Asthma and COPD

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Asthma and COPD

• November 28, 2002
• Cass Djurfors
• Dr. M. Betzner

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Objectives

• Asthma
• Definition
• Epidemiology
• Pathophysiology
• Clinical features
• Diagnostic tests
• Management
• Disposition

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Objectives

• COPD
• Definition
• Epidemiology
• Pathophysiology
• Clinical Presentation
• Diagnostic Criteria
• Treatment
• Chronic
• Acute

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Asthma definition

• Chronic inflammatory disease characterized by
  reversible airflow obstruction, exacerbations and
  remissions.

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NAEPP Diagnostic Criteria

• Intermittent airflow obstruction indicated by a
  history of nighttime cough, recurrent wheeze or
  recurrent chest tightness.
• Reversible airflow obstruction as documented by
  pulmonary function testing, worsening symptoms in
  the presence of any of several triggers, or
  symptoms that occur at night.
• All other possible diagnoses are excluded.
• National Asthma Education and Prevention Program.
  Expert panel report 2 Guidelines for the
  diagnosis and management of asthma. DHHS pub
  NIH 97-4051. 1997

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Epidemiology

• Affects 4-6 of population in the United States
• Most common chronic disease of childhood, fourth
  leading cause of disability in children,
  increasing in prevalence
• 30 of children will have persistent symptoms of
  asthma into adulthood
• Fatalities are real 4657 in U.S. in 1998

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Etiology

• Currently believed that asthma is the result of a
  combination of genetic predisposition and
  environmental exposures
• Common Triggers
• Tobacco smoke, air pollutants, animal allergens,
  dust mites, viral respiratory infections,
  cockroach allergens, weather changes, molds,
  outdoor allergens, gerd

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Pathophysiology

• Acute and chronic inflammation and airway
  hyperresponsiveness
• Partially reversible airflow obstruction results
  from bronchial smooth muscle constriction, airway
  edema and inflammation, and mucus plugging
  bronchoconstriction is superimposed in the acute
  setting
• Permanent changes can eventually be seen at the
  microscopic levelincluding collagen deposition
  and fibrosis below the basement membrane from
  mast cell activity and inflammatory cell migration

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History

• Symptoms
• Cough, wheeze, SOB, chest tightness, sputum,
  fever, poor feeding
• Pattern of disease
• Course, onset, duration, seasonal variation,
  frequency
• Aggravating factors/triggers
• Usual triggers, current trigger
• History of disease
• previous hospitalization
• previous intubation/ICU
• previous ED visits
• typical episode
• Age at onset and method of diagnosis
• Present management, meds and history of steroid
  use

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History

• Family History
• Social History
• Home environment (smoking, pets, allergens)
• Identification of precipitating cause
• Exacerbation profile
• Usual exacerbation pattern and outcome
• Past best spirometry measures
• Medical history, allergies, anaphylaxis
• Treatment
• Medications at home and timing of last dose
• Treatment before arrival

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Physical Exam

• Vital signs
• RR increases
• HR-tachycardia from anxiety, increased work of
  breathing, and hypoxia
• BP-hypotension may be present in patients with
  impending resp failure due to decreased venous
  return and increased pleural pressures. Pulsus
  paradoxus may be present

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Physical Exam

• Accessory muscle use
• Indrawing subcostal, intercostal,
  supraclavicular
• Paradoxical abdominal and chest wall movements
• Nasal flaring in young children

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Physical Exam

• Mental status
• Prolonged expiratory phase
• Lung findings
• Wheeze
• Silent chest

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Diagnostic Tests

• Pulse Oximetry
• Continuous monitoring
• lt91 may be a predictor of hospital admission in
  kids (Geelhoed et al, BMJ, 1988)
• PEF
• An approximation of FEV1
• Should be measured in all but the sickest of
  patients or those younger than 5 years
• Compare with predicted age/size appropriate value
  and with personal best

