Case Presentation COPD

CASE MANAGEMENT
DENISE NOELLE S. GONZALES

SEPTEMBER 28, 2022
LEILANIE S. SIA, MD
MODERATOR
OBJECTIVES
General objectives
● Approach to diagnosis and formulation of initial treatment plan to a patient presenting with
dyspnea
Specific objectives
● Is spirometry necessary to the diagnosis of a probable obstructive pulmonary disease?
● Are antibiotics warranted to in treating acute exacerbation of a probable obstructive pulmonary
disease?
● Follow up treatment plan to a patient with probable obstructive pulmonary pathology
2
HISTORY
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GENERAL DATA
● M. F. C. ● Iglesia Ni Cristo
● 71/M ● Previously a farmer
● Married ● Dingras, Ilocos Norte
● Filipino ● Poor reliability of patient
CHIEF COMPLAINT
Dyspnea
4
HISTORY OF PRESENT ILLNESS
Chronic cough for ~20 years
Episodes of dyspnea and increased sputum production  recurrent
hospitalizations, managed by nebulization and IV medications, (-)
intubation
Noncompliant with scheduled follow up consultations and medications
Baseline: stops for breath after walking a few minutes on the level
4 days PTA
(+) nasal secretions: mucoid
(+) cough: increased mucus production, mucoid
(-) dyspnea, (-) fever, (-) changes in sleeping pattern, (-) changes in
appetite, (-) orthopnea, (-) edema, (-) alteration in sensorium
No consult done
No medications taken
5
HISTORY OF PRESENT ILLNESS
2 days PTA (+) nasal secretions: mucoid, (+) cough: productive, mucoid
(+) progressive dyspnea: on tripod position, answers in phrases, walk a
few minutes on the level  breathless when dressing/undressing
(+) difficulty initiating sleep
(+) decreased appetite
(-) fever, (-) edema, (-) alteration in mental status
No consult done
Self-medicated with prescription for dyspnea from previous
hospitalizations:
Salbutamol (Hivent) 2.5mg/nebulization TID
No relief of dyspnea
Persistence of the above symptoms prompted consult at MMMH&MC ER
Admission 6
PAST HISTORY
● Childhood illness/hospitalizations
○ No episodes of shortness of breath, chest tightness, wheezing
○ No hospitalizations
● Adult illnesses/hospitalizations
○ July 2020: most recent hospitalization
■ Dyspnea and productive cough
■ Disclosed diagnosis: “Angkit”
■ No spirometry nor PEF done
■ Managed by nebulization, IV medications, O2 support
■ (-) Intubation
■ Prescribed take home meds:
● Salmeterol + Fluticasone 25/250 mcg MDI, 1 puff BID
● Salbutamol nebule prn dyspnea
● Cefuroxime 500 mg/tab, 1 tab BID for 5 days
● NAC 600 mg/tab, dissolved in ½ glass water OD
■ Noncompliant with medications and follow up consultations
7
PAST HISTORY
● Adult illnesses/hospitalizations
○ July and September 2017
■ Hospitalized for dyspnea and productive cough
■ Managed by nebulization, IV medications, O2 support
■ (-) Intubation
■ Noncompliant with medications and follow up consultations
○ Other hospitalizations unrecalled
○ (-) PTB, Kidney, Cardiac, Vascular, Clotting, Metabolic, Gastrointestinal, Rheumatic
diseases
● Surgeries/Injuries/Accidents: None
● Transfusions: None
● Allergies: No known food, dye, seasonal, environmental nor drug allergies
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CURRENT HEALTH STATUS /
RISK FACTORS
Health Screening Sleep pattern
● No prior blood chemistries or ● No insomnia, excessive daytime
ancillaries sleepiness no altered sleep wake cycle
● Sleeps 9PM – 4AM
Nutrition
● Home cooked food – prefers Exercise
vegetables ● None
● Purified water
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CURRENT HEALTH STATUS /
RISK FACTORS
Smoking Environmental exposures
● 33 pack years (15 to 48 y/o, 1 pack) ● Lives near highway: exposed to vehicle exhaust fumes
● Stopped at 48 y/o – perceived easy ● No history of recent travel
fatiguability ● No pets
● Current passive cigarette smoke exposure: 3
household members are active smokers Medication data
● Exposed to passive tobacco smoke during ● No antibiotic use for the past 3 months
