Acute exacerbation of Chronic obstructive pulmonary disease for emergency medicine

1. ACUTE EXACERBATION
OF COPD
DR KOSARAJU REVATI
JR. PAEDIATRICS
DR DRAVID M C
JR. EMERGENCY MEDICINE

2. INTRODUCTION
• COPD is a common, preventable, and treatable disease
characterized by persistent respiratory symptoms and airflow
limitation due to airway and/or alveolar abnormalities
• It is caused by significant exposure to noxious particles or gases
• The WHO Global Initiative for COPD encompasses chronic
bronchitis, emphysema, bronchiectasis, and asthma, recognizing
that most patients have a combination of the different diseases.

3. Risk Factors
• Tobacco smoke
• Indoor air pollution: Due to burning of wood and other biomass
fuels used for cooking and heating in poorly vented dwellings,
particularly affects women in developing countries
• Occupational exposures: Organic, inorganic dusts and chemical
agents and fumes

4. • Outdoor air pollution: Also contributes to the total burden of
inhaled particles
• Genetic factors: Alpha 1 antitrypsin deficiency,
Defective metaloproteinase 12 (MMP 12)
Glutathione S-transferase
• Age and sex: Aging and female sex increase COPD risk

5. • Lung growth and development: Any factor that affects the lung
growth during gestation and childhood (low birth weight,
respiratory infections etc) has potential to increase an individual’s
risk of developing COPD.
• Socio-economic status
• Asthma and hyper reactivity of airway
• Infections

7. PATHOPHYSIOLOGY
• These risk factors trigger an increase in inflammatory cells in the
airways, lung interstitium, and alveoli.
• Proteases break down lung parenchyma and stimulate mucus
secretion.
• Mucus-secreting cells replace cells that normally secrete
surfactant and protease inhibitors.

8. • These changes result in a loss of elastic recoil, narrowing, and
collapse of the smaller airways.
• Mucous stasis and bacterial colonization then develop in the
bronchi.
• The earliest objective changes are small increases in peripheral
airway resistance or lung compliance.

9. • Because dyspnea and hypersecretion often progress insidiously, it
may take decades before COPD becomes clinically evident.
• The central element of chronic lower airway obstruction is
impedance to expiratory airflow due to increased resistance or
decreased caliber of the small bronchi and bronchioles.

10. • Airflow obstruction results from a combination of airway
secretions, mucosal edema, bronchospasm, and
bronchoconstriction.
• Exaggerated airway resistance reduces total minute ventilation
and increases respiratory work.

12. OBSTRUCTIVE LD RESTRICTIVE LD
 Characterised by reduction in air flow
 So, shortness of breath in exhaling air
 Hence the air will remain inside the lung
after full expiration.
 Reduction in lung volume due to stiffness
of lung tissue or chest wall cavity
 So there will be difficulty in taking air
inside
EXAMPLES: COPD
Asthma
Bronchiectasis
EXAMPLES: ILD
Scoliosis, Neuromuscular
causes
Marked obesity
Idiopathic pulmonary fibrosis
Pneumoconiosis, sarcoidosis.
Decrease in both FEV1 and FEV1/FVC Normal FEV1/FVC ratio

14. PFT
• FVC : The maximum volume of air forcibly exhaling from the point of
maximum inhalation
• FEV1: Forced expiratory volume in 1 second during FVC maneuver.

15. COPD includes
1) Chronic bronchitis : Chronic productive cough in 3 months
in each of 2 successive years in a patient in whom other
causes of chronic cough been exculed

16. • Emphysema: Abnormal and permanent enlargement of the airspaces
distal to the terminal bronchioles i.e accompanied by destruction of air
space walls without obvious fibrosis.

18. ACUTE EXACERBATION OF COPD
• Acute exacerbations of COPD result in worsening of respiratory
symptoms beyond normal day-to-day variations and are usually
triggered by an infection or respiratory irritant.
• More than 75% of patients with acute exacerbations have evidence of
viral or bacterial infection, with up to half specifically due to bacteria.
• It is primarily due to ventilation–perfusion mismatch rather than the
expiratory airflow limitation which is seen with asthma exacerbations

19. CLINICAL FEATURES
• Dyspnoea : Progressive, persistent and characteristically worsen with
exercise
• Chronic Cough : May be intermitent and unproductive.
• Chronic sputum production
• Wheezing
• Chest tightness
• Weight loss
• Respiratory infections

20. CLINICAL PRESENTATION OF PATIENT TO
ER
• Signs of hypoxemia include tachypnea, tachycardia, systemic
hypertension, cyanosis, and a change in mental status.
• With increased work of breathing, carbon dioxide production
increases; alveolar hypoventilation creates arterial carbon
dioxide retention and respiratory acidosis.