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Diagnostic Tests

• CXR
• Of limited utility
• Useful in those with concern for complications of
  asthma (pneumothorax) or those patients in whom
  another diagnosis is suspected
• Recommended for children with first episode of
  wheeze to rule out foreign bodies, congenital
  anomalies (Scarfone, Emergency Asthma, 1999)

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Diagnostic Tests

• ABG
• Useful as supportive evidence for the clinical
  diagnosis of respiratory failure

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Asthma Severity CAEP

• Mild
• exertional dyspnea/cough
• nocturnal symptoms.
• Increased use of ß agonistfor symptom control.
• Good response to ß agonist
• FEV1,PEFR gt 60 predicted or best.
• (FEV1 gt 2.1L PEFR gt 300L/min)

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Asthma Severity CAEP

• Moderate
• dyspnea at rest, cough,congested, chest
  tightness,
• nocturnal symptoms.
• Partial relief from ß agonistand or ß agonist
  neededmore often than Q4h
• FEV1 PEFR 40-60 predicted or best.
• (FEV1 1.6-2.1L, PEFR 200-300L/min)

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Asthma Severity CAEP

• Severe
• laboured respirations
• agitated, diaphoretic
• difficulty speaking
• tachycardic,
• no prehospital reliefwith ß agonist
• FEV1,PEFR - unable or lt40 predicted or
  best(FEV1 lt1.6L PEFR lt200L/min O2 saturation
  lt90)

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Asthma Severity CAEP

• Near Death
• exhausted, confused,
• diaphoretic, cyanotic,
• silent chest, decreased resp. effort
• falling heart rate
• FEV1,PEFR not appropriate
• O2 saturation lt90 (despite supplemental O2)

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Treatment Goals

• Correct hypoxia
• Reverse airflow obstruction
• Treat underlying inflammatory response

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Management CAEP

• Mild
• O2
• ß agonist (MDI chamber)MDI (Metered Dose
  Inhaler) - MDI adapters available for ET
  tubeChamber (valved spacer device) - use of
  chamber is recommended

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Management CAEP

• Moderate
• O2
• ß agonist (MDI chamber)
• systemic corticosteroids
• anticholinergics may be helpful in some cases
• Frequent FEV1 /PEFR to evaluate response to
  treatment

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Management CAEP

• Severe
• 100 O2
• anticipate the need for intubation
• frequent/continuous ß agonistand anticholinergic
  (nebulized orMDI with chamber)

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Management CAEP

• Severe
• Systemic corticosteroids
• Cardiac monitoring
• Oximetry, ABG's, CXR
• Frequent reassessment
• Spirometry when possible
• Physician and nursingsupervision until clear
  signsof improvement
• UNRESPONSIVE Consider near death management

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Management CAEP

• Near Death
• 100 O2
• paralysis, intubation modified RSI technique
• Intubation is a clinical decision
• continuous ß agonist andanticholinergic
  (nebulized orMDI ETT adaptor)UNRESPONSIVE
• Rule out pneumothorax or upper airway obstruction
• consider alternative drugs I.V. ß agonists,
  inhalational anesthetic agents

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Management CAEP

• Near Death
• Systemic corticosteroids
• Cardiac monitoring
• Oximetry, ABG's, CXR
• Frequent reassessment
• Spirometry when possible
• Physician and nursingsupervision until clear
  signsof improvement

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Ventilatory Strategies

• Cautious CO2 reduction with permissive
  hypercapnea until lung function improves
• Controlled mechanical hypoventilation
• Bicarb as needed to keep pHgt7.2
• Slow RR (6-8 breaths/min) to reduce barotrauma
  and volutrauma
• Low IE ratios
• Low tidal volumes (6-8 mL/kg)
• Frequent suctioning of mucous secretions as
  required

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OXYGEN

• Will not suppress respiratory drive in acute
  asthma
• Start high FiO2 40-100
• Achieve O2Sat 92-95

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ß agonists first line therapy

• titrate to response (adults and children)
• e.g. inhaled salbutamol 100 µg/puff
• Relaxes bronchial smooth muscle and promotes
  mucociliary clearance
• MDI 4-8 puffs q15-20 min X 3 is usual, increase
  to 1 puff q 30-60 sec (4-20 puffs) prn
• wet nebulizer 5.0 mg ( 1 ml/3ml ns) q 15-20 min.
  X3 continuous if necessary
• administer with oxygen
• Increase dose for intubated patients

