copd review
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CHRONICOBSTRUCTIVE
PULMONARY DISEASE
Jongsiriyunyong K. EP rj
INTRODUCTION Progressive and Non fully reversible
airflow limitation
COPD is a disorder in which subsets have dominant features of
chronic bronchitis chronic productive cough for 3 months during
each of 2 consecutive years emphysema, or asthma
permanent enlargement of the air spaces distal to the terminal bronchioles, without obvious fibrosis
INTRODUCTION The Global Initiative for Chronic Obstructive
Lung Disease (GOLD) guidelines define COPD as a disease state characterized by
Airflow limitation that is not fully reversible, is usually progressive, and
Associated with an abnormal inflammatory response of the lungs to inhaled noxious particles or gases
Venn diagram of chronic obstructive pulmonary disease (COPD).
1 21
3 45
6 78
9 10
Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells
Gross pathology of advanced emphysema. Large bullae are present on the surface of the lung.
At high magnification, loss of alveolar walls and dilatation of airspaces in emphysema can be seen.
Pathophysiological
This phenomenon is called dynamic hyperinflation
ETIOLOGY I/II Cigarette smoking- 90%
Environmental factors Biomass fuels with indoor cooking and heating Traffic-related air pollution
Airway hyperresponsiveness
Alpha1-antitrypsin deficiency Panacinar emphysema Premature emphysema at an average age of 53 years for
nonsmokers and 40 years for smokers
Intravenous drug use Pulmonary vascular damage
Insoluble filler (eg, cornstarch, cotton fibers, cellulose, talc) contained in methadone or methylphenidate
Cocaine or heroin
ETIOLOGY II/II Immunodeficiency syndromes
Independent risk
Vasculitis syndrome Hypocomplementemic vasculitis urticaria syndrome
(HVUS)
Connective tissue disorders Cutis laxa is a disorder of elastin , various forms of
inheritance Marfan syndrome is an autosomal dominant inherited
disease of type I collagen Ehlers-Danlos syndrome
Salla disease Autosomal recessive storage disorder , sialic acid
PROGNOSIS For assess an individual’s risk of death or
hospitalization
History
Multifactorial with Individual lifestyle Socioeconomic factors Education / Knowledge
BODE INDEX
4-year survival
0-2 points = 80%
3-4 points = 67%
5-6 points = 57%
7-10 points = 18%
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CHARACTERISTIC I/II
Cough worsening dyspnea progressive exercise
intolerance sputum production alteration in mental
status Productive cough or
acute chest illness Breathlessness Wheezing
Systemic manifestations decreased fat-free mass impaired systemic
muscle function Osteoporosis Anemia Depression pulmonary hypertension cor pulmonale left-sided heart failure
Typically combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease.
CHARACTERISTIC II/II Hx of more than 40 pack-yrs of smoking
was the best single predictor of airflow obstruction
If all 3 signs are absent, airflow obstruction can be nearly ruled out Self-reported smoking Hx of > 55 pack-yrs Wheezing on auscultation Self-reported wheezing
PHYSICAL EXAMINATION Hyperinflation (barrel chest)
Wheezing – Frequently heard on forced and unforced expiration
Diffusely decreased breath sounds
Hyperresonance on percussion
Prolonged expiration phase
CHARACTERISTICS ALLOW DIFFERENTIATION
Chronic bronchitis Emphysema
obese Frequent cough and
expectoration Use of accessory
muscles of respiration is common
Coarse rhonchi and wheezing may be heard on auscultation
signs of right heart failure Cor pulmonale
edema and cyanosis
thin with a barrel chest little or no cough Breathing may be
assisted by pursed lips patients may adopt the
tripod sitting position hyperresonant, and
wheezing may be heard Distant Heart sounds
DIFFERENTIALS DIAGNOSIS Alpha1-Antitrypsin def
Bronchitis
Emphysema
Nicotine Addiction
Pulmonary Embolism
INVESTIGATION I/II Pulmonary Function Tests
For diagnosis Assessment of severity Following its progress
ABG Hypoxemia / hypercapnia Acidosis
Serum Chemistries Retain sodium /Lower potassium levels
/bicarbonate Chronic respiratory acidosis leads to compensatory
metabolic alkalosis
INVESTIGATION II/II CBC
Secondary polycythemia Hct>52% in men or 47% in women
Alpha1-Antitrypsin all patients < 40 yrs or Fm Hx of emphysema at
early age
Sputum Evaluation Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Pseudomonas aeruginosa
Chest Radiography +/- CT scan
COPD: Hyperinflation, depressed diaphragm, increased retrosternal space, and hypovascularity of lung parenchyma are demonstrated.
