

Contact Information

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Chronic Obstructive Pulmonary Disorder (COPD): A Breath of Fresh Air

Clare Hawkins, MD, MSC, FAAFP

ACTIVITY DISCLAIMERThe material presented here is being made available by the American Academy of Family Physicians for educational purposes only. Please note that medical information is constantly changing; the information contained in this activity was accurate at the time of publication. This material is not intended to represent the only, nor necessarily best, methods or procedures appropriate for the medical situations discussed. Rather, it is intended to present an approach, view, statement, or opinion of the faculty, which may be helpful to others who face similar situations.

The AAFP disclaims any and all liability for injury or other damages resulting to any individual using this material and for all claims that might arise out of the use of the techniques demonstrated therein by such individuals, whether these claims shall be asserted by a physician or any other person. Physicians may care to check specific details such as drug doses and contraindications, etc., in standard sources prior to clinical application. This material might contain recommendations/guidelines developed by other organizations. Please note that although these guidelines might be included, this does not necessarily imply the endorsement by the AAFP.

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DISCLOSUREIt is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflict of interest (COI), and if identified, conflicts are resolved prior to confirmation of participation. Only those participants who had no conflict of interest or who agreed to an identified resolution process prior to their participation were involved in this CME activity.

All individuals in a position to control content for this session have indicated they have no relevant financial relationships to disclose.

The content of my material/presentation in this CME activity will not include discussion of unapproved or investigational uses of products or devices.

Clare Hawkins, MD, MSC, FAAFPLead physician, Aspire Health in Texas

Dr. Hawkins splits his time between practicing family medicine in private practice in Houston, Texas, and managing a palliative care home-visiting service in Texas and Louisiana for Aspire Health. He also manages Renaissance Physicians, a large independent physician association (IPA). He is a recent past president of the Texas Academy of Family Physicians, is a member of the AAFP’s Commission on Health of the Public and Science, and is a chair of the commission’s Subcommittee on Clinical Practice Guidelines. With 30 years of experience as a family medicine educator and more than 15 years serving as faculty for the AAFP, Dr. Hawkins has presented on a variety of medical topics. In addition, he has a long-term interest in the physician-patient relationship and physician resilience.

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Learning Objectives1. Evaluate patients who are current or former smokers, and

those who develop frequent viral infections, for symptoms that may indicate COPD or related conditions.

2. Interpret and validate results in symptomatic patients.

3. Prepare treatment plans that include a combination approach to therapy for patients who have COPD.

4. Counsel patients who have COPD on the importance of quitting smoking and receiving annual vaccinations for influenza and pneumonia.

Audience Engagement SystemStep 1 Step 2 Step 3

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Epidemiology of COPD

• Third leading cause of death in the US1

• 15.2% of adults had a diagnosis of COPD in 20102

• $36 billion dollars annually in 2010, and costs are expected to rise to $49 billion for medical costs alone by 20203

• Worldwide, an estimated 74 million deaths were caused by COPD in 20154

1 CDC 2016,  2Adeloye et al 2015, 3Ford et al, 2015, 4WHO Fact sheet 2016

COPD Phenotypes• Overlapping

• Some COPD without classic features

NoPhenotype

Chronic Bronchitis

Asthma

Emphysema

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2. Testing for COPD

• Physical Exam*

• Office Spirometry

• Other Pulmonary Function Testing

• Chest Xray & CT

• ECG*Hilleman 1995

Diagnosis• Spirometry as the mainstay of diagnosis• Simple, inexpensive, but sometimes

confusing• Spirometry classification of COPD patients by

GOLD COPD has utility but does not easily explain illness trajectory

• Health Status Measures assist (CAT and MRC dyspnea Scale)

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Three Numbers• FVC: Forced Vital Capacity• FEV1: Amount breathed out in 1 second• FEV1/FVC: How much of your lung’s air can be

exhaled in the first second– Measure of caliber or function of airway – NOT A COMPARISON TO REFERENCE

VALUES • More accurate than Peak Flow

Lung Volumes

InspiratoryCapacity

Tidal Volume

Functional Residual Capacity)

Expiratory Reserve Volume

Residual Volume

VitalCapacity

(ERV + RV = 

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Dynamic Hyperinflation

InspiratoryCapacity

Tidal Volume

Expiratory Reserve Volume

Residual Volume

VitalCapacity

Severity of obstruction (GOLD)

FEV1 % of predicted

Mild >80

Moderate 50 to 79

Severe 30 to 49

Very severe <30 *

Severity of restriction

FVC % of predicted

Mild >65 to 80

Moderate >50 to 64

Severe <50

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FEV 1 Thresholds (GOLD) • Grade 1: Mild FEV1 > 80%• Grade 2: Moderate 50% < FEV1 < 80%• Grade 3: Severe 30% < FEV1 < 50%• Grade 4: Very Severe FEV1 < 30%

• Compared with predicted values in patients with post-bronchodilator FEV1/FVC < 70

Caveat

• FEV1/FVC 70 – Overestimates COPD diagnosis in Elderly

– Underestimates COPD diagnosis in those under age 45

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0

2

4

6

8

10

12

0 1 2 3 4 5 6Volume (L)

Flow(L/sec)

PEFR

FEV1

Normal Flow Volume Curve (Expiratory)

Flow (L/sec)

0

2

4

6

8

10

12

0 1 2 3 4 5 6

Volume (L)

NormalObstructionRestriction

Normal, Obstructed, & Restrictive Curves

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AES Question #1

The most common cause of an Obstructive Pattern is:

A. Pleural Effusion

B. Pulmonary Fibrosis

C. COPD and Asthma

D. Pulmonary Embolus

Inspiratory Volume Loop

Expiratory 

Flattened Inspiratory LoopIndicating possibleExtrathoracic Obstruction

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NoYes

Obstructive Defect

Is FVC Low? (<80% pred)

Combined Defect of Obstruction and Restriction /or Hyperinflation

Pure Obstruction

Reversible Obstructionand improved FVC with

ß-agonist

Reversible Obstruction

with ß-agonist

Further Testing with Full PFT’s

Suspect Asthma

SuspectCOPD

Is FEV1 / FVC Ratio Low? (<70%)Yes

NoYes

NoYes

Adapted with permission from J S Lowry 

Common Obstructive Disorders• Diffuse Airway Disease

– Asthma

– COPD

– Bronchiectasis

– Cystic Fibrosis

• Upper Airway Obstruction– Foreign Body– Neoplasm– Tracheal

Stenosis– Tracheomalaca– Vocal Cord

Paralysis

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NoYes

Is FVC Low?(<80% predicted)