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ß agonists first line therapy

• Several RCTs have shown equivalent efficacy
  between MDI spacer and nebulizers in the
  emergency treatment of acute asthma
• Rodrigo et al, American Journal of Emergency
  Medicine, 1998
• Schuh et al, J Pediatr, 1999
• For outpatient ß agonist use, MDIs are
  equivalent to all other hand held inhaler
  devices, and remain the most cost effective
  delivery system.
• Ram et al, BMJ, 2001

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Anticholinergics

• e.g. inhaled ipratropium bromide (20 µg/puff)
• Inhibits acetylcholine-mediated
  bronchoconstriction and decreases mucous
  production.
• Not systemically absorbed
• Peak effect in 60 minutes
• Indicated for moderate and severe asthma in both
  adults and children

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Anticholinergics

• Zorc et al, Pediatrics, 1999
• 427 childrengt12 months were randomized in a
  blinded fashion to either ipratropium (250
  mcg/dose) or normal saline with each of the first
  three nebulized albuterol doses.
• The addition of the ipratropium to a standard ED
  treatment protocol for acute asthma was
  associated with reductions in duration and amount
  of treatment before discharge

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Anticholinergics

• MDI 4-8 puffs q15-20 min X 3 is usual, increase
  to 1 puff q 30-60 SEC (4-20 puffs) prn
• Wet nebulizer .25. - .5 mg ( 1 -2ml/3ml NS) q
  15-20 min. X3 continuous if necessary
• Decrease frequency in recovery phase
• May be mixed with ß agonists

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Corticosteroids

• All patients seen in ER for asthma should be
  considered for oral or IV steroids
• Associated with rapid resolution of airflow
  obstruction and decreased relapse rate
• Oral and IV are equally efficacious
• No good evidence regarding best dose
• Accepted doses are 100-200 mg of
  methylprednisolone or equivalent or 500-1000mg of
  hydrocortisone or equivalent, oral doses should
  be in the range of 40mg of prednisone or
  equivalent

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Corticosteroids at d/c

• Patients discharged from the ED who require
  steroid therapy should be given 30-60 mg of
  prednisone orally for 7-14 days (CMAJ, Guidelines
  for the emergency management of asthma in adults,
  1999)
• Children 1-2 mg/kg per day for a total of 5 days
• Decadron has not been widely used or studied but
  may be an alternative in children

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Inhaled Corticosteroids

• Should be prescribed at discharge but not a
  component of emergency management
• CMAJ, Guidelines for the emergency management of
  asthma in adults, 1999
• Dose-related systemic adverse effects, especially
  at doses gt0.8mg/d of fluticasone or equivalent
• Lipworth, Systemic Adverse Effects of Inhaled
  Corticosteroid Therapy, Arch Intern Med, 1999.

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Intubation agents

• Induction Ketamine 1.5 mg/Kg I.V.
• Add atropine in kids
• Paralysis
• Succinylcholine 1.5 mg/Kg I.V.
• Roc/vec/pavulon for maintenanceof paralysis only

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Alternative Drugs

• (Not usually required) May be Associated With
  More ToxicityPatients unresponsive to treatment
  may benefit from I.V. ß agonists or inhalational
  anesthetic agents. These forms of therapy may
  require consultation with respirology, ICU,
  anesthesia or internal medicine.

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Alternative Drugs

• Adrenaline (11000) S.C. 0.3 - 0.5 ml q 15 - 20
  min prn (1 ml 11000 in 250 D5W 4 µg/ml) I.V.
  Infusion 4-8 µg/minKids 0.01mL/kg of 11000
  S.C.