Emphysema : increased AP diameter, increased retrosternal airspace, and flattened diaphragm on lateral chest radiograph.
A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragm on posteroanterior chest radiograph
A computed tomography (CT) scan shows hyperlucency due to diffuse hypovascularity and bullae formation, predominantly in the upper lobes.
Severe bullous disease as seen on a computed tomography (CT) scan in a patient with chronic obstructive pulmonary disease (COPD).
TREATMENT Acute exacerbation
Stable COPDRx base on severity of disease
TREATMENT
Severity evaluateMild to moderate
เหนื่��อยเพิ่�มขึ้� นื่ไม�มาก Hemodynamic stable เพิ่�มขึ้นื่าดยาและความถี่��ขึ้อง bronchodilator Pred 30-40 mg/dy for 7dy
Moderate to severe Risk for respiratory failure
AOC Accessory muscle used: paradoxical chest/abd motion SpO2 < 90% or PaO2 < 60 mmHg PaCO2 > 45 mmHg or pH < 7.35
Acute exacerbation
TREATMENT
Indication for admit
Severe exarcerbation Severe stage of COPD New onset of : cyanosis, peripheral edema Unimprove after appropriated Tx Multi-Comorbit : CAD, DM, HT New onset Arrhythmia Undefinite Diagnosis Old age or Homeless
ACUTE EXACERBATION
treatment
TREATMENTAcute exacerbation : 1-3 wk onset Bronchodilator
Beta2-agonist Anticholinergic Methylxantine
Corticosteroid Systemic corticosteroids
Oxygen All pt with SpO2 < 90% keep SpO2 90-94%
Antibiotic Cover Streptococcus pneumoniae, Hemophilus influenza,
Morexella catarrhalis, Klebsiella pneumoniae ; Pseudomonas aeruginosa
Machanical ventilation Non-invasive positive pressure ventilation: NIPPV Invasive mechanical ventilation
TREATMENTAcute exacerbation : 1-3 wk onset
Short acting Beta2-agonist is first line but recommended combine of SABA and Anticholinergic for limited S/E (palpitation, tachycardia, tremor)
Fenoterol/Ipratropium bromide Every 15-20 min in 1st hour then 4-6 hr interval Addition SABA every 1-2 hr
BRONCHODILATOR
Medication type Onset (min)
duration (hour)
Route drug
Beta2agonist Short 3-5 4-6 InhaleOralIV
Salbutamol(ventolin®)
TerbutalineFenoterol
8-12 InhaleOral
Procaterol
Long 30-45 > 12 Inhale SalmeterolFormoterol
Anticholinergic Short 10-15 6-8 Inhale Ipratopium bromide
Long 5 >24 Inhale Tiotropium (Spiriva®)
Methylxanthine Uncertained in sustained release OralIV
TheophyllineAminophylline
TREATMENTAcute exacerbation : 1-3 wk onset
Systemic corticosteroid
Limited systemic inflammation and airway inflammation Decrease sputum eosinophil Decrease serum CRP Improve FEV1 and PaO2 Minimize treatment failure / Length of stay in Hospital/
Exacerbation No improve of mortality
Prednisoline 30-40 mg/dy for 7-14 dy or
Dexamethasone 5- 10 mg q 6 hr orHydrocortisone 100-200 mg q 6 hr
TREATMENTAcute exacerbation : 1-3 wk onset
Oxygen All pt with SpO2 < 90% keep SpO2 90-94%
Limited S/E of Oxygen supplement ลด hypoxic drive ทำ�าให�เกด hypoventilation เพิ่�ม ventilation / perfusion mismatch (เพิ่�ม
deadspace ) Haldane effect
rightward displacement of the CO2-hemoglobin dissociation curve in the presence of increased oxygen saturation, increasing the amount of CO2 dissolved in blood
TREATMENTAcute exacerbation : 1-3 wk onset
Machanical ventilation
Indication of NIPPV เหนื่��อยมากร่�วมก!บ accessory muscle with abd paradox Acidosis pH 7.25-7.35 and/or PaCO2 > 45 mmHg RR > 24 / min