Restrictive Defect Normal Spirometry

Further Testing with Full PFT’s and

consider referral

Is FEV1 / FVC Ratio Low? (<70%)

NoDiagnostic Flow Diagram, Restriction 

Common Restrictive Disorders

Parenchymal• Interstitial Lung Diseases

– Fibrosis– Granulomatosis (TB)– Pneumoconiosis– Pneumonitis (lupus)

• Loss of Functioning Tissue – Atelectasis– Large Neoplasm– Resection

Pleural– Effusion– Fibrosis

Chest Wall– Kyphoscoliosis– Neuromuscular

Disease– Trauma

Extrathoracic– Abdominal

Distension– Obesity

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Coding and ReimbursementDiagnosis Code

Cough 786.2

Simple chronic bronchitis 491.0

Mucopurulent chronic bronchitis 491.2

Acute bronchitis 466.0

Chronic obstructive pulmonary disease 496.0

Shortness of breath 786.5

Restrictive lung disease 515

Asthma 493.91

Coding and ReimbursementProcedure CPT Code Reimbursement*

Single spirometry 94010 $32.82

Pre‐post spirometry 94060 $57.71

Pulmonary stress test simple 94620 $71.77

Medication administration bronchodilator supply separate  94640 $13.34

Demonstration / instruction  94664 $14.79

Smoking Cessation <8x/ yr  99406 $12.98

Equipment Cost

Office spirometer $1,500 – 2,500

Reimbursements based on Medicare payments 2009  Trailblazer Spirometry cost estimated from several vendors

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COPD Assessment Test (CAT): • CAT: An 8-item measure of health status impairment in

COPD • CCQ: Clinical COPD Questionnaire (CCQ):

– Self-administered questionnaire developed to measure clinical control in patients with COPD (http://www.ccq.nl)

• mMRC dyspnea: Breathlessness Measurement using the Modified British Medical Research Council :

– relates well to other measures of health status and predicts future mortality risk

http://catestonline.org

CAT (COPD Assessment Test) I never cough 1 2 3 4 5 I cough all the time

I have no phlegm in my chest at all 1 2 3 4 5 My chest is full of phlegm

My chest does not feel tight at all 1 2 3 4 5 My chest feels very tight

When I walk up a hill or one flight of stairs I am not breathless

1 2 3 4 5 When I walk up a hill or one flight of stairs I am very breathless

I am not limited doing any activities at home

1 2 3 4 5 I am very limited doing activities at home

I am confident leaving my home despite my lung condition

1 2 3 4 5 I am not at all confident leaving my home because of my lung condition

I sleep soundly 1 2 3 4 5 I don’t sleep soundly because of my lung condition 

I have losts of energy  1 2 3 4 5 I have no energy at all

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CATscore

Impact level Possible management considerations

<10 Low

• Smoking Cessation• Annual influenza vaccination• Reduce exposure to exacerbation risk factors• Therapy as warranted by further clinical assessment.

10–20 Medium

• Reviewing maintenance therapy – is it optimal?• Referral for pulmonary rehabilitation• Ensuring best approaches to minimising and managing exacerbations

• Reviewing aggravating factors –still smoking? 

21–30 High • Referral to specialist care (if you are in general practice) • Additional pharmacological treatments

mMRC Dyspnea Scale

0 I only get breathless with strenuous exercise

1 I get short of breath when hurrying on the level or walking up a slight hill

2 I walk slower than people of the same age on the level because of my breathlessness, or I have to stop for breath when walking on my own pace on the level

3 I stop for breath after walking about 100 meters or a few minutes on the level

4 I am too breathless to leave the house or I am breathless when dressing or undressing 

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Prognosis Model in COPD

Characteristics SpirometricClass

Exac/ yr CAT mMRC

A Low Risk, Less Symptoms Gold 1‐2 <1 <10 0‐1

B Low Risk, More Symptoms Gold 1‐2 <1 >10 >2

C High Risk, Less Symptoms Gold 3‐4 >2 <10 0‐1

D High Risk, More Symptoms Gold 3‐4 >2 >10 >2

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3. Treatment Plans

• Medications for Stable COPD• Medications for COPD Exacerbations• Pulmonary Rehabilitation• Oxygen Therapy• Comorbidities• End of Life Care

GOALS

• Relieving symptoms• Slowing disease progression• Enhancing exercise tolerance and

functional status• Preventing and treating complications• Improving overall health

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Grade 1Mild

Grade 2Moderate

Grade 3Severe

Grade 4 Very Severe

FEV1 > 80 FEV1 50‐80 FEV1 30‐50 FEV1 < 30Or < 50 with Cor Pulmonale

PCV 23,13

Influenza LABA and/or LAMA

& SABA ICS for recurrent exacerbations

Pulmonary  Rehab

Oxygen & LVRS?

3. Treatment Plans: Stable COPD

Medication Categories

• Short Acting Beta Agonist (SABA)

• Short Acting Anticholinergic

• Long Acting Anticholinergic (LAMA)

• Long Acting Beta Agonist (LABA)

• Inhaled Corticosteroid (ICS)

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Spacer

Long Acting Beta Agonists LABA

• SERAVENT diskus, (salmeterol) DPI device

• FORADIL Aerolizer, (formoterol) DPI

• BROVANA, (arformoteral) nebulized

• PERFORMIST, (salmeterol) DPI

• STRIVERDI Respimat, (olodaterol) DPI

• ARCAPTA Neohaler, (indacaterol) DPI

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Inhaled Corticosteroid, ICS• FLOVENT MDI or Diskus (44, 110, 220 fluticasone) DPI

Device• QVAR MDI (40 & 80 beclomethasone) HFA MDI • ASMANEX Twisthaler• PULMICORT Tubohaler, (200 budesonide) (DPI Device)• PULMICORT Flexhaler, (90 & 180 budesonide) DPI Device• PULMICORT Respules (budesonide) Neb bid • AEROSPAN Aerosol, (80 & 160 flunisolide) HFA MDI• ALVESCO Aerosol, (80 & 160 ciclesonide) HFA MDI• ASMANEX HFA MDI, (100 & 200 mometasone) DPI• ARNUITY Ellipta, (100 & 200 fluticasone) DPI

Combo LABA & ICS

• ADVAIR Diskus, salmeterol & fluticasone, 250/50, (230/21 bid MDI)

• SYMBICORT, formoterol & budesonide) (80/45, 160/45

• BREO Ellipta, daily (vilanterol & fluticasone)• DULERA Aerosol, (100/5 and 200/5 ii bid

(formoterol & mometasone)

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Anticholinergic LAMA

• SPIRIVA Handihaler or Respimat, tiotropium DPI

• INCRUSE Ellipta, (umeclidinium) DPI

• SEEBRI Neohaler, (glycopyrrolate) DPI

LAMA & LABA

• ANORO Ellipta (umeclidinium & vilanterol)

• STIOLTO Respimat (tiotropium & olodaterol)

• UTIBRON Neohaler (glycopyrrolate & indacaterol)

• BEVESPI Aerosphere (formoterol & glycopyrrolate)

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ICS, LAMA, LABA ?