21. • The patient tries to overcome severe dyspnea and orthopnea
by sitting in an up-and-forward position, using pursed-lip
exhalation and engaging accessory muscles to breathe.
• Pulsus paradoxus (a decrease of >10 mm Hg in systolic
blood pressure during respiratory cycles) may be noted
during palpation of the pulse or during blood pressure
recording.

22. Modified MRC Dyspnoea Scale
Grade Symptoms
mMRC Grade 0 Breathlessness only on strenuous activity
mMRC Grade 1 Breathlessness while hurrying on the level or
walking slight uphill
mMRC Grade 2 Walking slower on the level than the same
age group
mMRC Grade 3 Breathlessness while walking about 100m, or
after few minutes on walking level ground
mMRC Grade 4 Breathlessness on doing daily routine
activities

23. PHYSICAL SIGNS
• INSPECTION
Barrel shaped chest
Accessory respiratory muscle participation
Prolonged expiration during quiet breathing
Expiration through pursed lip
Paradoxical retraction on lower intercostal spaces
Tripod position

26. • PALPATION
Decreased tactile vocal fremitus
• PERCUSSION
Hyper-resonant
Depressed diaphragm
Diminision of the area of absolute cardiac dullness.

27. • AUSCULTATION
Prolonged expiration
Reduced breath sounds
The presence of wheeze during quiet breathing
Crackles can be heard if infection exist.

28. Critical differential diagnosis of COPD
exacerbations

30. DIAGNOSIS OF COPD
Symptoms : chronic cough , SOB and sputum production
+
Exposure to risk factor : tobacco, occupation and indoor/outdoor
pollution
+
SPIROMETRY is required to establish the diagnosis.

31. • The presence of post bronchodilator FEV1/FEV <0.70 Confirms the
presence of persistent airflow limitation and thus of COPD
SPIROMETRY : Normal trace showing FEV1 and FEV

32. SPIROMETRY: Obstructive disease

33. Classification of COPD severity

34. Arterial Blood Gas analysis
• The best tool in acute evaluation for assessing oxygenation, ventilation, and acid-
base disturbances.
• Arterial blood gases clarify the severity of exacerbation and the probable clinical
course.
• Respiratory failure typically shows an arterial Pao2 of <60 mm Hg or an arterial
Sao2 <90% in room air.
• Respiratory acidosis is present if the partial pressure of carbon dioxide (Pco2) is
>44 mm Hg.

35. • If the pH is <7.35, there is an acute and uncompensated component of
respiratory or metabolic acidosis present
• While arterial blood is best potentially useful screening tool.
• In acute respiratory acidosis, the serum bicarbonate rises by 1 mEq/L
for each 10-mm Hg increase in Pco2, and the pH will change
• In chronic respiratory acidosis, the bicarbonate rises by 3.5 mEq/L for
each 10-mm Hg increase in Pco2, and the pH will Changes outside of
these ranges suggest an accompanying metabolic disorder

36. Chest x ray –Emphysema
• Marked over inflation is noted with flattend and low diaphragm
• Intercostal space becomes widen
• Horizontal pattern of ribs
• Long thin heart shadow
• Decreased marking of lung peripheral vessels

38. CT findings
• Greater sensitivity and specificity for emphysema

39. Laboratory examination
Blood examination
• CBC -In exacerbation or acute infection in airway , leucocytosis may
be seen
Sputum culture
• Streptococcus pneumonia
• Hemophilus influenzae
• Moraxella catarrhalis
• Klebsiella pneumonia

40. TREATMENT
Based on the principles of
• Prevention of further progress of disease
• Preservation and enhancement of pulmonary functional capacity
• Avoidance of exacerbations in order to improve the quality of life.