C/I of NIPPV Uncooperation เสมหะมาก หย$ดหายใจ Cardiovascular instability Life-threatening hypoxemia Severe acidosis : pH < 7.25
TREATMENTAcute exacerbation : 1-3 wk onset
Machanical ventilationIndication of Invasive mechanical
ventilation Respiratory failure
Severe acidosis : pH < 7.25RR > 35/minAccessory muscle used
with C/I for NIPPV Fail NIPPV
STABLE COPD
treatment
TREATMENTStable COPD : base on severity Bronchodilator
Beta2-agonist Anticholinergic Methylxantine
Corticosteroid inhaled corticosteroids
Vaccination Annual influenza vaccine Pneumococcal vaccination
Pulmonary rehabilitation Improve quality of life
Oxygen therapy Short term Long term
sugery
TREATMENTStable COPD : at ALL stage
Avoidance of risk factor(s)
Influenza vaccination
Pneumococcal vaccination
TREATMENTStable COPD : Mild COPD
Short-acting bronchodilator when needed
TREATMENTStable COPD : Moderate COPD
Short-acting bronchodilator when needed
Regular treatment with one or more long-acting bronchodilators
Rehabilitation
TREATMENTStable COPD : Severe COPD
Short-acting bronchodilator when needed
Regular treatment with one or more long-acting bronchodilators
Rehabilitation
Inhaled glucocorticoids if significant symptoms, lung function response, or if repeated exacerbations
COMBINATION ICS/LABA
Combination Dose(ug/dy) Trade name
Fluticasone/Salmeterol 500/100-1000/100
Seretide®
Budesonide / Formeterol 320/9-640/18 Symbicort®
BRONCHODILATOR
Medication type Onset (min)
duration (hour)
Route drug
Beta2agonist Short 3-5 4-6 InhaleOralIV
Salbutamol(ventolin®)
TerbutalineFenoterol
8-12 InhaleOral
Procaterol
Long 30-45 > 12 Inhale SalmeterolFormoterol
Anticholinergic Short 10-15 6-8 Inhale Ipratopium bromide
Long 5 >24 Inhale Tiotropium (Spiriva®)
Methylxanthine Uncertained in sustained release OralIV
TheophyllineAminophylline
TREATMENTStable COPD : Very severe COPD
Short-acting bronchodilator when needed
Regular treatment with one or more long-acting bronchodilators
Inhaled glucocorticoids if significant symptoms, lung function response, or if repeated exacerbations
Treatment of complications : CHF, infection, nutrition
Rehabilitation
Long-term oxygen therapy if chronic respiratory failure
Consider surgical treatment
VACCINATION
PULMONARY REHABILITATION
OXYGEN THERAPY ม� 3 แบบ ค�อ
Short-term therapyLong-term continuous therapyDuring exercise
เป้'าหมายค�อเพิ่�ม PaO2 ให�ได�อย�างนื่�อย 60 mmHg ขึ้ณะพิ่!ก และ/หร่�อ SaO2อย�างนื่�อย 90% ซึ่��งจะทำ�าให�อว!ยวะทำ��ส�าค!ญได�ร่!บ O2
SHORT TERM OXYGEN THERAPY Indication for STOT
Recent Exacerbation with new hypoxemia
Re-evaluate at wk 4 Continue STOT if still hypoxemia
Re-evaluate at Mo 3Treat as LTOT
LONG TERM OXYGEN THERAPY Continue Oxygen supplement > 15 hr/dy
ลด mortality เพิ่�ม exercise toleranceQuality of life: psychotherypyPrevent pulmonary HT
Ind for LTOTPaO2 < 55 mmHg or SaO2 < 88%
PaO2 < 56-59 mmHg or SaO2 < 89% with sign of chronic hypoxemia Pul HT Peripheral edema จาก CHF Polycythemia (Hct > 55%)
Failed STOT
OXYGEN THERAPY
Oxygen therapy via nasal cannulaHome supplemental
oxygen
Bilevel positive airway pressure (BiPAP)
DISPOSITION Hemodynamic stable
Bronchodilator supply less than every 4 hr
SpO2 >90% w/o O2 supplement at least 24 hr
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