• TRELIGY: Fluticasone, Umeclidinium, vilanterol

Inhaler Technique

• 50% of people use their inhaler incorrectly• Many health care providers can’t demonstrate• Have them line up their inhalers

– Have them contrast rescue from maintenance– Have them store or d/c ones from previous formulary

• Have them take them out and show you how they use them (and how often)

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Medication Adherence• Review dose counter to see if “on track”• LABA & LAMA don’t have immediate effect

that patients expect• Outline refill rate. Is it monthly? • Review “donut hole” and formulary issues

– Consider using Needy Meds or Low income Subsidy

• www.needymeds.com

MDI vs “NEBS”

• Nebulized medications may be necessary if patient has severely limited inspiratory capacity

• Beta Agonist excess = Tremor, Anxiety, Tachycardia (But similar to popular caffeine supplement drinks)

• “Part B” Medicare not “Part D”, so can be used in the donut hole

• Ie. “Brovana” LABA ~ $800/month

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• 58 yo Asian Male

• COPD x 5 years

• Continues to smoke

• Dyspnea with minimal exertion

• Increased cough with sputum

• Increased sputum purulence

• Three similar exacerbations in past 12 months

ARS CASE COPD Exacerbation

AdobeStock License#91249577

AES Question #2

The Best Treatment for this Exacerbation is?

A. Tapering dosage of methylprednisilone

B. Guerilla-cillin in high doses

C. Prednisone 40 mg daily x 5 days

D. Immediate hospital admission

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3. Treatment Plan: Exacerbations• Oral Steroids = IV steroids within 1 hour.

Prednisone 40 mg daily 5 days1

• Antibiotics: Amox/Clav, Doxicycycline, TMP/SMX, Quinolone, or others

• Bronchodilators

• Oxygen +/- hospitalization if desaturating1 Leuppi 2013

COPD Interventions #1 E-kit• Prednisone 40 mg daily x 5 days

– No other doses, no medrol dose pack, …. • Antibiotic of choice

– Bactrim, Doxicycline, Azithromycin, Amox-Clav• Fill Prescription• Keep in Fridge• Begin if; Change in Volume or Purulence

– Change in Dyspnea

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Infectious vs Non Infectious Exacerbations

• 2/3 will need antibiotics

• If no change in sputum or fever, but only dyspnea, and no evidence of pneumothorax then may just need steroid

Anthonisen 1987

Preventing Recurrent Exacerbations

• LABA/LAMA therapy with good technique • Macrolide Therapy Daily or 3 x per week

– Antibiotic resistance, hearing loss, QT interval• PDE4 Inhibitor Roflumilast

– diarrhea, weight loss, nausea, headache, back pain, influenza, insomnia, dizziness, decreased appetite 1, 2

1Chong 2013, 2Martinez 2015

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Oxygen

• Evidence equivocal – If < 88% sat

– > 16-18 h per day for decreased mortality

– For exercise desaturation? • Improves exercise duration, no improvement in

outcomes1

GOLD 2018

What is Pulmonary Rehab• Comprehensive, interdisciplinary intervention that

includes;– supervised exercise training– Patient education– Behavioral therapy– Lifestyle management

• Programs last from 8 to 12 weeks, with 2 to 3 weekly sessions

• Some evidence for home-based rehab especially for maintenance

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Pulmonary Rehabilitation• Should be prescribed for symptomatic

patients with FEV1 < 50%, (SORT A)

• Could be considered for symptomatic or exercise limited patients FEV1 >50% (SORT B)

• Pulmonary rehabilitation improved quality of life dyspnea, and exercise capacity compared to standard care. (SORT A)

ACP Updates Guideline on Diagnosis and Management of Stable COPD Aug 2, 2011  www.aafp.org/fpm 2012

Roman et al. 2013

3. Treatment Plans: Comorbidities• Cardiovascular Disease • Heart Failure • Atrial Fibrillation • Hypertension • Osteoporosis • Anxiety & Depression • Diabetes • Impaired cognitive function

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3. Treatment Plans: End of Life Care

• COPD as third most common cause of death• A story without a (well defined), Beginning,

Middle or End– Dyspnea at Rest– Frequent Exacerbations– Weight Loss – Recurrent Intubation/ Ventilation

Case II Roger

• Roger is a 65 yo with advanced COPD, who you have seen for many years, and treated with multiple inhalers, oxygen and a few hospitalizations for exacerbations

• He has begun to lose weight and has severe exercise restriction in spite of maximal treatment

• Can you enter a conversation about prognosis? • How?

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Case II Roger 65 COPD “D” • Multiple inhalers, oxygen and a

few hospitalizations for exacerbations

• Has begun to lose weight and has severe exercise restriction in spite of maximal treatment

• How would you bring up the topic?

Adobe Stock License # 64486308

AES Question #3

How would you bring up the topic?A. Tell him, there is nothing more medicine can

doB. Discuss how if he is intubated he will never

come off the ventilatorC. Say, “I’m worried about you because I see

signs that your disease is getting much worse”

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Illness Trajectory: Chronic IllnessOrgan Failure COPD or CHF

Exacerbation

Introducing The Topic• “After looking at what has been going on in the

past year, I think we should talk about where this appears to be going”

• “How do you feel about continuing to go to the hospital?”

• “When this happens again do you want to go on a breathing machine?”

• “Since we know that COPD will likely take your life, have you thought what it will be like to die?”

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AES Question #4

The only thing which changes the natural history of COPD is;

A. Anti-inflammatory therapy

B. Smoking cessation

C. Combined LABA and LAMA therapy

D. Pulmonary rehabilitation

Adapted from: Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J 1977; 1: 1645–1648.

