CHRONIC OBSTRUCTIVE

PILMONARY DISEASE

Kreshimaricon Furigay
•INFORMANT
PATIENT

•RELIABILITY
95%
GENERAL DATA
• C.R.
• 58 years old
• Male
• Amulung, Cagayan
• Filipino
• Roman Catholic
• Admission: August 18, 2018
 Chief Complaint:

DIFFICULTY OF BREATHING
 HISTORY OF PRESENT ILLNESS
• 4 DAYS PRIOR TO ADMISSION

NO
CONSULT
 Productive cough  Undocumented fever
 Whitish to yellowish sputum,  Relieved by Paracetamol
non-bloody tablet
HISTORY OF PRESENT ILLNESS
• FEW HOURS PRIOR TO ADMISSION

 Productive cough Body weakness

ADMISSION
Difficulty of breathing
PHYSICAL EXAMINATION
• GENERAL:
• Ambulatory, conscious, coherent, in respiratory distress

• Vital signs:
BP- 130/80
HR – 81 bpm
Temperature – 36.8 C
RR- 29cpm
O2 sat- 91%
SKIN
• No cyanosis, no pallor, no lesions. Warm to touch; Good skin turgor

HEAD
• Evenly distributed hair, no scalp lesion

EYES
• Anicteric sclera, pink palpebral conjunctiva

EARS
• No deformities, no discharges

NOSE
• (-)nasal discharge, (-) nasal flaring

Mouth
• Dry lips but with moist oral mucosa, no cleft lip and palate.
NECK
• No cervical lymphadenopathy, no mass
LUNGS
• Symmetrical chest expansion, (+) intercostal retractions, (+) coarse
crackles & wheezes on bilateral lung fields

HEART
• Adynamic precordium, PMI at 5th ICS left mid clavicular line, normal rate,
regular rhythm, no murmurs
ABDOMEN
• Flat, normoactive bowel sound, (-) palpable mass, soft abdomen, (-)
tenderness
GENITALIA
• Grossly male

EXTREMITIES
• No deformities, no clubbing, CRT of 1-2 seconds.
PAST MEDICAL HISTORY
• (+) Hypertension
• (-) Diabetes mellitus
• (-) Heart disease
• (-) Allergies
FAMILY HISTORY
• (+) Hypertension
• (-) Diabetes mellitus
• (-) Heart disease
• (-) Allergies
PERSONAL AND SOCIAL HISTORY
Alcoholic
beverages
Sari-sari Lives in a semi
concrete,
drinker
store Smoker 30 Loves to eat
bungalow type • Gin ½
owner/ of house with pack years vegetables
vendor glass, 3-
1 bedroom
5x/week
 REVIEW OF SYSTEMS
head • no headache, with dizziness

Eye • no BOV, discharges , or excessive tearing

Eras • no ear pain, discharge, tinnitus

Nose • no allergies, obstruction, polyps, or change in sense of smell.

Throat • no hoarseness, dysphagia

Cardio-
Respirat • no orthopnea
ory

Gastroin
testinal
• no vomiting, no LBM, constipation, melena

Endocrine
• no cold intolerance, polyuria, polydipsia, polyuria
SALIENT FEATURES
• 58 years old
• Male
• Dyspnea
• Productive cough
• Whitish to yellowish sputum
• Undocumented fever
• In respiratory distress
• Tachypneic
• O2 sat 91%
• Intercostal retractions
• Coarse crackles on bilateral lung fields
• Wheezes on bilateral lung fields
• Smoker 30 pack years
DIFFERENTIAL DIAGNOSIS
 COPD
PULMONARY Asthma
Pleural effusion
Pneumonia
Congestive heart failure
CARDIAC Metastatic tumor
Atrial fibrillation
GERD
DYSPNEA
GASTROINTESTINAL Aspiration
Neoplasia
Metabolic Acidosis
NEUROMUSCULAR Phrenic Nerve
Palsy
Anxiety/Hyperventilation
OTHERS
Pain
 COPD
PULMONARY Asthma
Pleural effusion
Pneumonia
Congestive heart failure
CARDIAC Metastatic tumor
Atrial fibrillation
GERD
DYSPNEA
GASTROINTESTINAL Aspiration
Neoplasia
Metabolic Acidosis
NEUROMUSCULAR Phrenic Nerve
Palsy
Anxiety/Hyperventilation
OTHERS
Pain
COPD
RULE IN
• Dyspnea • Retractions
• Productive cough • Coarse crackles on
• Whitish to yellowish sputum bilateral lung fields
• In respiratory distress • Wheezes on bilateral
• Tachypneic lung fields
• Smoker 30 pack years
ASTHMA
RULE IN RULE OUT
• Dyspnea • Smoker 30 pack years
• Cough
• Sputum production Cannot totally rule out
• Wheezes on auscultation
PNEUMONIA
RULE IN RULE OUT
• Cough • CANNOT TOTALLY
• Sputum production RULE OUT
• Dyspnea
• Tachypneic
• Crackles on auscultation
PLEURAL EFFUSION
RULE IN RULE OUT
• Sputum production • Productive cough
• Dyspnea • No decreased breath
• Tachypneic sounds
• Crackles on auscultation
CONGESTIVE HEART FAILURE
RULE IN RULE OUT
• Dyspnea • No orthopnea
• Wheezing • No paroxysmal
• Cough nocturnal dyspnea
• Smoker • No edema
• Coarse crackles on chest
auscultation
ADMITTING DIAGNOSIS