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Alternative Drugs

• Salbutamol (I.V. solution only) Load 4µg/Kg
  (over 2-5 min) I.V. Infusion 0.1 - 0.2 µg/Kg/min
• Methylxanthines (Aminophylline) Load 3 - 6 mg/Kg
  I.V. over 30 min (1/2 if already taking)
  infusion 0.2 - 1 mg/Kg/Hour (follow levels). Not
  usually recommended as Bronchodilator in the
  first 4 hours of treatment.

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Alternative Drugs

• Magnesium
• Controversial Some evidence for IV use in severe
  asthma
• Smooth muscle relaxant
• Adults (AMA guidelines)
• Severe / Near Death Asthma satslt90,
  PEF/FEV1lt40
• consider 2gm MgSO4 IV over 20 mins
• Peds
• Severe / Near Death Asthma (satslt92,PEF/FEV1lt50
  of pb/predicted
• consider 25mg/kg MgSO4 IV over 20 mins

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Alternative Drugs

• Heliox
• Mixture of helium and oxygen
• Low-density gas mixture which is thought to
  reduce turbulent airflow
• Must be at least 60 helium which presents a
  problem in hypoxic patients
• Evidence is limited
• Can be considered in a limited group of
  nonhypoxic severe asthmatics

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Alternative Drugs

• Leukotriene Modifiers
• Potent bronchodilator with additive effect to
  B2-agonists
• Direction for the future
• May have a role in acute treatment of asthma, but
  that remains to be investigated

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Disposition CAEP guidelines

• Pretreatment
• lt 25 predicted or best(FEV1 lt 1.0 L PEFR lt 100
  L/min)
• Admission isusually necessary

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Disposition CAEP guidelines

• Post Treatment
• 1. lt 40 predicted or best(FEV1 lt 1.6 L PEFR lt
  200 L/min)
• Admission recommended
• 2. 40-60 predicted or best(FEV1 lt 1.6-2.1 L
  PEFR lt 200-300 L/min)
• Discharge Possible
• 3. gt 60 predicted or best(FEV1 gt 2.1 L PEFR gt
  300 L/min)
• Discharge likely

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Patients at Risk for Relapse

• 1. Previous near death episode.2. Recent
  E.D. visits.3. Frequent hospitalizations.4.
  Steroid dependent or recent use.5. Sudden
  attacks.6. Allergic/anaphylactic triggers.7.
  Prolonged duration of recent attack.8. Poor
  compliance or understanding.9. Returning to same
  environmental triggers.

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Discharge instructions

• MEDICATIONS
• A. ß agonists
• Regular use often required for 48 hours (2-4
  puffs Q4h).
• PRN use after 48 hours if symptoms controlled
• If unable to control symptoms with ß agonists
  return to E.D. or see your physician.

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Discharge instructions

• B. Corticosteroids - indicated for most patients
• Prednisone 30-60 mg/day for 7-14 days taper or
  discontinue based on asthma control/physician
  advice
• Individual plans based on past treatment/recent
  symptoms
• Inhaled Continue at previous dose even if taking
  prednisone. Initiate at 500-1000 ug/day
  (Beclomethasone/Budesonide or equivalent). Higher
  doses may be necessary. Consider as integral part
  of long term management.

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Discharge instructions

• Anti inflammatory medications (non-steroid)
• To be continued on discharge.
• Role in long term management to be assessed by
  family physician or consultant.

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PATIENT INSTRUCTIONS

• Review
• 1) Drug Delivery Technique (puffer, spacer
  device, powder delivery)
• 2) Role of relievers (ß agonists) and preventers
  (anti inflammatory)
• Explain
• Treatment failure indications for emergency
  assessment or physician advice. This should be
  based on signs, symptoms and medication
  requirements, e.g. dose (number and frequency of
  puffs) of ß agonist required for relief or
  control of symptoms.

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PATIENT INSTRUCTIONS

• Educate
• The Lung Association, Asthma and Allergy
  Information Association and the Asthma Society of
  Canada has educational materials and some
  communities have formal education programs.
• Refer
• Consider respirology, internal medicine, allergy/
  immunology consultation for high risk patients.
  Worsening/ persisting symptoms, modify dose and
  schedule of steroid therapy. Follow up with
  family MD or consultant in 1-7 days to assess
  response.