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4. Smoking Cessation & Vaccination

• Ask: At every visit about smoking status

• Advise: the hazards and impact of smoking

• Assess: readiness to quit, set a quit-date

• Assist: prescribe

• Arrange: follow-up in person, telephonic or on-linehttps://www.cdc.gov/tobacco/quit_smoking/cessation/nqdw/index.htm

Medical Assistance with Quitting

• Nicotine Replacement (17% patch, 12.5% lozenges/gum, 2.4% spray/ inhaler )

• Varenicline (Chantix) (7.9%)

• Bupropion (Wellbutrin XL 150 / d- 300 mg / d) -2.7%

Quitting Smoking Among Adults — United States, 2000–2015  MMRW. January 6, 2017 / 65(52);1457–1464https://www.cdc.gov/mmwr/volumes/65/wr/mm6552a1.htm?s_cid=mm6552a1_w

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Varenicline (Chantix)

Initiate regimen 1 week before quit smoking date Days 1-3: 0.5 mg PO qDay Days 4-7: 0.5 mg PO BID Day 8 to end of treatment: 1 mg PO BID If quitting is successful after 12 weeks,

continue another 12 weeks at 1 mg q12hr

Varenicline (Chantix) SLOW QUIT METHOD: reduce smoking by 50%

from baseline within the first 4 weeks, by an additional 50% in the next 4 weeks Side Effects Psychiatric relative contraindication (depression/

suicide) Seizure contraindication Reduce dose if GFR < 30 0.5 mg/d increase to bid If on hemodialysis; maximum 0.5 mg / d

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Vaccinations

• PCV 13 “Pneumococcal Conjugate” • PCV 23 “Pneumococcal Polysaccharide”

– Before and second dose after 65 (five years apart)

– One year between Conjugate and Polysaccharide

• Influenza– Annually

Practice Recommendations 1. Spirometry should be used to diagnose symptomatic

patients (SOR A)

2. Spirometry should not be used to screen asymptomatic patients (SOR A)

3. Bronchodilators should be used for those with FEV1 60-80% predicted (SOR B)

4. Bronchodilators should be used for those with FEV1 < 60% (SOR A)

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Practice Recommendations5. Oral Steroids = IV steroids within 1 hour.

Prednisone 40 mg daily 5 days1 (SOR A)6. Macrolide daily or 3 x week can reduce

exacerbation frequency for those with FEV1 < 60% (SOR B)2

7. Pulmonary Rehabilitation should be offered for those with FEV1 < 60% predicted3

1 Lueppi REDUCE 2013, 2 GOLD 2018 3Pradella 2015

Questions

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Contact Information

[email protected]

• 713-417-6894

References• GOLD COPD 2018

– https://goldcopd.org/gold-reports/ accessed Aug 5, 2018• Holleman DR, Jr, Simel DL. Does the clinical

examination predict airflow limitation? JAMA. 1995;273(4):313-9.

• Pradella CO, Belmonte GM, Maia MN, Delgado CS, Luise AP, Nascimento OA, et al. Home-Based Pulmonary Rehabilitation for Subjects With COPD: A Randomized Study. Respiratory Care. 2015;60(4):526-32.

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References• Centers For Disease Control and Prevention. Chronic obstructive

pulmonary disease (COPD). 2016. Accessed at https://www.cdc.gov/copd/index.html on 15 May 2017.

• Adeloye D, Chua S, Lee C, Basquill C, Papana A, Theodoratou E, et al. Global and regional estimates of COPD prevalence: Systematic review and meta-analysis. J Glob Health. 2015;5(2):020415.

• Ford E, Murphy LB, Khavjou O, Giles WH, Holt JB, Croft JB. Total and state-specific medical and absenteeism costs of COPD among adults aged ≥ 18 years in the United States for 2010 and projections through 2020. CHEST. 2015;147(1):31-45.

• World Health Organization. Chronic obstructive pulmonary disease (COPD): Fact Sheet. 2016. Accessed at http://www.who.int/mediacentre/factsheets/fs315/en/ on 15 May 2017.

References• Leuppi JD. Short-term vs Conventional Glucocorticoid

Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease The REDUCE Randomized Clinical Trial. JAMA. 2013;309(21):2223-2231

• Roman M, Larraz C, Gomez A, Ripoll J, Mir I, Miranda EZ, et al. Efficacy of pulmonary rehabilitation in patients with moderate chronic obstructive pulmonary disease: a randomized controlled trial. BMC Family Practice. 2013;14:21.

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References• Wellington Respiratory Study. Thorax

2008;63:761-7 • ACP Updates Guideline on Diagnosis and

Management of Stable COPD Aug 2, 2011 www.aafp.org/fpm 2012

• Armstrong C. ACP guideline on stable COPD. Am Fam Physician. 2012 Jan 15;85(2):204-205.

References

• Lee H, Kim J, Tagmazyan K. Treatment of stable COPD: the GOLD guidelines. Am FamPhysician. 2013;88(10):655-663.

• Lenney J, Innes JA, Crompton GK. Inappropriate inhaler use: assessment of use and patient preference of seven inhalation devices. Respir Med. 2000;94(5):496-500.

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References • Chong J, Leung B, Poole P. Phosphodiesterase 4 inhibitors

for chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews. 2013;11:CD002309.

• Martinez FJ, Calverley PM, Goehring UM, Brose M, FabbriLM, Rabe KF. Effect of roflumilast on exacerbations in patients with severe chronic obstructive pulmonary disease uncontrolled by combination therapy (REACT): a multicentrerandomised controlled trial. Lancet. 2015;385(9971):857-66.

• Anthonisen NR, et al. Antibiotic therapy in exacerbations of chronic obstructive pulmonary disease. Ann Intern Med. 1987 Feb;106(2):196-204.

References• Qaseem A, WT, Weinberger SE, Hanania NA, Criner G, van der

Molen T, Marciniuk DD, Denberg, T, Schünemann H, Wedzicha W, MacDonald R, Shekelle P; American College of Physicians; American College of Chest Physicians; American Thoracic Society; European Respiratory Society. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Ann Intern Med. 2011 Aug 2;155(3):179-91. 2011.

• Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J 1977; 1: 1645–1648

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Pneumonia: The Forgotten Killer

William R. Sonnenberg, MD, FAAFP

ACTIVITY DISCLAIMERThe material presented here is being made available by the American Academy of Family Physicians for educational purposes only. Please note that medical information is constantly changing; the information contained in this activity was accurate at the time of publication. This material is not intended to represent the only, nor necessarily best, methods or procedures appropriate for the medical situations discussed. Rather, it is intended to present an approach, view, statement, or opinion of the faculty, which may be helpful to others who face similar situations.

The AAFP disclaims any and all liability for injury or other damages resulting to any individual using this material and for all claims that might arise out of the use of the techniques demonstrated therein by such individuals, whether these claims shall be asserted by a physician or any other person. Physicians may care to check specific details such as drug doses and contraindications, etc., in standard sources prior to clinical application. This material might contain recommendations/guidelines developed by other organizations. Please note that although these guidelines might be included, this does not necessarily imply the endorsement by the AAFP.

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DISCLOSUREIt is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed for potential conflict of interest (COI), and if identified, conflicts are resolved prior to confirmation of participation. Only those participants who had no conflict of interest or who agreed to an identified resolution process prior to their participation were involved in this CME activity.