COPD IN AE
CAP - MR
COURSE IN THE WARD
ON ADMISSION (8/18/18)

S O A P
Difficulty of Conscious, coherent, in DAT
COPD
breathing respiratory distress
BP: 130/80 IN AE Diagnostics:
CR: 81 CBC with PC Chest xray- PA/Lat
Productive Na, K, crea, BUN 12 Lead ECG
T: 36.8
cough RR: 29 CAP Sputum GS/CS Urinalysis
O2 sat: 91% CBG – 140 ABG
Body MR
(-)cyanosis, (-) gross Pallor Therapeutics:
weakness anicteric sclerae, pink PNSS 1 L x 12
conjunctiva Ampicillin-Sulbactam 1.5g/now then q6 (-)
symmetrical chest expansion, ANST
(+)subcostal retractions (+) Azithromycin 500 mg/tab OD
crackles & wheezes BLF Hydrocortisone 250 mg/IV now then 100 mg/IV
adynamic precordium, no q6
murmurs, Salbutamol + Iprat neb q15 x 3 doses then q4
Flat,NABS, soft, nontender O2 inhalation at 2 LPM via NC
full and equal pulses (-) VS q1
clubbing I & O qshift
UREA 3.4
CREA 66.2
1ST HD (8/19/18)

S O A P
(-) Difficulty Conscious, coherent, not in DAT
COPD
of breathing respiratory distress
BP: 130/80 IN AE Diagnostics:
CR: 91 Blood CS x 2 sites
Productive Facilitate Sputum GS/CS
T: 36.8
cough RR: 20 CAP
O2 sat: 98% Therapeutics:
MR PNSS 1 L x 12
(-)cyanosis, (-) gross Pallor Ampicillin-Sulbactam 1.5g/IV q6 (D1)
anicteric sclerae, pink Azithromycin 500 mg/tab OD (D1)
conjunctiva Hydrocortisone 100 mg/IV q6
symmetrical chest expansion, Salbutamol + Iprat q6
(-)subcostal retractions (+) VS q4
crackles BLF, (-) wheezes I & O qshift
adynamic precordium, no WOF DOB and desaturation
murmurs,
Flat,NABS, soft, nontender
full and equal pulses (-)
clubbing
2nd HD (8/20/18)

S O A P
(-) Difficulty Conscious, coherent, not in DAT
COPD
of breathing respiratory distress
BP: 140/90 IN AE Diagnostics:
CR: 70 Repeat CBC w/ pc in AM
Productive Repeat K STAT
T: 36
cough RR: 20 CAP
O2 sat: 98% Therapeutics:
MR PNSS 1 L x 12
(-)cyanosis, (-) gross Pallor Ampicillin-Sulbactam 1.5g/IV q6 (D1)
anicteric sclerae, pink Azithromycin 500 mg/tab OD (D1)
conjunctiva Hydrocortisone 100 mg/IV q8
symmetrical chest expansion, Salbutamol + Iprat q6
(-)subcostal retractions (+) Start Kalium durule tab q8
crackles BLF, (-) wheezes VS q4
adynamic precordium, no I & O qshift
murmurs, May D/C O2 inhalation, may hook back if w/
Flat,NABS, soft, nontender DOB or desaturation <94%
full and equal pulses (-)
clubbing
3nd HD (8/21/18)