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Chronic Management Considerations

• Environmental control
• Short-acting B2-agonists on demand
• Regular inhaled glucocorticoid for all but the
  mildest of asthmatics (if B2-agonist is neededgt3
  times per week, other than for exercise, inhaled
  glucocorticoid should be added)
• If asthma is not adequately controlled by
  moderate doses (500-1000mcg/d of beclomethasone
  or equivalent) additional therapy should be
  addedconsider long-acting B2-agonists,
  leukotriene antagonists or other medications
• Severe asthma may require additional treatment
  with prednisone
• CMAJ, Canadian Asthma Consensus Report, 1999

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COPD

• ATS Definition
• A disease state characterized by the presence of
  airflow obstruction due to chronic bronchitis or
  emphysema
• Progressive
• Airway hyperactivity, if present, may be
  partially reversible

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COPD Definitions

• Chronic Bronchitis
• Presence of chronic productive cough for 3 months
  in each of 2 successive years in a patient in
  whom other causes of chronic cough have been
  excluded
• Emphysema
• Abnormal permanent enlargement of the airspaces
  distal to the terminal bronchioles, accompanied
  by destruction of their walls and without obvious
  fibrosis
• Tintinalli, Emergency Medicine, 2000

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Epidemiology

• Sixth leading cause of death in the world in 1990
  (WHO)
• Leading cause of morbidity and mortality among
  smokers gt 55 yrs
• Rare in those under age 40
• Mengtwomen, but this is changing as more women
  smoke
• Mortality for patients hospitalized with a COPD
  exacerbation is estimated at 5-14

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Pathophysiology

• Smoking accounts for 80-90 of risk
• Environmental factors have been suggested
  occupational exposure, air pollution, second hand
  smoke
• Genetic factorsa1-antitrypsin deficiency
• Earliest detectable changes in COPD evolution are
  evident as small increases in peripheral airway
  resistance or lung compliance

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Pathophysiology

• Disease progression is slow and insidious,
  spanning decades may be masked by sedentary
  lifestyle of most smokers
• Abstinence from smoking is most advantageous
  during early course of disease
• Variability in disease pattern and progression
  between similar patientsmuch is still unknown

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Pathophysiology

• Airflow impedance (expiratory mostly) results
  primarily from increased resistance or decreased
  caliber of the small bronchi and bronchioles
• Airway secretions, mucosal edema, bronchospasm,
  and bronchoconstriction from decreased airway
  elasticity are all responsible for airflow
  obstruction
• Increased airway resistance reduced minute
  ventilation /- increased work of breathing

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Pathophysiology

• Alveolar hypoventilation hypoxemia
  hypercarbia
• V/Q mismatching
• Pulmonary hypertension
• RV hypertrophy then dilatation
• Cor pulmonale

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Clinical Presentation

• Chronic Stable COPD
• Symptoms
• Exertional dyspnea
• Cough
• Exam
• Tachypnea
• Accessory muscle use
• Pursed-lip breathing
• Expiratory wheeze
• Coarse crackles
• Reduced air entry

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Clinical Presentation

• Acute exacerbation of COPD
• Patients present complaining of
• Worsening dyspnea
• Increased sputum volume
• Increased sputum purulence
• Hypoxemia, tachypnea, cyanosis, agitation,
  tachycardia, hypertension, acc mm use, pursed-lip
  exhalation, sitting up leaning forward posture
• Hypercapnea may result in confusion, tremor,
  decreased LOC
• Respiratory failure

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Causes of AECOPD

• Superimposed respiratory infection
• Cardiovascular deterioration
• Smoking
• Noncompliance with meds
• Environmental exposures
• Meds e.g. ß-blockers, benzos, narcotics
• Misuse of oxygen therapy
• Metabolic derangements

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DDX AECOPD

• Pneumonia
• IHD
• CHF
• Asthma
• PE
• Pneumothorax
• Etc.

