Weekly endorsement during our rotation in the Department of Family and Community Medicine. This is the case of a 72-year-old male who came in due to difficulty of breathing

1. Igbaras, Iloilo
CC Jackie Lou C. Acha

2. General Data
 M.E.
 72 years old
 Male
 Mantangan, Igbaras
Chief complaint:
Difficulty of breathing

3. History of Present Illness
 1 week PTC
(+) productive cough with whitish phlegm
(+) intermittent undocumented fever x 1 day
relieved by Paracetamol
(+) chills
(+) headache
(+) body malaise
(+) loss of appetite

4. History of Present Illness
 Day of consult
(+) persistent cough, loss of appetite, body
malaise
(+) sudden onset DOB

5. History of Present Illness
 Pertinent negatives
(-) chest pain/tightness
(-) dizziness
(-) hemoptysis
(-) weight loss
(-) orthopnea
(-) PND

6. Past Medical History
 Diagnosed with bronchial asthma 3 years
PTC
(-) HPN
(-) DM
(-) FDA
(-) PTB

7. Family History
(+) Bronchial asthma – maternal aunt
(-) DM
(-) HPN
(-) FDA
(-) heredo-familial diseases

8. Personal/Social History
- High school graduate
- Works as a farmer
(+) 8.5-pack-year smoker
- smokes 3 sticks per day since 15 years old
up to present
(+) alcoholic beverage drinker
- ½ bottle whisky, 1-2x a week since 15
years old

9. PHYSICAL EXAMINATION
- General Appearance
- Awake, conscious, coherent
- In CPD
- Prefers to sit with upper body forward

10. PHYSICAL EXAMINATION
- Vital Signs
- Temperature - 37.8 degrees Celsius
- RR - 28 cpm
- CR - 120 bpm
- O2 sat - 97%

11. PHYSICAL EXAMINATION
- Skin
- warm to touch, dry, wrinkled, good skin
turgor
- no skin lesions or edema noted

12. PHYSICAL EXAMINATION
- HEENT
• Head: Normocephalic, no lesions or masses
• Eyes: Anicteric sclerae, pinkish conjunctivae
Pupils ~3 mm diameter, equally reactive
to light and accommodation, both direct and
consensus
• Ears: No ear discharges
• Nose: no discharges, non hyperemic nasal
mucosa, (-) alar flaring

13. PHYSICAL EXAMINATION
- HEENT
• Mouth
- moist lips and buccal mucosae
- non-hyperemic, non-enlarged tonsils
• Neck
(+) Left cervical lymphadenopathy
(-) NVE

14. PHYSICAL EXAMINATION
- Chest P.E.
• Heart
- adynamic precordium
-PMI at 5th ICS Left MCL
-NCRRR
-no murmurs

15. PHYSICAL EXAMINATION
- Chest P.E.
• Lungs
- Symmetrical chest expansion
(+) suprasternal, supraclavicular retractions
- Resonant lungs
- Equal vocal and tactile fremiti
(+) wheezing on all lung fields
(+) fine crackles at the R lung base

16. PHYSICAL EXAMINATION
- Abdomen
- No lesions
- Normoactive bowel sounds
- Soft, nontender abdomen; no palpable
masses
- Liver not enlarged; spleen and kidneys non
palpable

17. PHYSICAL EXAMINATION
- Extremities
Grossly normal, no deformities
No edema
Warm to touch
CRT < 2 seconds
Full pulses

18. Primary Impression
T/C Chronic Obstructive Pulmonary Disease
in Acute Exacerbation;
Community Acquired Pneumonia
- Moderate Risk

19. Differentials
 Congestive heart failure
 Bronchiectasis
 Chronic asthma
 Pulmonary tuberculosis

21. Chronic Obstructive Pulmonary
Disease
A disease state characterized by airflow limitation
that is not fully reversible
-Harrison’s
A common preventable and treatable disease
characterized by persistent airflow limitation
that is usually progressive and associated with
an enhanced chronic inflammatory response in
the airways and the lung to noxious particles
or gases
- GOLD

22. COPD
 Emphysema
- an anatomically defined condition
characterized by destruction and
enlargement of the lung alveoli
 Chronic bronchitis
- clinically defined condition with chronic
cough and phlegm
 Small airways disease
- a condition in which small bronchioles
are narrowed

23. COPD
 Emphysema
- a pathological term
- often (but incorrectly) used clinically
- describes only one of the several
structural abnormalities present in
COPD patients