childhood ● No herbal medications
● Denies illegal drug/substance use
Alcohol
● Previous (19 to 48 y/o): 1 bottle of gin Immunization history
(350mL, 80 proof) for 2-3 days in a week ● Childhood immunization: unrecalled
● Adult immunization: none
○ (-) COVID-19, (-) Influenza, (-) Pneumococcal
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FAMILY HISTORY
● (-) Cancer ● (-) Clotting disorders
● (-) Kidney diseases ● (-) Constitutional disorders
● (-) Lung diseases ● (-) Dementia/Alzheimer’s
○ (-) Asthma
○ (-) COPD ● (-) Metabolic disorders
○ (-) Tuberculosis
○ (-) DM
● (-) Psychiatric ● (-) Gastrointestinal disorders
● (-) Cardiac and vascular ● (-) Rheumatic disorders
○ (-) Hypertension
○ (-) Dyslipidemia ● (-) Skin disorders
○ (-) Stroke
○ (-) Sudden death
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PERSONAL AND SOCIAL HISTORY
● Lives with wife and 3 sons. Good relationship among the household members.
● Financial support: 3 sons
● No clear understanding among family members regarding his diagnosis / medications
12
REVIEW OF SYSTEMS
● GENERAL: (-) weight changes (loss or gain)
● SKIN, HAIR, NAILS: (-) itchiness, (-) rashes, vasomotor changes, (-) texture changes, (-)
photosensitivity, (-) changes in the hair (growth, loss, thickness, brittleness), (-) abnormal nail
growth color, (-) mole changes, (-) excessive sweating
● HEENT / NECK: (-) blurring of vision, (-) photophobia, (-) doubling of vision, (-) deafness, (-)
tinnitus, (-) aural discharge, (-) epistaxis, (-) bleeding gums, (-) disturbance of taste (metallic), (-)
tonsillar pain, (-) neck stiffness, (-) sensation of lump in the throat
● CARDIAC: (-) chest pain, (-) nocturnal dyspnea, (-) orthopnea, (-) palpitations, (-) syncope, (-) leg
swelling
● GASTROINTESTINAL: (-) nausea,(-) vomiting, (-) hematemesis, (-) melena, (-) hematochezia, (-)
dysphagia, (-) distention, (-) abdominal masses, (-) hemorrhoids, (-) change in stool color or
contents
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REVIEW OF SYSTEMS
● GENITOURINARY: (-) urinary frequency, urgency, hesitancy, dribbling, weak urinary stream, (-)
urinary incontinence, (-) dysuria, (-) hematuria, (-) nocturia, (-) flank pain, (-) stone passage, (-)
passage of bubbly urine, (-) urethral discharge, (-) genital lesions
● VASCULAR: (-) claudication, (-) extremity temperature changes (coldness / warmness)
● ENDOCRINE: (-) heat-cold intolerance, (-) palpitations, (-) voice changes, (-) polydipsia,
polyphagia, polyuria, (-) irritability, (-) slowness in mentation, (-) distribution and changes in facial or
body hair, (-) increased hat or glove size
● HEMATOLOGIC: (-) abnormal bleeding, (-) bruising, (-) pallor, (-) adenopathy
● NEUROLOGIC: (-) headache, (-) seizure, (-) loss of consciousness, (-) abnormalities of sensation,
(-) motor dysfunction or weakness or paralysis, (-) abnormalities of coordination, (-) speech
disturbance, (-) mental changes, (-) head trauma, (-) tremors, (-) loss of memory
● PSYCHIATRIC: (-) anxiety, (-) depression, (-) hallucinations, (-) delusions, (-) paranoia, (-) violent
behavior, (-) mood changes, (-) agitation
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PHYSICAL
EXAMINATION
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PHYSICAL EXAMINATION
General Survey: Conscious, wheelchair-borne, in cardiopulmonary distress, tripod position, talks
in words, not agitated, asthenic, no characteristic facies, no characteristic body odor/breath
Vital Signs: BP 120/70, CR 126, RR 25, T 37.0, SpO2 80s% at RA
Anthropometrics: Ht 157 cm, Wt 42 kg, BMI: 17 kg/m2 (overweight by Asia Pacific)
Skin: No cyanosis, no pallor, no jaundice, nails apparently normal in color and shape, no abnormal
pigmentations, no abnormal hair growths
Head: Overall facial structure symmetrical, no abnormal head/facial movement, (+) bitemporal muscle
wasting