41. ED management of COPD Exacerbation
• Assess severity of symptoms
• Administer controlled oxygen (target arterial oxygen saturation of88%–92%)
• Continuous cardiovascular status monitoring
• Perform arterial blood gas measurementafter20–30 min if arterial oxygen
saturation remains <90% or if concerned about symptomatic hypercapnia
• Administer bronchodilators

42. • β2-Agonists and/or anticholinergic agents by nebulization or
metered-dose inhaler with spacer
• Add oral or IV corticosteroids
• Consider antibiotics if increased sputum volume, change in sputum
color , fever ,or suspicion of infectious etiology of exacerbation
• Consider noninvasive mechanical ventilation
• Evaluation may include chest radiograph ,CBC with differential ,basic
metabolic panel , ECG

43. Oxygen Administer
• Oxygen to achieve a Pao2 of 60 to 70 mm Hg or an Sao2 between 88% and
92%.29
• There is potential harm in targeting higher oxygen levels.
Use any of the following devices
• standard dual-prong nasal cannula
• simple facemask
• Venturi mask.

44. • It may take 20 to 30 minutes from administration of supplemental oxygen for
improvement to occur.
• Be aware that oxygen administration may produce hypercapnia through
worsening ventilation–perfusion mismatching
• this is one reason non-rebreathing masks are best used cautiously.
• If adequate oxygenation does not exist or respiratory acidosis develops, assisted
ventilation is an option
• Long term oxygen therapy improves survival , exercise and cognitive performance
in patients with respiratory failure

45. Bronchodilators
• Beta2- agonists
• Medications that increase FEV1 and/or change other spirometric
variables.
• MOA: Relaxes airway smooth muscle by stimulating beta2 adrenergic
receptors, which increases cAMP and produces functional antagonism
to bronchoconstriction.
• Adverse effects: Sinus tachycardia, tremors

46. Bronchodilators
Three major classes of bronchodilators:
β2 - agonists:
•Short acting: Salbutamol & terbutaline
•Long acting: Salmeterol & formoterol
•Anticholinergic agents: Ipratropium,tiotropium
•Theophylline: a weak bronchodilator but has some anti
inflammatory properties.

47. • Levalbuterol (MDI, nebulizer): 6-8hours
Nebuliser: 0.63mg three times TID
MDI: 90mcg (2 actuations of MDI)
• Salbutamol (MDI, nebulizer, DPI): 12 hours ext. release
Nebuliser: 0.63mg three times TID
MDI: 90mcg (2 actuations of MDI)
• Terbutaline (DPI): 4-6hours, 5mg TID
SABA

48. LABA
• Formoterol (DPI, neb): 12 hours, 20mcg BD
• Salmeterol (MDI, DPI): 12 hours, 50mcg BD, maintainence dose in
COPD
• Indacaterol (DPI, neb): 24 hours, 75mcg OD

49. Anti muscarinic drugs
• MOA: Blocks the bronchoconstriction effects of the Ach on M3
muscarinic receptors expressed in smooth muscle.
• Adverse effects: produces dry mouth. Cardiovascular events
(Ipratropium> tiotropium). Bitter metallic taste in ipratropium inhalers

50. SAMA:
• Ipratropium bromide (MDI, Neb): 6-8 hours,
MDI: 2 actuations (34mcg), not to exceed 12 actuations per day
Neb: 500mcg (2.5ml) TID
LAMA:
• Tiotropium bromide (DPI, SMI, MDI): 12 hours, 1.25mcg per
actuation
• Aclidinium bromide (DPI, MDI): 12 hours, 400mcg/ actuation
• Umeclidinium (DPI): 24 hours, 62.5mcg/ actuation

51. GLUCOCORTICOIDS
• Regular treatment with inhaled glucocorticoids is
appropriate for symptomatic patients with an FEV1 <50%
(pred) and repeate exacerbation.
• Chronic treatment with systemic glucocorticoids should be avoided
because of unfavorable benefit to risk ratio
• Hyperglycemia is the most common adverse effect.

52. • A short course (5 to 7 days) of systemic steroids
• improves lung function and hypoxemia and shortens recovery time in
acute COPD exacerbations
• Use of corticosteroids in the ED does not affect the rate of
hospitalization but decreases the rate of return visits
• There appears to be no benefit from oral prednisone > 40 to 60 mg as
• a single or divided twice daily total dose
• There is also no benefit to IV administration of glucocorticoids except
in patients who cannot tolerate oral intake or are in shock and have
impaired absorption of medication from the GI tract

53. COMBINATION THERAPY
• Combination therapy of long acting beta 2 agonists and inhaled
corticosteroids and show a significant additional effect on pulmonary
function and a reduction in symptoms
• Mainly in patient with an FEV1 < 50%