All individuals in a position to control content for this session have indicated they have no relevant financial relationships to disclose.

The content of my material/presentation in this CME activity will not include discussion of unapproved or investigational uses of products or devices.

William R. Sonnenberg, MD, FAAFPFamily physician, Titusville, Pennsylvania; Clinical Assistant Professor of Family and Community Medicine, Penn State College of Medicine, Hershey, Pennsylvania

Dr. Sonnenberg earned his medical degree from the University of Pittsburgh and completed his family medicine residency at McKeesport Hospital in Pennsylvania. A former president of the Pennsylvania Academy of Family Physicians, he has been in private practice in the Titusville, Pennsylvania, area since 1983. In 2017, he was a featured speaker about pneumonia and inflammatory bowel disease in three issues of the AAFP’s FP Audio™. His lectures at national meetings have been selected for publication by Audio-Digest seven times. 2018 marks his 11th time presenting at the AAFP’s annual meeting.

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Learning Objectives1. Monitor the health of patients who have weakened immune systems to mitigate risk

factors that increase their risks of developing pneumonia.

2. Prescribe appropriate empiric therapy for CAP based on suspected pathogen and local susceptibility patterns.

3. Identify risk factors for multidrug-pathogens in patients who have HAP or VAP.

4. Prescribe appropriate antibiotic therapy for HAP or VAP based on risk factors for multidrug-resistant pathogens, predominant pathogens in the clinical setting and local susceptibility patterns.

5. Provide appropriate vaccines for prevention of pneumococcal pneumonia and influenza per current guidelines.

Audience Engagement SystemStep 1 Step 2 Step 3

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Target Audience

• Alabama

• Illinois

• Maine

• Michigan

• Washington

Jim Henson

• May 4, 1990 had sore throat

• May 13, saw doctor in North Carolina, aspirin suggested

• May 15, 2am, SOB and coughing blood

• 5 am ventilator

• Died may 16 1:21 am

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Maimonides and Pneumonia

• Acute fever

• Sticking pain in the chest

• Short breaths

• Serrated pulse

• Cough mostly with sputum

Epidemiology

• 8th leading cause of death in USA

• Most common infection-related mortality

• Main cause of sepsis worldwide

• 2nd leading cause of hospitalization

• 2nd highest % of ER visits admitted

• Most in winter months

• 52,700 deaths in 2007

• $17 billion per year

Am Fam Physician. 2011 Jun 1;83(11):1299-1306

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8th Leading Cause of Death - 2013

27,682

41,32553,282

0

10,000

20,000

30,000

40,000

50,000

60,000

Prostate Cancer Breast Cancer Pneumonia

DEA

THS

30 Day Readmission Rate

23.5%20.0%

15.5% 14.7%

0%

5%

10%

15%

20%

25%

CHF COPD Pneumonia AMI

Agency for Healthcare Research and Quality, Feb 23, 2016

$2 Billion Cost$2 Billion Cost

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Stagnation

• No mortality decrease since routine use of penicillin – 14%

• Guidelines work!

• 28,661 pneumonias, 7,719 admissions

• 30 day mortality for admitted patients

• 11.0% v 14.2% (RR 0.69)Dean, NC et al. Am J Med. 2001 Apr 15;110(6):451-7

Community Acquired Pneumonia

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Risk Factors for CAP

• Male

• Underweight

• >65 years

• Smoking

• Alcohol

• Immunosuppression

• COPD

• HIV

• Asplenia

• Contact with children

• Bad teeth

• Crowding (>10/household)Torres A, Peetermans WE, Viegi G, Blasi F. Thorax. 2013;68(11):1057-1065

Smoking and Invasive Pneumococcus

Current Smokers

Cigs/day Odds Ratio

1-14 2.3

15-24 3.7

>24 5.5

All 4.1

Passive Smokers

Hours/day Odds Ratio

≤4 2.4

>4 3.9

All 2.5

J. Pekka Nuorti, M.D, et al. N Engl J Med 2000; 342:681-689

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Medications that Increase Risk• Proton pump inhibitors• Tumor necrosis factor-alpha inhibitors• Amiodarone• N-acetylcysteine, • Oral or inhaled steroids • Benzodiazepines• Eszopiclone

Remington LT, Sligl WI. Community-acquired pneumonia. Curr Opin Pulm Med. 2014;20(3):215-224

PPI’s and CAP

• 463 patients, 29% using PPI’s

• Doubled risk of S. pneumoniae

• 28% v. 14%

• No increased risk for other bacteria

de Jager CPC et al. Aliment Pharmacol Ther 2012 Nov.

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Inhaled Corticosteroids

• Cohort 163,514 pts, 20,344 developed severe pneumonia over 5.4 years of follow-up

• Current use, RR 1.69• Risk disappeared after stopping for 6 months

• Higher with fluticasone, RR 2.01

• Lower with budesonide, RR 1.17Samy Suissa, et al. Thorax. 2013;68(11):1029-1036

Benzodiazepines and CAP

• Case controlled study over 4,900 patients

• 54% ↑ pneumonia

• 22% ↑ dying in 30 days

• 32% ↑ dying in 3 years

Thorax doi:10.1136/thoraxjnl-2012-202374

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Anticholinergic and Pneumonia• Case-controlled study adults 64-94, 1039

pneumonia cases

• Acute use • 59% cases of pneumonia

• 35% of controls

• aOR = 2.55

J Am Geriatr Soc. 2015 Mar;63(3):476-85

Symptoms• Cough – 90%• Fever – 80%• Dyspnea – 66%• Pleuritic chest pain – 50%• Tachypnea

• Most consistent sign• Can occur 3-4 days before other signs

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Normal Vitals?• All normal vital signs → < 1% risk of pneumonia

• RR > 20

• HR > 100

• Temp > 37.8⁰C

Metlay JP, et al, JAMA 1997; 278:1440-1445

Findings• Rales or crackles present 75-

80% of the time

• Less than 1/3 have dullness on percussion or egophony

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Physical Exam v. CXR• 52 males with lower respiratory Sx

• 24 had pneumonia on CXR

• 3 physicians, blinded to Hx, labs, CXR• Sensitivity 47% - 69%

• Specificity 58% - 75%

Wipf JE et al. Arch of Int Med 159(10):1082-7

Pneumonia in Elderly• Weaker immunity, less symptoms• Insidious onset• Chest pain uncommon• Fever may be absent, 30%• May have normal WBC• Cough weak or absent• Delirium common• Sputum minimal or absent

Daniel M. Musher, M.D., and Anna R. Thorner, M.D. NEJM 2014; 371:1619-1628

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Osler on Pneumonia

"In old age, pneumonia may be latent, coming on without a chill; the cough and expectoration are slight.. ..”