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Diagnostic Tests

• Pulse Oximetry
• Easy, immediate, noninvasive test that provides
  information about the severity of respiratory
  compromise in an acute exacerbation
• ABG
• Provides accurate information about pH, PaO2 and
  PaCO2
• Consider in most if not all patients presenting
  with an acute exacerbation

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Diagnostic Tests

• PFTs
• FEV1 as compared to percent predicted is an
  excellent measure of disease severity
• As FEV1 falls below 25-30 of predicted, both
  hypoxemia and hypercarbia usually occur
• PEF can be used in ED to estimate FEV1, with the
  understanding that PEF is effort dependent and
  tends to overestimate lung function in the mid
  ranges

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Diagnostic Tests

• CXR
• Almost always abnormal, comparisons with prior
  exams should be made
• Helpful in the diagnosis of complications such as
  pneumothorax, pneumonia, pleural effusions,
  pulmonary neoplasia

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Infectious Precipitants

• Viral infections often implicated in COPD
  exacerbations influenza, PAI, RSV
• Atypical organisms may also be involved
  Mycoplasma, Chlamydia pneumoniae, Legionella
• Chronic colonization also occurs, most often with
  H. flu, Strep pneumo, and Moraxellarole of these
  organisms in exacerbations is controversial.

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CAP in AECOPD

• COPD patients are at high risk for CAP
• Symptoms of CAP are similar to those of AECOPD
  sputum, fever, cough
• Strep pneumo is most common, followed by H flu,
  and Moraxella Catarrhalis
• Legionella and Pseudomonas should always be
  considered
• Pneumovax and yearly influenza vaccines are
  important prevention

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Antibiotics in AECOPD

• Controversial and difficult to study
• Currently accepted practice based on the best
  evidence is that patients presenting with
  infectious symptoms
• Fever
• Increased sputum production
• Change in character of sputum
• will have a better outcome with the use of
  empiric antibiotic therapy

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Antibiotics in AECOPD

• Increasing evidence for newer antibiotics as
  first line therapy azithromycin, respiratory
  fluoroquinolones, ß-lactamase inhibitors.

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Antibiotics in AECOPD

• CHA recommendations
• lt4 exacerbations/year
• Amoxicillin 500mg po tid x 7-10d
• Doxycycline 200mg po x 1d then 100mg po od x
  7-10d
• TMP/SMX 1 DS tablet po bid x 7-10d

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Antibiotics in AECOPD

• CHA recommendations
• gt or 4 exacerbations per year or failure of
  first line agent or Abx last 6 weeks
• Cefuroxime axetil 250-500mg bid x 7-10d
• Amoxicillin-clavulanate 875mg po bid x 7-10 d
• For pen allergic patients
• Azithromycin 500mg x 1d then 250mg po od x 4d
• Clarithromycin 250-500mg po bid x 7-10d
• Levofloxacin 500mg po od x 5-10d
• Moxifloxacin 400mg po od x 5-10d

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Management of stable COPD

• Lifestyle modifications
• Smoking cessation
• Regular exercise
• Weight control
• Pulmonary rehabilitation
• Prevention
• Pneumovax
• Influenza

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Management of stable COPD

• Oxygen
• Started after room air ABGs document PaO2lt55 or
  56-59 in the face of cor pulmonale
• Bronchodilators
• ß-agonists
• Ipratropium bromide
• Long acting ß-agonists
• /- Theophylline

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Management of stable COPD

• Steroids
• 20-30 are steroid responders
• Inhaled or oral

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Management AECOPD

• Goals of therapy
• Relieve bronchoconstriction
• Improve oxygenation
• Approach to treatment
• Multi-modal
• Be cognizant of previous disease pattern

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Management AECOPD

• Oxygen
• All patients in respiratory distress should
  receive supplemental oxygen
• Target O2satgt90
• Be aware that patients known to be CO2-retainers
  may require controlled oxygen therapy
• Hypercarbia is likely secondary to the Haldane
  effect a shift of the hemoglobin-CO2 binding
  curve, as well as due to increased CO2 production
  and changes in physiologic dead space

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Management AECOPD

• ß2-agonists
• COPD patients will have some reversibility to
  their airflow obstruction that can effectively be
  relieved by inhaled short acting ß2-agonist
  therapy
• Long acting ß2-agonist therapy should be reserved
  for chronic management only
• No evidence that one specific agent has any
  greater efficacy than any other
• Little evidence regarding timing of
  administration (q60 min vs. q20 min etc.)