54. Combination (SAMA/ SABA)
• Salbutamol/ ipratropium (SMI/ MDI):
MDI- 100mcg/20mcg, QID
Neb- 2.5mg/0.5mg, QID
LABA/ ICS
• Formoterol/ beclametasone (MDI, DPI)
• Formoterol/ budesonide (MDI, DPI)
• Salmeterol/ Mometasone (MDI)
• Salmeterol/ fluticasone propionate (MDI, DPI)

55. Methylxanthines
• Theophylline most commonly used methylxanthine, is metabolised by
cytochrome p450.
• Addition of theophylline to salmeterol produces a greater
improvement in FEV1 and breathlessness than salmeterol alone.
• However large placebo controlled trial showed no effect of oral
theophylline alone or in combination with T.Pred

56. Antibiotics
• In moderately or severely ill patients if there is evidence of infection,
such as change in volume of sputum and increased purulence of
sputum
• most common pathogens associated with COPD exacerbation:
• Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella
catarrhalis. T
• Initial antibiotics for uncomplicated COPD include
 macrolides (azithromycin)
 tetracyclines (doxycycline)
 trimethoprim-sulfamethoxazole.

57. • Consider providing coverage for Pseudomonas aeruginosa in patients
with one or more of the following risk factors:
 admission and/or antibiotic course in past 3 months,
 prior culture showing Pseudomonas infection,
 concomitant bronchiectasis.
There is little evidence regarding the duration of treatment, which
ranges from 3 to 14 days.

58. CEFTRIAXONE 2GM IV Q12HR
PIPERACILLIN-TAZOBACTAM 4.5GM IV Q6H
MEROPENEM 1GM IV Q8H/AZTREONAM 1GM IV
PLUS
AZITHROMYCIN 500MG IV OD
OR
LEVOFLOXACIN 750MG IV OD/ MOXIFLOXACIN 400MG IV OD

64. Other treatments
• Anti oxidants
• Mucolytic agents
• Pulmonary rehabilitation
• Nutrition
• Surgery
Bullectomy
Lung volume reduction surgery
Lung transplantation

65. Indications for Hospital Admission
• Marked increase in intensity of symptoms, such as sudden
development of resting dyspnea or inability to walk from room to
room
• Failure of exacerbation to respond to initial medical management
• Significant comorbidities
• Newly occurring dysrhythmias, heart failure
• Frequent exacerbations and/or frequent relapse after ED treatment
• Older age
• Insufficient home support

66. Indications and Relative Contraindications for Noninvasive
Ventilation
Selection criteria
• Acidosis (pH <7.36)/hypercapnia(Paco2 >50 mm Hg)/oxygenation
deficit (Pao2 <60 mm HgorSao2 <90%)
• Severe dyspnea with clinical signs such as respiratory muscle fatigue
or increased work of breathing

67. Exclusion criteria
• Respiratory arrest
• Cardiovascular instability(hypotension , arrhythmias, myocardial infarction)
• Change in mental status ;uncooperative patient
• High aspiration risk
• Viscous or copious secretions
• Recent facial or gastroesophageal surgery
• Craniofacial trauma
• Fixed nasopharyngeal abnormalities
• Burns
• Extreme obesity

68. Indications for Intubation With Mechanical
Ventilation
• Unable to tolerate noninvasive ventilation (NIV)or NIV failure
• Respiratory or cardiac arrest
• Respiratory failure
• Decreased consciousness or increased agitation
• Massive aspiration
• Persistent inability to remove respiratory secretions
• Hypotension
• Persistent hypoxemia despite optimal respiratory treatment
• Hemodynamic instability

69. Indications for Intensive Care Admission
• Severe dyspnea that responds inadequately to initial emergency
therapy
• Changes in mental status (confusion, lethargy, coma)
• Persistent or worsening hypoxemia(Pao2 <40 mm Hg) and/or
severe/worsening respiratory acidosis (pH<7.25)despite supplemental
oxygen and NIPPV
• Need for invasive mechanical ventilation
• Hemodynamic instability
• (Local resources and capabilities may dictate different decision
making; with NIPPV patients in particular , different systems dictate
different dispositions.)
• NIPPV = noninvasive positive-pressure ventilation

70. Complication of COPD
1. Pneumothorax
2. Cor pulmonale
3. Exacerbation of COPD
4. Respiratory failure

71. Comorbidities assossiated with COPD
 Cardiovascular diseases
 Osteoporosis
 Respiratory infection
 Anxiety and depression
 Diabetes
 Lung cancer
 Bronchiectasis

72. Thank you