“In senile and alcoholic patients, the temperature may be low but the brain symptoms pronounced.”

CAP Pathogens

Typical

• S. pneumoniae

• H. influenzae

Atypical

• Mycoplasma

• Chlamydophilia pneumonia

• Legionella

• Viruses

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Atypicals

• Don’t Gram Stain

• Don’t grow on routine culture

• Present in 25% of all pneumonias

• Always treat

Typical v. Atypical PneumoniaTypical

• Memorable onset• Unilateral• Pleuritic• Cough with purulent phlegm• Fever, chills, sweats• Dyspnea• Few extrapulmonary symptoms

Atypical• Slow onset• “Walking pneumonia”• Extrapulmonary symptoms

• Myalgias• Diarrhea• Abdominal pain• Sore throat, ear pain

• Dry cough• Little fever, dyspnea

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Pneumococcal Pneumonia• 95% in past, now 10-15%

• Vaccines, ↓smoking

• Abrupt onset, high fever, shaking chill

• Productive cough• Pleuritic chest pain• 75% bacteremia• CXR consolation, primarily RLL

Daniel M. Musher, M.D., and Anna R. Thorner, M.D. NEJM 2014; 371:1619-1628

Risk of Pneumococcal Pneumonia• 50x higher < 2 years or > 65 years

• ≈ 1.5-2.1 times more likely in males

• Smoking, active and passive, most important risk factor ages 18-64

• Living with child < 6 years in daycare

• Dementia, seizure, HF, COPD, HIV, influenza

• Proton pump inhibitors

• Influenza may be responsible for 40% of cases at peak of flu seasons

Semin Respir Crit Care Med. 2005;26(6):563-574.

Sci Transl Med 2013 Jun 26;5(191)

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H. Flu Pneumonia

• Subacute onset of fever, less fulminant

• Associated with COPD

• Productive cough

• CXR patchy bronchopneumonia or RLL pneumonia

Legionella Infection• Peaks in late summer

• Incubation 2-10 days

• Fever > 104° F or 40° C

• Relative bradycardia

• GI – diarrhea, abnormal LFTs

• CNS symptoms – confusion, ataxia, headache, seizures

Cunha BA. Clinical features of legionnaires' disease. Semin Respir Infect. 1998;13(2):116–127

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Legionella Infection Risk Factors• Male • Long-term smoking• 20% travel associated• No person-to-person

transmission• Survives in water, biofilms• Unused hotel rooms, long pipe

runs, many water outlets• Cooling towers, cruise ships,

fountains, dipping flower pots Lancet Infect Dis, Vol 14, Iss 10, Oct 2014, Pages 1011–1021

Mycoplasma Pneumonia• Most common cause under 40

• Incubation 2-3 weeks, 5-10% develop pneumonia

• Otitis media, pharyngitis

• 20% of CAP requiring hospitalization

• 75% have normal white counts

• Burrows between cilia

• No cell wallClin Microbiol Rev. 2004; 17(4):697-728

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Chlamydophila pneumoniae• Up to 10% of all pneumonias in USA

• Most adults have been infected

• 3-4 week incubation

• 2 week prodrome of sore throat

• Mild infiltrates

• May be severe with COPD

• Association with CAD (foam cells) and Alzheimer’s disease (ε4 allele)Blasi F, Tarsia P, Aliberti S. Chlamydophila pneumoniae. Clin Microbiol Infect 2009;15:29-35.

Moraxella Pneumonia

• Subacute, follows chronic bronchitis

• Predilection for patients with CAD

• Productive cough

• Purulent sputum

• Chills infrequent

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Community Acquired MRSA• More antibiotic susceptibility

• More virulent

• More necrotizing pneumonia

• Linezolid may reduce toxin production better

Wunderink RG, et al. Clin Infect Dis. 2012;54(5):621.Curr Ther Res Clin Exp. 2012 Jun; 73(3): 86–102.

Hageman JC et al. Emerg Infect Dis. 2006;12(6):894

Features Suggesting CAP MRSA

• Cavitary infiltrate or necrosis

• Rapidly increasing pleural effusion

• Gross hemoptysis (not just blood-streaked)

• Concurrent influenza• Neutropenia

• Erythematous rash• Skin pustules• Young, previous sly healthy

patient• Severe pneumonia during

summer months

N Engl J Med 2014; 370:543-551

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MRSA Pneumonia

• Multiple nodular lesions

• Some with cavitation

• Bilateral pleural effusions

CAP Pathogens, 2010-2012

Jain S et al. N Engl J Med

2015;373:415-427.

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Testing

Laboratory Studies

• CBC• BMP• LFT• Sputum Gram Stain• Blood cultures before antibiotics• PCR, Urine antigen, viral studies• IgG and IgM not useful

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When to Chest X-RayOne Abnormal Vital Sign

• Temp > 100⁰F (37.8⁰C)

• HR > 100

• RR > 20

Two Clinical Signs

• ↓ Breath sounds

• Crackles (rales)

• Absence of asthma

Ebell MH. Predicting pneumonia in adults with respiratory illness. Am Fam Physician. 2007;76(4):562

False Negative CXR’s

• Pneumocystis

• Early pneumonia

• First 24 hours

• Severe neutropenia

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Lung Ultrasound

• Sensitivity 94%, specificity 96% in adults

• No radiation, bedside

• Pregnancy

• More accurate for pleural effusion and consolidation

G Volpicelli, M Elbarbary, M Blaivas, the International Liaison Intensive Care Med, 38 (2012), pp. 577–591

Blood Cultures

• Positive 4% - 18% in CAP

• Add little

• Highly specific if positive

• Obtain in severe CAP

• Yield halved by prior antibiotic treatment

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Impact of Blood Cultures

•13 studies

•Positive BC in 0% - 14%• Narrowed antibiotics 0% - 3%

• Broadening 0% - 1 %

Journal of Hospital Medicine 01/2009; 4(2):112 - 123

Who Needs Blood Cultures?• Cavitation

• Alcoholics

• End stage liver disease

• Critically ill

• Neutropenia

• Asplenia

• Pleural effusion

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Sputum Cultures Value

• Lung cavities

• Poor response to outpatient therapy

• Pleural effusion

• ICU admissions

Sputum Studies Value

• 40% - 60% unable to produce sputum

• 45% - 50% inadequate because of contamination

• 80% yield with pneumococcal pneumonia

• 40% pneumonias multiple organisms, can‘t narrow antibiotics based on culture

Musher DM, et al. Clin Infect Dis 2004; 30:165-169

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Pulse Oximetry• All admitted patients - CMS guideline

• pO2 ≤ 90% good specificity for adverse outcomes

• Admit all hypoxic patients

• Oxygen saturation < 90%

• Arterial saturation < 60 mm Hg on room air

Primary Care Respiratory Journal (2010) 19(4): 378-382

Urine Antigen Testing• Useful on day one to several weeks thereafter• Antibiotics little effect• Pneumococcal testing

• 60-80% sensitive• Greater than 90% specific

• Legionella testing• 70%-90% sensitive• 99% sensitive for serogroup 1 (80%-95% of legionella CAP)

Mandell LA, Wunderink RG, Anzueto A, et al. Clin Infect Dis. 2007;44(suppl 2):S27–S72.