Eyes: No lid swelling, lashes not matted, nonhyperemic conjunctiva, anicteric sclera, pink palpebral
conjunctiva, no exudates
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Ears: No pinna deformities, no tragal tenderness, no auricular discharge
Nose: No alar flaring, nasal septum midline, no blood clots
Oral Cavity and Throat: Moist lips and buccal mucosa, tongue and uvula midline, tonsils not enlarged,
posterior pharyngeal wall non-hyperemic
Neck: Trachea midline, no palpable cervical lymphadenopathy, thyroid not enlarged, neck veins not
distended
Thorax/Lungs: No chest wall deformities, (+) intercostal and supraclavicular retractions, symmetrical
chest expansion, hyperresonant on percussion, tight air entry with expiratory wheezes
Cardiovascular: Adynamic precordium, apex beat at 5th LICS MCL, S1 louder than S2 at mitral and
tricuspid area, S2 louder than S1 at aortic and pulmonic area, no murmur
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Gastrointestinal: Flat nondistended abdomen, no discolorations, normoactive bowel sounds, tympanitic,
no palpable masses, no direct nor rebound tenderness, DRE not done
Extremities: no edema, symmetrical right and left upper and lower limbs, no bruising, no masses, no
limitations in ROM, full equal pulses
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NEUROLOGIC EXAMINATION
GCS GCS 15 (E4V5M6)
CEREBRUM Oriented to Time, Place and Person
CEREBELLUM Intact balance/equilibrium
CRANIAL I: Not tested

NERVES II: OD 2mm ERTL
III, IV, VI: OD EOMS intact in all fields, No nystagmus
V: Able to move jaw side-to-side with resistance
VII: No facial asymmetry
VIII: Gross hearing intact
IX, X: Symmetric soft palate and tonsillar pillar elevation
XI: Can shrug can turn head
XII: No tongue deviation
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NEUROLOGIC EXAMINATION
MOTOR Right upper ext: 5/5

Left upper ext: 5/5
Right lower ext: 5/5
Left lower ext: 5/5
SENSORY No sensory deficit
REFLEX ++ bilateral
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SALIENT FEATURES
SUBJECTIVE OBJECTIVE
SUBJECTIVE POSITIVES OBJECTIVE POSITIVES
● 71/M ● In cardiopulmonary distress, tripod position, talks in
● 33 pack year smoker, current passive smoke words
exposure ● BP 120/70, CR 126, RR 25, T 37.0, SpO2 80s% at
RA
● Chronic cough ~20 years ● Ht 157 cm, Wt 42 kg, BMI: 17 kg/m2
● Recurrent hospitalizations: “Angkit” ● No chest wall deformities, (+) intercostal and
Salmeterol + Fluticasone 25/250 mcg MDI supraclavicular retractions, symmetrical chest
Salbutamol nebule prn dyspnea expansion, hyperresonant on percussion, tight air
● CC: 2-day history of progressive dyspnea entry with expiratory wheezes
● 4-day history of increased mucoid sputum production ● (+) bitemporal muscle wasting
and colds
● Not relieved by Salbutamol nebulization
OBJECTIVE NEGATIVES
● Neck veins not distended
SUBJECTIVE NEGATIVES ● Adynamic precordium, apex beat at 5th LICS MCL,
● (-) Orthopnea, PND, edema S1 louder than S2 at mitral and tricuspid area, S2
● No childhood illness/hospitalizations louder than S1 at aortic and pulmonic area, no
● No allergies murmur
● No adult immunization ● (-) Peripheral edema
● No family history of lung diseases (BA, COPD, PTB)
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DIFFERENTIAL
DIAGNOSIS
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PATIENT CHRONIC OBSTRUCTIVE PULMONARY DISEASE
IN ACUTE EXACERBATION
● 71/M Considered MOST PROBABLE diagnosis:

● 33 pack year smoker, current passive smoke ● May present with exacerbations (dyspnea)
exposure ● Dyspnea persistent
● Chronic cough ~20 years ● Onset often mid-life (>40 years old)
● Recurrent hospitalizations: “Angkit” ● History of smoking, toxic exposures
Salmeterol + Fluticasone 25/250 mcg MDI ● Limited relief of bronchodilators
Salbutamol nebule prn dyspnea
● CC: 2-day history of progressive dyspnea
● 4-day history of increased sputum production
● (-) Orthopnea, PND, edema