24.  Chronic bronchitis
 Presence of cough or sputum production for
at least 3 months in each of the 2
consecutive years
 An independent disease entity that may
precede or follow the development of airflow
limitation
 Also exists in patients with normal
spirometry

25. Epidemiology
 COPD is a leading cause of morbidity
and mortality worldwide
 Estimates suggest that COPD will rise
from the sixth to the third most common
cause of death worldwide by 2020
 due to continued exposure to COPD risk
factors and the changing age structure of
the world’s population

26. Risk Factors
 Cigarette Smoking- major risk factor
 Airway responsiveness
 Respiratory infections
 Occupational exposures
 Ambient air pollution
 Passive or second-hand smoke
exposure
 Genetic – Severe α 1 antitrypsin ( α 1AT)
deficiency

28.  Effects of smoking on pulmonary
function depend on
 Intensity of smoking exposure
 Timing of smoking exposure during growth
 Baseline lung function

29. (Intensity of
smoking)
(Timing of smoking
exposure)
(Baseline lung function)
Natural
History of
COPD

30. PATHOPHYSIOLOGY

31.  Oxidative Stress
Oxidative stress may be an important amplifying
mechanism in COPD. Oxidants are generated
by cigarette smoke and other inhaled
particulates, and released from activated
inflammatory cells such as macrophages and
neutrophils
 Protease-Antiprotease Imbalance
Protease-mediated destruction of elastin, a major
connective tissue component in lung
parenchyma, is an important feature of
emphysema and is likely to be irreversible

32. Protease-Antiprotease
Imbalance

33. Chronic airflow limitation
Inflammation
Small airway disease
-Airway inflammation
-Airway fibrosis
-Luminal plugs
-Increased airway resistance
Parenchymal destruction
-Loss of alveolar attachments
-Decrease of elastic recoil
Airflow limitation
Decreased
FEV1
Decreased
gas transfer

35. Diagnosis
 A clinical diagnosis of COPD should be
considered in any patient who has
dyspnea, chronic cough or sputum
production, and a history of exposure
to risk factors for the disease
 Spirometry is required to make the
diagnosis in this clinical context
 Post-bronchodilator FEV1/FVC <0.70 is
confirmatory

36. Key indicators for considering a
diagnosis of COPD
 Dyspnea
 Progressive (worsens over time)
 Usually worse with exercise
 Persistent (present every day)
 Described by the patient as an
○ “Increased effort to breathe”
○ “Heaviness”, “air hunger”, or “gasping”

37. Key indicators for considering a
diagnosis of COPD
 Chronic cough
 May be intermittent and may be
unproductive
 Chronic sputum production
 Any pattern
 History of exposure to risk factors
 Tobacco smoke, occupational dusts and
chemicals, smoke from home cooking and
heating fuels

38. Spirometric Classification of COPD
Severity Based on Post-Bronchodilator
FEV1
 Stage I: Mild COPD –
 Characterized by mild airflow limitation
(FEV1/FVC < 0.70; FEV1 ≥ 80% predicted).
 Symptoms of chronic cough and sputum
production may be present, but not always.
At this stage, the individual is usually
unaware that his or her lung function is
abnormal.

39.  Stage II: Moderate COPD –
 Characterized by worsening airflow limitation
(FEV1/FVC < 0.70; 50% ≤ FEV1 < 80%
predicted), with shortness of breath typically
developing on exertion and cough and
sputum production sometimes also present.
 This is the stage at which patients typically
seek medical attention because of chronic
respiratory symptoms or an exacerbation of
their disease.

40.  Stage III: Severe COPD –
 Characterized by further worsening of airflow
limitation
 (FEV1/FVC < 0.70; 30% ≤ FEV1 < 50%
predicted), greater shortness of
breath, reduced exercise
capacity, fatigue, and repeated
exacerbations that almost always have an
impact on patients’ quality of life.