S O
(-) Difficulty Conscious, coherent, not in
of breathing respiratory distress
BP: 140/90
CR: 82
T: 36
RR: 18
O2 sat: 95%
(-)cyanosis, (-) gross Pallor
anicteric sclerae, pink
conjunctiva
symmetrical chest expansion,
(-)subcostal retractions (-)
crackles BLF, (-) wheezes
adynamic precordium, no
murmurs,
Flat,NABS, soft, nontender
full and equal pulses (-)
clubbing
A P
MGH
COPD
IN AE THM:
1. Sultamicillin 750 mg/cap q12 x 7 days
2. Prednisone 20 mg/tab q12 x 5 days
CAP 3. Salbutamol + IPA neb PRN for DOB
4. Tiotropium bromide 18 mcg/cap in
MR turbohaler, 1 puff/day
5. Start Amlodipine 10 mg/tab OD
For Pulmonary Function Test as OPD Basis
For FBS, Lipid profile test as OPD Basis
OPD follow up on Aug 31, 2018
 FINAL DIAGNOSIS

CHRONIC OBSTRUCTIVE PULMONARY

DISEASE IN ACUTE EXACERBATION

COMMUNITY ACQUIRED PNEUMONIA –

MODERATE RISK
CASE DISCUSSION
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
INCIDENCE
►COPD is currently the fourth leading cause of death in the
world.
►COPD is projected to be the 3rd leading cause of death by
2020.
►More than 3 million people died of COPD in 2012
accounting for 6% of all deaths globally.
►Globally, the COPD burden is projected to increase in
coming decades because of continued exposure to COPD
risk factors and aging of the population.
COPD
• a common, preventable and treatable disease
that is characterized by persistent respiratory
symptoms and airflow limitation that is due to
airway and/or alveolar abnormalities usually
caused by significant exposure to noxious
particles or gases.
• a disease state characterized by airflow
limitation that is not fully reversible.
 COPD

Chronic Small
Emphysema Bronchitis Airways
Disease
Anatomically defined
condition Clinically Small
characterized by defined
condition with bronchioles
destruction and
enlargement of the chronic cough are narrowed
lung alveoli and sputum
PATHOGENESIS

antielastases
1. Chronic exposure to cigarette smoke leads to inflammatory
and immune cell recruitment within the terminal air spaces of
the lungs

2. These inflammatory cells release elastolytic and other

proteinases that damage the extracellular matrix of the lung

3. Structural cell death (endothelial and epithelial cells) occurs

directly through oxidant-induced cigarette smoke damage
and senescence as well as indirectly via proteolytic loss of
matrix attachment

4. Ineffective repair of elastin and other ECM components result

in air space enlargement that defines pulmonary emphysema
PATHOLOGY
• Chronic inflammation
• Increased numbers of goblet cells
• Mucus gland hyperplasia
• Fibrosis
• Narrowing and reduction in the number of small
airways
• Airway collapse due to the loss of tethering caused by
alveolar wall destruction in emphysema
Lung Parenchyma
• Destruction of gas exchanging
air-spaces, usually the structures
distal to the terminal bronchiole:
EMPHYSEMA • Respiratory bronchiole
• Alveolar ducts
• Alveoli

ACINI
NORMAL ACINUS
 TYPES OF EMPHYSEMA
CENTRIACINAR
• Abnormal dilation or
destruction of the
respiratory bronchiole,
the central portion of the
acinus.
• It is commonly
associated with cigarette
smoking
 TYPES OF EMPHYSEMA
PANACINAR
• Refers to enlargement
or destruction of all
parts of the acinus.
• Seen in alpha-1
antitrypsin deficiency
and in smokers
 TYPES OF EMPHYSEMA
PARASEPTAL
• The alveolar ducts are
predominantly affected.
RISK FACTORS OF COPD
Genes
Infections

Socioeconomic
status

Aging Populations
GENETICS
• Alpha 1-antitrypsin deficiency is a genetic
condition that is responsible for about 2% of cases of
COPD.
• In this condition, the body does not make enough of
a protein, alpha 1-antitrypsin.
• Alpha 1-antitrypsin protects the lungs from damage
caused by protease enzymes, such as elastase and
trypsin, that can be released as a result of an
inflammatory response to tobacco smoke.
CLINICAL MANIFESTATIONS