● No childhood illness/ hospitalizations/ allergies/
adult immunization
● No family history of lung diseases
● In cardiopulmonary distress, tripod position, talks
in phrases
● BP 120/70, CR 126, RR 25, T 37.0, SpO2 80s%
● (+) intercostal and supraclavicular retractions,
hyperresonant, tight air entry with expiratory
wheezes
● AP, PMI 5th LICS MCL, no murmur
● (-) Peripheral edema
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PATIENT BRONCHIAL ASTHMA IN ACUTE EXACERBATION
● 71/M Considered a primary diagnosis:

● 33 pack year smoker, current passive smoke ● May present with exacerbations (dyspnea)
exposure
● Chronic cough ~20 years Ruled out:
● Recurrent hospitalizations: “Angkit” ● Onset often in childhood
Salmeterol + Fluticasone 25/250 mcg MDI ● Symptoms vary from day to day and worse at
night and early morning
● Associated with allergy, rhinitis, eczema
● Family history of asthma
● No childhood illness/ hospitalizations/ allergies/
adult immunization
● No family history of lung diseases
● In cardiopulmonary distress, tripod position, talks
in phrases
● BP 120/70, CR 126, RR 25, T 37.0, SpO2 80s%
wheezes
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PATIENT LEFT-SIDED HEART FAILURE
● 71/M Considered a primary diagnosis:

● 33 pack year smoker, current passive smoke ● Dyspnea is a cardinal manifestation of left heart
exposure failure
● Chronic cough ~20 years
● Recurrent hospitalizations: “Angkit” Ruled out:
Salmeterol + Fluticasone 25/250 mcg MDI ● May arise with increasing severity as exertional
dyspnea, orthopnea, paroxysmal nocturnal
dyspnea, and dyspnea at rest.
● Rales, wheezing and rhonchi can occur with
● No childhood illness/ hospitalizations/ allergies/ congestion of the bronchial mucosa.
adult immunization ● Chronic HF is accompanied by cardiac
● No family history of lung diseases enlargement. Apical impulse is displaced
● In cardiopulmonary distress, tripod position, talks downward and to the left and may be diffuse in
in phrases dilated cardiomyopathy or sustained in pressure
● BP 120/70, CR 126, RR 25, T 37.0, SpO2 80s% overloaded states such as aortic stenosis.
wheezes
25
Chronic Obstructive Pulmonary Disease Probable
in Acute Exacerbation
CLINICAL IMPRESSION
26
D0
Subjective
09/21/22 Objective Findings Assessment Management
Complaints
2:30 PM
ER • (+) Dyspnea • Tripod position, answers • COPD probable in • Diet: Full LSLF with SAP
• (+) Increased in words acute exacerbation
sputum • GCS 15 (E4V5M6) • IVF: PNSS 1L to run at 80cc/hr
production, • BP 120/70, CR 126, RR
mucoid 25, T 37.0, SpO2 80s% • Diagnostics:
• (+) Decreased • (-) cyanosis Chest xray (upright), 12L ECG
appetite • No chest wall deformities, CBC, BUN, Crea, Na, K
• (+) Difficulty (+) intercostal and AST, ALT, ABG
initiating sleep supraclavicular FBS, Sputum GS/CS
• (-) Fever retractions, symmetrical SARS-Cov 2 RT-PCR
chest expansion,
hyperresonant on • Therapeutics:
percussion, tight air entry Hydrocortisone 50mg IV q6
with expiratory wheezes Salbutamol 200mcg/puff MDI, 2
• Adynamic precordium, puffs q6 and prn for dyspnea
apex beat at 5th LICS Azithromycin 500mg/tab, 1 tab OD
MCL, no murmur x 5 days
• Abd flat, soft, nontender NAC 600mg dissolved in ½ glass
• No edema water OD in PM
Chlorhexidine oral care BID
• Maintain O2 via FM at 5LPM to

maintain O2 sats >88%
27
ANCILLARIES
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ANCILLARIES
EGFR 70
Compensated primary metabolic alkalosis

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CHRONIC OBSTRUCTIVE PULMONARY
DISEASE
● Persistent respiratory symptoms and airflow limitation that is not fully
reversible
● COPD include:
○ Emphysema
■ Anatomically defined condition characterized by destruction of the lung
alveoli with air space enlargement
○ Chronic bronchitis
■ Clinically defined condition with chronic cough and phlegm
○ Small airway disease
■ Small bronchioles are narrowed and reduced in number.