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Other Studies• PCR for mycoplasma

• Chlamydophila antigen and/or PCR detection tests when psittacosis suspected

• Viral studies – 25% of al CAP

Thorax 2009;64:iii1-iii55 doi:10.1136/thx.2009.121434

Procalcitonin• Upregulated in bacterial infection

• Down regulated in viral infections

• Best studied in respiratory infections

• Use with clinical judgement

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Procalcitonin Level Antibiotics?

< 0.1 ng/ml Strongly discouraged

0.1 to o.25 ng/ml Discouraged

0.26 to 0.5 ng/ml Encouraged

> 0.5 ng.ml Strongly encouraged

Pleural Effusions

• 20% - 60% of CAP

• Tap most mild to moderate effusions

• Treat transudates with antibiotics

• Repeat taps or chest tube for exudates

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Inpatient or Outpatient?

Reasons to Avoid Hospitalization• 25 times greater cost

• 80% prefer outpatient

• Faster return to activity

• Lower mortality

• Thromboembolic events

• Hospital resistant bacteriaATS pneumonia guidelines, 2007

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CURB-65 Scoring• One point for each

• Confusion

• Uremia (BUN > 19)

• Respiratory Rate > 30

• Blood pressure (SBP < 90, DBP < 60)

• Age ≥ 65

British Thoracic Society

CURB-65 Treatment SiteScore Mortality % Risk Suggested Site

0 0.6%Low Outpatient

1 2.7%

2 6.8% Moderate Short stay/Supervised outpatient

3 14.0% Moderate to high Inpatient

4 or 5 27.8% High Inpatient/ICU

British Thoracic Society

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Hospital Acquired Pneumonia

Health Care-Associated Pneumonia

Inpatient for ≥ 2 days in previous 90 days

Nursing home or ECF

Home infusion therapy

Hemodialysis in previous 30 days

Family member with multidrug-resistant pathogen

Immunosuppressive disease or therapyATS and IDSA

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Inpatient Pathogens

Non-ICU

• S. pneumoniae• M. pneumoniae• C. pneumoniae• H. influenza• Legionella species• Aspiration• Viruses

ICU

• S. pneumoniae• Staphylococcus aureus• Legionella species• Gram-negative Bacilli• H. influenza

Mandell et al. Clin Infect Dis 2007;44:S27-72

Prevention of HAP• Hand washing

• Non invasive ventilation

• Breaks in sedation

• Assess for extubation

• Head of bed at 30⁰ to 45⁰

• Control glucose

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Treatment of Pneumonia

CAP Guidelines

• First dose soon and before leaving ER

• Treat all for Atypicals and pneumococcus

• Macrolide monotherapy only if on cardiopulmonary disease and no recent antibiotics

• Anti-pseudomonal treatment for those at risk

• MRSA therapy for those at risk

• No monotherapy in ICU

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Antibiotic Timing• Antibiotics within 4 hours of arrival to

hospital

• Mortality 6.8% v. 7.4%

• 0.4 day shorter LOS

• May increase pressure for misuse

• Guideline retired in 2012 in favor of prompt treatment where Dx first made

Houck PM et al. Arch Intern Med. 2004;164(6):637

IDSA Empiric Antibiotics for CAP (Outpatient)

70

Mandell et al. Clin Infect Dis 2007;44:S27-72

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IDSA Empiric Antibiotics for CAP (Inpatient)

71

Mandell et al. Clin Infect Dis 2007;44:S27-72

IDSA Empiric Antibiotics for CAP (Inpatient)

Pseudomonas Antipseudomonal β lactam +

antipseudomonal quinoloneor

Antipseudomonal β lactam + aminoglycoside + azithromycin

orAntipseudomonal β lactam (PCN

allergy→ aztreonam) + aminoglycoside + antipseudomonal quinolone

MRSA

Add Vancomycin orLinezolid or ceftaroline

Mandell et al. Clin Infect Dis 2007;44:S27-72

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Macrolide Resistance

49% Nationally

Keedy K, et al. Poster presented at: 19th Annual MAD-ID Conference; May 5-7, 2016; Orlando, FL.

Macrolides in Pneumonia?• High pneumococcal resistance• Decrease inflammatory mediators and adhesion molecules• Many retrospective studies show reduced morbidity and

mortality• 187 pts, crude mortality 5.6% v. 23.6% with azithromycin

• Clarithromycin probably should not be used• Interaction with CCB’s – kidney injury, hypotension, death• Statin interactions

Shorr AF, et al. BMJ Open 2013

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Fluoroquinolones Have Issues

• Hypertoxic C. diff; NAP1

• Worse than clindamycin

• Prolonged QT interval

• Tendon rupture and tendonitis

• Black box neuropathy warning

• Aortic dissection, aneurysm

Risk Factors Resistant Pneumococcus

• Age > 65 years• β-lactam, macrolide, or

fluoroquinolone past 3-6 months• Alcoholism• Comorbidities• Immunosuppressive illness or

therapy• Exposure to child in day care

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Steroids For Inpatient CAP• Meta analysis 13 RCT trials (>2000 pts)

• 20-60 mg prednisone or equivalent

• All-cause mortality RR 5.3% v. 7.9%

• Only benefited severe pneumonia 7.4% vs. 22.0%

• Mechanical ventilation RR 3.1% v. 5.7%

• ARDS 0.4% vs. 3.0%

• Shortened hospital stay one day.