•Exertional dyspnea
•Cough
•Sputum production
PHYSICAL EXAMINATION
INSPECTION
• Barrel-shaped chest
• Accessory respiratory muscle participate
• Prolonged expiration during quiet breathing
• Expiration through pursed lips
• Paradoxical retraction of the lower interspaces
during inspiration (hoover's sign)
• Tripod Position
TRIPOD POSITION
• Patients with end-stage
COPD may adopt
positions that relieve
dyspnea, such as leaning
forward with arms
outstretched and weight
supported on the palms
or elbows.
PHYSICAL EXAMINATION
Palpation
• Decreased fremitus vocalis
Percussion
• Hyperresonant
• Depressed diaphragm
Auscultation
• Prolonged expiration
• Reduced breath sounds
• The presence of wheezing
during quiet breathing
• Crackles can be heard if
infection exist
DIAGNOSIS OF COPD
SYMPTOMS EXPOSURE TO RISK FACTORS
Dyspnea Tobacco
Cough Occupation
Sputum production Indoor/Outdoor Pollution

SPIROMETRY
Required to establish diagnosis
DIAGNOSIS OF COPD
The presence of a post-bronchodilator
FEV1/FVC < 0.70 confirms the presence
of persistent airflow limitation and thus
of COPD.
SPIROMETRY: NORMAL TRACE
SPIROMETRY: OBSTRUCTIVE DISEASE
SIGNS OF HYPERINFLATION
• Low set diaphragm
• Flat diaphragm best
determined by lateral chest.
• Hyperlucent lung fields
• Increased AP diameter.
• Increased retrosternal air
• Vertical heart
Classification of severity of airflow limitation
Choice of thresholds
►COPD Assessment Test (CAT TM )
►Chronic Respiratory Questionnaire (CCQ® )
►St George’s Respiratory Questionnaire (SGRQ)
►Chronic Respiratory Questionnaire (CRQ)
►Modified Medical Research Council (mMRC) questionnaire
 Assessment of Exacerbation Risk
• COPD exacerbations are defined as an acute worsening of
respiratory symptoms that result in additional therapy.
• Classified as:
• Mild (treated with SABDs only)
• Moderate (treated with SABDs plus antibiotics and/or oral
corticosteroids) or
• Severe (patient requires hospitalization or visits the emergency
room). Severe exacerbations may also be associated with acute
respiratory failure.
• Blood eosinophil count may also predict exacerbation rates (in patients
treated with LABA without ICS).
ABCD ASSESSMENT TOOL
EXAMPLE
Consider two patients:
Both patients with FEV1 < 30% of predicted
Both with CAT scores of 18
But, one with 0 exacerbations in the past year and the
other with 3 exacerbations in the past year.
 PREVENTION AND
MANAGEMENT OF COPD
SMOKING CESSATION
►Smoking cessation has the greatest capacity to influence the
natural history of COPD.
►If effective resources and time are dedicated to smoking cessation,
long-term quit success rates of up to 25% can be achieved.
VACCINATION
►Influenza vaccination can reduce serious illness (such as
lower respiratory tract infections requiring
hospitalization)24 and death in COPD patients.
►Pneumococcal vaccinations, PCV13 and PPSV23, are
recommended for all patients ≥ 65 years of age
PHARMACOLOGIC THERAPY
PHARMACOLOGIC THERAPY
NON-PHARMACOLOGIC TREATMENT
• Education and self-management
• Physical activity
• Pulmonary rehabilitation programs
• Exercise training
• Self-management education
• End of life and palliative care
• Nutritional support
• Vaccination
• Oxygen therapy
OXYGEN THERAPY
• Oxygen -- >15 h /d
• Long-term oxygen therapy (LTOT) improves
survival, exercise, sleep and cognitive
performance in patients with respiratory failure.

• The therapeutic goal is to maintain SaO2 ≥ 90%

and PaO2 ≥ 60mmHg at sea level and rest .
OTHER TREATMENTS
•Pulmonary rehabilitation
•Nutrition
•Surgery:
• Bullectomy
• Lung volume reduction surgery
• Lung transplantation
COPD AND COMORBIDITIES
►Cardiovascular ►Anxiety and
disease (CVD) depression
►Heart failure ►COPD and lung
cancer
►Ischaemic heart ►Metabolic
disease (IHD) syndrome and
►Arrhythmias diabetes
►Peripheral ►Gastroesophageal
vascular disease reflux (GERD)
►Hypertension ►Bronchiectasis
►Obstructive sleep
►Osteoporosis apnea
THANK YOU!