Silverman, E. K., Make, B. J., Crapo, J. D. (2022). Chronic Obstructive Pulmonary Disease, 32
Harrison's Principles of Internal Medicine (21st ed., Vol. 2, pp. 2180–2189), McGraw Hill LLC.
CHRONIC OBSTRUCTIVE PULMONARY
●
DISEASE
Classic definition: Chronic airflow obstruction, determined by spirometry, that usually
occurs in the setting of noxious environmental exposures (products of combustion,
cigarette smoking and biomass fuels)
● Host factors such as abnormal lung development and genetics can lead to COPD
● 4th leading cause of death and affects >10 million persons in the US
● Globally, there are an estimated 250 million with COPD
PATHOGENESIS
● Airflow obstruction
○ Physiologic marker of COPD
○ Can result from airway disease and/or emphysema
○ Small airways may become narrowed by cells (hyperplasia and accumulation),
mucus, and fibrosis, and extensive small airway destruction
○ Pulmonary vascular destruction occurs in concert with small airway disease and
emphysema.
Silverman, E. K., Make, B. J., Crapo, J. D. (2022). Chronic Obstructive Pulmonary Disease, Harrison's
35
Principles of Internal Medicine (21st ed., Vol. 2, pp. 2180–2189), McGraw Hill LLC.
PATHOLOGY
● Cigarette smoke exposure: affect large airways, small airways (≤2 mm diameter), and
alveoli
○ Changes in large airways
■ Mucus gland enlargement and goblet cell hyperplasia  cough and mucus production
■ Bronchial squamous metaplasia  predisposed to carcinogenesis and disrupting
mucociliary clearance.
■ Smooth-muscle hypertrophy and bronchial hyperreactivity (not as prominent)
○ Changes in small airways and alveoli
■ Goblet cell metaplasia (mucus-secreting cells replacing surfactant-secreting Club cells)
 predisposed airway narrowing or collapse
■ Luminal narrowing by fibrosis, excess mucus, edema, and cellular infiltration
■ Inflammatory cells may cause proteolytic destruction of elastic fibers
PATHOPHYSIOLOGY
● Airflow obstruction
○ Determined for clinical purposes by spirometry
○ Involves maximal forced expiratory maneuvers after the subject has inhaled to
total lung capacity
○ Key parameters
■ Forced expiratory maneuver (FEV1): volume of air exhaled within the first
second
■ Forced vital capacity (FVC): Total volume of air exhaled during the entire
spirometric maneuver
○ COPD: Chronically reduced ratio of FEV1/FVC
○ Reduced FEV1 seldom shows large improvements to inhaled
bronchodilators, although improvements up to 15% are common
RISK FACTORS
● Cigarette smoking
○ Additional environmental and/ or genetic factors contribute to the impact of
smoking
○ Impact of electronic cigarettes and vaping on the development and progression of
COPD has not yet been determined
● Airway responsiveness
○ Particularly relevant for childhood asthmatic subjects who become chronic
smokers
○ Asthmatics with reduced lung function early in life were more likely to meet
spirometric criteria for COPD in early adulthood.