Siemieniuk RAC et al. Ann Intern Med 2015 Oct 6

Using Steroids in CAP

• Worsens influenza and aspergilla pneumonia

• Best in severe pneumonia

• Dose

• IV Methylprednisolone 0.5 mg/kg every 12 hours

• PO prednisone 50 mg daily

• Duration 5-7 days

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Switch to Oral Therapy• Meet following criteria for 24 hours

• Able to ingest oral medications• HR <100, SBP > 90 • RR < 25• O2 sat > 90%, pO2 > 60 on room air or low-

flow O2 via nasal cannula, or return to baseline O2 for pts on long-term O2 therapy

• Return to baseline cognition• Temp < 100.9⁰F (38.3⁰C)

Lee JS, Giesler DL, Gellad WF, Fine MJ. Antibiotic therapy for adults hospitalized with community-acquired pneumonia: a systematic review. JAMA. 2016;315(6):593–602

Duration of Antibiotic Therapy• Minimum of 5 days

• 7 days if fever persists after 4 days

• Expect improvement at day 3

Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44:Suppl 2:S27-S72

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Response to Therapy

• Expect improvement in 3 days

• 6% - 15% may not respond

• Pneumococcal pneumonia

• Cough resolves in 8 days

• Crackles clear in 3 weeks

Risk Factors for Response Failure• Multilobar

• Cavitation

• Pleural effusion

• Liver disease

• Leukopenia

• High PSI IndexMenéndez R et al. Thorax. 2004;59(11):960

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Treatment Failures, Further Evaluation

• Repeat history – travel, pet exposure

• Repeat CXR, sputum and blood cultures

• Chest CT

• Bronchoscopy

• Lung biopsy

Clin Infect Dis. 2007;44 Suppl 2:S27

Cardiac Complications of Pneumonia

• Influenza and bacterial pneumonia

• MI and afib in 7-10% of admitted VA patients

• Worsening heart failure in 20%

• Up regulation of cytokines

• Afib usually resolves in few weeks

Daniel M. Musher, M.D., and Anna R. Thorner, M.D. N Engl J Med 2014; 371:1619-162

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Stable for Discharge?• Temp > 37.8⁰C• RR > 24• HR > 100• SBP ≤ 90• O2 sat < 90% on room air• Can‘t eat• No mental status improvement

• If one parameter of instability present at discharge then

• Death rate 14.6% v. 2.1%

• Readmission 14.6% v. 6.5%

Dagan E et al. Scand J Infect Dis. 2006;38(10):860

Follow-up Chest X-ray?• CXR responses lags behind clinical response

• CXR response varies (age, #lobes)

• Under 50, no pulmonary disease; clears in 4 weeks

• Older with underlying lung disease; clears in 12 weeks

• Get follow-up CXR with

• Pleural effusion

• Endotracheal tubeMitl RL et al. Am J Respir Crit Care Med. 1994;149(3 Pt 1):630.

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Simple RecommendationsMild CAP, no resistance Doxycycline

Moderate CAP, recent ABX use Azithromycin + high dose amoxicillin

Moderate CAP with comorbidity Azithromycin + cefuroxime

Inpatient moderate CAP IV azithromycin + ceftriaxone

Severe inpatient CAP Cefapime + Fluoroquinolone

Prevention of Pneumonia

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Why Prevent Pneumonia?

• Mortality hazard ratio for CAP 1.65

• Average age 59

• Inpatient cost $11,000 to $55,000

• Outpatient cost $1,000 to $5,600

Wyrwich KW et al. Patient Relat Outcome Meas. 2015;6:215-223

Pneumococcal Vaccination, Polysaccharide

Hazard Ratio

CAP Hospitalization 1.21

Outpatient pneumonia 1.14

Pneumococcal bacteremia 0.58

Death from any cause 0.88

Jackson LA et al. N Engl J Med 2003;348:1747-1755

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Problems with Polysaccharide Vaccine• Ineffective under age 2• Not lifelong• No mucosal immunity

• No protection from upper or lower tract infection

• Little herd immunity• No help with carrier rates

Conjugated Vaccine (PCV 13)• Mucosal immunity and longer lasting

• Adults 19 and older with

• asplenia, sickle cell disease, cerebrospinal fluid leaks, cochlear implants, or other immunosuppressing conditions

• Should get PCV13 first followed in 8 weeks by PPSV23

• If PPSV23 already given, give PCV13 one year later

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Pneumococcal VaccinesPVC13 PPSV23

Prevents bacteremia + +Limits non-Bacteremic pneumonia + ?Prevents colonization +Response in young children +Faster immune response +More strains +

PPSV23 blunts response to PCV13

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Giving Both PCV13 and PPSV23

• Ages 2-18 – Give 1st PPSV23 at least 8 weeks after final dose of PCV13

• If immunocompromised or asplenia, give 2nd dose PPSV23 after 1st PPSV23

• Age 19-64, high risk – give PCV13 followed by PPSV23 at least 8 weeks later

• >Age 65 – give PCV13 first followed by PPSV23 12 months later

• Wait one year after any dose of PPSV23

Influenza Vaccination • 17,393 admissions for CAP in 4 year study

• November → April

• 1590 vaccinated patients significantly less likely to die (odds ratio = 0.30)

• Influenza may increase pneumococcal susceptibility by 100 fold

Spaude KA, et al.. Arch Intern Med. January 8, 2007;167:53–9

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Antibiotics for Acute Respiratory Infection• 814,000 patients, 1.5 million visits

• 65% were diagnosed with bronchitis

• Significant minor adverse side effects in treated group

• Less hospitalizations for pneumonia in antibiotic group

• NNT is 12,225Meropol SB et al. Ann Fam Med March/April 2013 vol. 11 no. 2 165-172

Antibiotics for “Almost Pneumonia?”

• 2000 patients with “moderately bad” bronchitis or worse randomized to amoxicillin or placebo

• NNT 30 to prevent new or worsening symptoms

• Number needed to harm 21

• Nausea, rash, diarrhea

• One anaphylaxis

Little P et al. Lancet 13:2, p123–129,

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Time for a Vitamin D Slide• Finnish study of 1,421 subjects from

1998-2001

• Lowest 1/3 had 2.5 risk of pneumonia than those with high levels

University of Eastern Finland. "Low vitamin D levels a risk factor for pneumonia." ScienceDaily. ScienceDaily, 30 April 2013

Other Risk Reducers

• High socioeconomic status

• Recent dental examination

• Statins

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Dentures and Pneumonia

• 2.3x higher risk of pneumonia if dentures worn at night

• 1.6x higher risk with poor oral hygiene in nursing homes

T. Iinuma, et al. Journal of Dental Research, October 2014

Statins and Pneumonia• 18 studies

• RR 0.84 for CAP

• RR 0.68 short term mortality

• Dampens inflammatory response

• No benefit in VAP

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Practice Recommendations • Learn guidelines, they have potential to improve

mortality

• Discharge when switched to orals

• Trim use of anticholinergics, PPIs, sedatives

• Immunize against pneumococcal disease with both vaccines and influenza

• Be rich with nice teeth

Rocky Graziano

I quit school in the sixth grade because of pneumonia.

Not because I had it, but because I couldn't spell it.

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