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Management AECOPD

• Anticholinergics
• Preferentially dilate larger central airways
  compared to ß2-agonists which dilate peripheral
  airways
• Slower onset of action than ß2-agonists
• Thought to inhibit vagal stimulation of the
  bronchithereby promoting smooth muscle
  relaxation
• Atropine and glycopyrrolate have been used
• Most common agent is ipratropium bromide q4-6h by
  neb or MDI

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Management AECOPD

• Theophylline
• Controversial
• Narrow therapeutic window
• Significant side effects dysrhythmias, seizures
• Limited evidence for efficacy

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Management AECOPD

• Corticosteroids
• Conflicting results in the literature
• In acute exacerbation, there is likely a role for
  systemic steroids, but not for inhaled
• Steroid response is likely a continuum rather
  than an all or none phenomenon

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Management AECOPD

• Magnesium
• Studied mostly in asthma
• One study showed benefit in COPD, used as 1-2g IV
  over 20 min
• Heliox
• No large-scale studies
• Probably should only be considered as a last
  alternative

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Mechanical Ventilation the controversies

• Widespread fear among healthcare workers that
  patients will become ventilator dependent
• Evidence suggests that most patients in fact will
  be extubated around day 10 but that 1-5 year
  mortality rate following an episode of
  respiratory failure is very high
• Likely a decision that should be addressed by the
  patient, family, primary health care provider
  PRIOR to the actual event

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Mechanical Ventilation

• Decision to begin assisted ventilation is a
  clinical one
• Noninvasive ventilation (BiPAP)
• BiPAP works by providing nasal, bilevel positive
  airway pressure. This overcomes the intrinsic
  PEEP of most COPD patients, and significantly
  reduces work of breathing, thereby improving gas
  exchange
• Response is usually seen within the first hour
• Should be considered first line before
  endotracheal intubation unless patient has
  impaired mental status or cardiovascular
  instability

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Mechanical Ventilation

• Kramer et al
• Selection criteria for NPPV (any two)
• Moderate to severe dyspnea with use of accessory
  muscles and paradoxical abdominal motion
• Moderate to severe acidosis (pH 7.3-7.35) and
  hypercapnia (PaCO2 45-60)
• Respiratory frequency gt 25 breaths/min

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Mechanical Ventilation

• Kramer et al
• Exclusion Criteria for NPPV (any one)
• Respiratory arrest
• Cardiovascular instability (hypotension,
  dysrhythmias, AMI)
• Somnolence, impaired mental status, uncooperative
  patient
• High risk of aspiration
• Viscous or copious secretions
• Recent facial or gastroesophageal surgery
• Craniofacial trauma with fixed nasopharyngeal
  abnormalities
• Extreme obesity

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Mechanical Ventilation

• Indications for invasive mechanical ventilation
  in AECOPD (Pierson, Respiratory Care, 2002)
• Severe dyspnea with accessory muscle use and
  paradoxical abdominal motion
• RRgt35
• Life-threatening hypoxemia (PaO2lt40)
• Severe acidosis (pH lt 7.25) and hypercapnea
  (PaCO2 gt 60)
• Respiratory arrest
• Somnolence or impaired mental status
• Cardiovascular complications
• Other complications (sepsis, pneumonia, PE)
• Failure of NPPV

106
Disposition

• Consider
• Overall respiratory status post-treatment
• Home environment
• Mental status
• Comorbid illness
• Age
• Compliance
• Previous pattern of illness
• Keep in mind high relapse rate

107
Disposition

• Treatment at home
• O2 if needed
• Inhaled ß2-agonists
• Inhaled anticholinergic agents
• Proper inhaler technique (review prior to
  discharge)
• Corticosteroids
• /- Theophylline
• /- Antibiotics