○ Both asthma and airway hyperresponsiveness are risk factors for COPD
RISK FACTORS
● Respiratory Infections
○ Adult respiratory infections on decline in pulmonary function is controversial, but
significant long-term reductions in pulmonary function are not typically seen
following an individual episode of acute bronchitis or pneumonia
○ Recent studies have suggested that childhood pneumonia may lead to increased
risk for COPD later in life
● Occupational Exposure
○ Coal mining, gold mining, and cotton textile dust - COPD risk is likely substantially
less important than effect of cigarette smoking
RISK FACTORS
● Ambient air pollution
○ Relationship of air pollution to chronic airflow obstruction remains unproved
○ Prolonged exposure to smoke produced by biomass combustion appears to be a
significant risk factor for COPD, particularly among women
● Passive or second-hand smoking exposure

○ Exposure of children to maternal smoking results in significantly reduced lung
growth
○ In utero: significant reductions in postnatal pulmonary function
○ Passive smoke exposure as risk factor in development of severe pulmonary
function reductions often observed in COPD remains uncertain
● Genetic considerations: α1 Antitrypsin Deficiency

CLINICAL PRESENTATION
HISTORY PHYSICAL FINDINGS
• Cough • Early stages: normal PE
• Sputum production • More severe disease: prolonged expiratory phase,
• Exertional dyspnea expiratory wheezes
• Careful history usually reveals • Signs of hyperinflation
presence of respiratory symptoms • Barrel chest
prior to acute exacerbation • Enlarged lung volume with poor
• Advanced stage: breathless doing diaphragmatic excursion (percussed)
basic activities of daily living • Tripod position
• Resting hypoxemia  may require • Cyanosis: lips, nail beds
supplemental O2 • Advanced stage: cachexia, significant weight loss,
bitemporal wasting, diffuse loss of subcutaneous
adipose tissue  poor prognostic factor
• Hoover’s sign: paradoxical inward movement of rib
cage with inspiration
CLINICAL PRESENTATION
LABORATORY FINDINGS RADIOGRAPHIC FINDINGS
• Airflow obstruction - hallmark of • CXR
COPD • Obvious bullae, paucity of parenchymal
• Reduction in FEV1 and markings, or hyperlucency suggests
FEV1/FVC presence of emphysema
• ABG and oximetry • Increased lung volumes and flattening of the
• Resting or exertional diaphragm suggest hyperinflation
hypoxemia • Chest CT
• Elevated hematocrit: chronic • Current definitive test for establishing
hypoxemia presence or absence of emphysema, pattern
of emphysema, and presence of significant
disease involving medium and large airways
43
© 2022 Global Initiative for Chronic Obstructive Lung Disease
• Spirometry is required to
make the diagnosis
• Post-bronchodilator FEV1/FVC
<0.70 confirms the presence of
persistent airflow limitation
44
SPIROMETRY
● Most reproducible and objective measurement of airflow limitation
● Despite of its good sensitivity, PEF measurement alone cannot be reliably used as
the only diagnostic test because of its specificity
● Assessing degree of reversibility of airflow limitation (e.g., bronchodilator challenge)
to inform therapeutic decisions is no longer recommended
○ Degree of reversibility has not been shown to augment the diagnosis of COPD, differentiate
diagnosis from asthma, or predict response to long-term treatment with bronchodilators or
corticosteroids
● GOLD advocates active case finding (spirometry if with symptoms and/or risk factors)
but not screening spirometry (asymptomatic without significant risk factors)
45
DIAGNOSIS OF COPD
● PROBABLE COPD case: history and PE is compatible with COPD
● The only confirmatory test for the diagnosis of COPD is spirometry (FEV1/FVC <0.70)
● Spirometry be performed within 3 months after the patient’s first consultation
● Spirometry should be performed:
○ All patients who are suspected to have COPD
○ Clinically stable
○ No active infection or exacerbation
○ Have not taken medications that might interfere with the spirometry’s result (e.g. short-acting
bronchodilator in the previous 6 hours, long-acting Beta-2-agonist (LABA) in the previous 12
hours or sustained release theophylline in the previous hours)
46
2021 Summary of Consensus Statements on the Diagnosis and Management of COPD in the
COPD EXACERBATION
● Acute worsening of respiratory symptoms that results in additional therapy
● Increased dyspnea, increased sputum purulence and volume, increased cough and
wheeze
● Mainly triggered by respiratory viral infections
● COPD exacerbations contribute to disease progression
● Mild: treated with short acting bronchodilators (SABDs) only  Outpatient clinic
● Moderate: SABDs plus antibiotics and/or oral corticosteroids  Outpatient clinic or
Level 2 health facility
● Severe: require hospitalizations or visits to ER  Level 2 or Level 3 health facility
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ANTIBIOTICS IN COPD EXACERBATION?