41.  Stage IV: Very Severe COPD
 Characterized by severe airflow limitation
(FEV1/FVC < 0.70; FEV1 < 30% predicted
or FEV1 < 50% predicted plus the presence
of chronic respiratory failure)
 At this stage, quality of life is very
appreciably impaired and exacerbations
may be life threatening

42. Treatment of
Stable COPD

43. COPD Exacerbations
 an event in the natural course of the
disease characterized by a change in the
patient’s baseline dyspnea, cough, and/or
sputum that is beyond normal day-to-day
variations, is acute in onset, and may
warrant a change in regular medication in a
patient with underlying COPD
 Triggered by infection with bacteria or
viruses, environmental pollutants, or
unknown factors
 Increased hyperinflation and gas trapping
accounting for the increased dyspnea

44. Assessment of COPD
Exacerbations

45. Management of Severe but Not life-
threatening Exacerbations of COPD
 Assess severity of symptoms
 Administer controlled oxygen therapy
 Bronchodilators
 Increase doses and/or frequency
 Combine beta2-agonists and anticholinergics
 Use spacers or nebulizers
 Add oral or IV glucocorticoids
 Consider antibiotics if with signs of
bacterial infection
 Closely monitor condition of the patient

46. Indications for hospital
admission

48. Definition
 Pneumonia
 Infection of the pulmonary parenchyma
 Community acquired pneumonia
 a lower respiratory tract infection acquired in the
community within 24 hours to less than 2 weeks
 It commonly presents with an acute
cough, abnormal vital signs of tachypnea
(respiratory rate >20 breaths per
minute), tachycardia (cardiac rate
>100/minute), and fever (temperature >37.8ºC)
with at least one abnormal chest finding of
diminished breath sounds, rhonchi, crackles, or
wheeze

49. Epidemiology
 Pneumonia is the third leading cause of
morbidity (2001) and mortality (1998) in
Filipinos
-Philippine Health Statistics, DOH
 The incidence rates are highest at the
extremes of age

50. Risk factors for CAP
 asthma
 immunosuppression
 institutionalization
 age of 70 years
 heart failure
 cerebrovascular disease
 alcoholism
 tobacco smoking
 COPD
 HIV infection

51. Epidemiologic Factors Suggesting
Possible Causes of CAP
Factor Possible Pathogen
Alcoholism Streptococcus pneumoniae, oral anaerobes,
Klebsiella pneumoniae, Acinetobacter spp.,
Mycobacterium tuberculosis
COPD and/or smoking Haemophilus influenzae, Pseudomonas
aeruginosa, Legionella spp.,
S. pneumoniae, Moraxella catarrhalis,
Chlamydia pneumoniae
Structural lung disease (e.g.
bronchiectasis)
P. aeruginosa, Burkholderia cepacia,
Staphylococcus aureus

52. Pathophysiology
 Pneumonia results from the proliferation
of microbial pathogens at the alveolar
level and the host's response to those
pathogens
 Microorganisms gain access to the
lower respiratory tract commonly by
aspiration from the oropharynx

53. Pathophysiology
 Mechanical factors are critically
important in host defense
 hairs and turbinates of the nares
 branching architecture of the
tracheobronchial tree
 gag reflex and the cough mechanism
 Normal flora in oropharynx

54. Pathophysiology
 When barriers are overcome, resident
alveolar macrophages are extremely
efficient at clearing and killing pathogens
 When the capacity of the alveolar
macrophages to ingest or kill the
microorganisms is exceeded
=> clinical pneumonia
 The host inflammatory response, rather
than the proliferation of
microorganisms, triggers the clinical
syndrome of pneumonia

55. Pathophysiology
 The release of inflammatory
mediators, such as interleukin (IL)-1 and
tumor necrosis factor (TNF), results in
fever
 Chemokines, such as IL-8 and
granulocyte colony-stimulating
factor, stimulate the release of
neutrophils and their attraction to the
lung, producing both peripheral
leukocytosis and increased purulent
secretions

56. Diagnosis and
Management of CAP

57. Empiric Antibiotic Therapy
 For moderate-risk CAP
a combination of an IV non-
antipseudomonal β-lactam
(BLIC, cephalosporin or carbapenem)
with either an extended macrolide or
respiratory fluoroquinolone is
recommended as initial antimicrobial
treatment

58. Prevention
 Influenza vaccination is recommended
for the prevention of CAP
 Pneumococcal vaccination is
recommended for the prevention of
invasive pneumococcal disease in
adults
 Smoking cessation is recommended for
all persons with CAP who smoke

59. What was done to the patient?
 Given O2 at 2 lpm via nasal prong
 Given PAI with Salbutamol + Ipratropium
bromide neb 1 neb q15 mins x 3 doses
 Chest physiotherapy after nebulization
 Referred to Guimbal hospital for
admission
 Encouraged smoking and alcohol
cessation