● Antibiotics should be given in COPD exacerbation:
○ Three cardinal symptoms: increase in dyspnea, sputum volume and sputum
purulence
○ Two of the cardinal symptoms, if increased purulence of sputum is one out of two
symptoms
○ Require mechanical ventilation (invasive or noninvasive)
● Choice of antibiotic should be based on local bacterial resistance patterns
○ Aminopenicillin with clavulanic acid
○ Macrolide
○ Tetracycline
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ANTIBIOTICS IN COPD EXACERBATION?
● Increased sputum purulence as cardinal symptom, accompanied by increase in sputum volume or increased
dyspnea
● Initial empiric antibiotic therapy be guided by the following parameters:
○ Severity of exacerbation
○ Presence of comorbidities
○ Severity of airflow limitation (FEV1 < 30% of predicted)
○ Previous use of antimicrobial therapy within the past 3 months
○ Frequency of exacerbations (>3/year)
● Antibiotics targeted against Pseudomonas as empiric treatment:
○ Severe exacerbations
○ Need for mechanical ventilation
○ Hemodynamically unstable
○ With antibiotic use within the previous 3 months
○ Presence of bronchiectasis
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OXYGEN THERAPY
● Key component of hospital treatment of an exacerbation
● Target saturation 88 – 92%
● Once oxygen is started, blood gases should be checked frequently to ensure
satisfactory oxygenation without CO2 retention and/or worsening acidosis
● Use of noninvasive mechanical ventilation is preferred over invasive ventilation
(intubation and positive pressure ventilation) as initial mode
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57
D0
Subjective
Complaints
2:30 PM
ER • (+) Dyspnea • Tripod position, answers • COPD probable in • Diet: Full LSLF with SAP
mucoid 25, T 37.0, SpO2 80s% • Diagnostics:
• (+) Decreased • (-) cyanosis Chest xray (upright), 12L ECG
appetite • No chest wall deformities, CBC, BUN, Crea, Na, K
• (+) Difficulty (+) intercostal and AST, ALT, ABG
initiating sleep supraclavicular FBS, Sputum GS/CS
• (-) Fever retractions, symmetrical SARS-Cov 2 RT-PCR
chest expansion,
hyperresonant on • Therapeutics:
percussion, tight air entry Hydrocortisone 50mg IV q6
with expiratory wheezes Salbutamol 200mcg/puff MDI, 2
• Adynamic precordium, puffs q6 and prn for dyspnea
apex beat at 5th LICS Azithromycin 500mg/tab, 1 tab OD
MCL, no murmur x 5 days
• Abd flat, soft, nontender NAC 600mg dissolved in ½ glass
• No edema water OD in PM
Chlorhexidine oral care BID
• Maintain O2 via FM at 5LPM to

maintain O2 sats >88%
58
D0
Subjective
Complaints
11:00 PM
GFEW • (+) Dyspnea • Tripod position, answers • COPD probable in • Diet: DAT with SAP
mucoid 27, T 36.8, SpO2 92% @ • Therapeutics:
• (+) Decreased 5LPM FM Hydrocortisone 50mg IV q6
appetite • (-) cyanosis Salbutamol 200mcg/puff MDI, 2
• (+) Difficulty • No chest wall deformities, puffs q6 and prn for dyspnea then
initiating sleep (+) intercostal and shift to Salbutamol + Ipratropium
• (-) Fever supraclavicular neb q8 once RTPCR negative
retractions, symmetrical Azithromycin 500mg/tab, 1 tab OD
chest expansion, x 5 days
hyperresonant on NAC 600mg dissolved in ½ glass
percussion, tight air entry water OD in PM
with expiratory wheezes Discontinue Chlorhexidine oral care
• Adynamic precordium, BID
apex beat at 5th LICS
MCL, no murmur • Maintain decrease O2 support at
• Abd flat, soft, nontender 2LPM via NC
• No edema
59
D1
Subjective
Complaints
10:00 AM
GFEW • (+) Dyspnea • Tripod position, answers • COPD probable in • Diet: DAT with SAP
• (+) Productive in words acute exacerbation
cough, mucoid – • GCS 15 (E4V5M6) • IVF: PNSS 1L to run at 80cc/hr
difficulty • BP 120/70, CR 89-92, RR
expectorating 22-23, T 36.5, SpO2 99- • Diagnostics:
• (+) Decreased 100% at 2LPM NC Sputum gene xpert
appetite • (-) cyanosis Procalcitonin
• (+) Difficulty • No chest wall deformities,
initiating sleep (+) intercostal and • Therapeutics:
• (-) Fever supraclavicular Give Salbutamol + Ipratropium neb
retractions, symmetrical q15mins x 3 doses then q1 x 3
chest expansion, doses then q4
hyperresonant on HOLD Salbutamol MDI
percussion, tight air entry, Hydrocortisone 50mg IV q6
occasional wheezes Azithromycin 500mg/tab, 1 tab OD
• Adynamic precordium, x 5 days
apex beat at 5th LICS Increase NAC 600mg dissolved in
MCL, no murmur ½ glass water to BID in PM
• Abd flat, soft, nontender HOLD Chlorhexidine oral care BID
• No edema
• May wean off O2 support
60
D2
Subjective
Complaints
2:00 PM
4FM • (-) Dyspnea • Comfortable on bed • COPD probable in • Diet: DAT with SAP
• Decreased • GCS 15 (E4V5M6) acute exacerbation
Cough • BP 120/70-80, CR 66-91, • IVF: PNSS 1L to run at 80cc/hr
• Improved RR 20-23, T 36.5-36.7,
appetite SpO2 98-99% @ RA • Therapeutics:
• Improved sleep • (-) cyanosis Decrease Salbutamol + Ipratropium
• (-) Fever • No chest wall deformities, neb to q8
(-) retractions, Decrease Hydrocortisone 50mg IV
symmetrical chest to q12
expansion, resonant on Azithromycin 500mg/tab, 1 tab OD
percussion, clear breath x 5 days
sounds Decrease NAC 600mg dissolved in
• Adynamic precordium, ½ glass water to OD in PM
apex beat at 5th LICS Start Glycopyrronium + Indacaterol
MCL, no murmur cap, 1 cap inhaled via inhaler
• Abd flat, soft, nontender device ODHS
• No edema
61
D3
Subjective
Complaints
3:30 PM
4FM • (-) Dyspnea • Comfortable on bed • COPD probable in • May go home with take home
• (-) Cough • GCS 15 (E4V5M6) acute exacerbation - medications:
• Improved • BP 110-120/70, CR 79- resolved Glycopyrronium + Indacaterol cap,
appetite 81, RR 20-21, T 36.5, 1 cap inhaled via inhaler device
• Improved sleep SpO2 98% @ RA ODHS
• (-) Fever • (-) cyanosis Salbutamol + Ipratropium neb q8
• No chest wall deformities, and prn for dyspnea
(-) retractions, Azithromycin 500mg/tab, 1 tab OD
symmetrical chest x 1 more day
expansion, resonant on NAC 600mg dissolved in ½ glass
percussion, clear breath water to OD in PM
sounds Doxofylline 400mg/tab, ½ tab
• Adynamic precordium, ODHS
apex beat at 5th LICS
MCL, no murmur • Ff up at IM OPD after 2 weeks
• Abd flat, soft, nontender
• No edema • For COVID-19, Influenza and
Pneumococcal immunizations as
OPD
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80 – 50 – 30
69
ASSESSMENT OF SYMPTOMS
70
30
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ANTIBIOTICS IN STABLE COPD?
● Later studies have shown that regular use of some antibiotics may reduce exacerbation
rate
● Azithromycin (250mg/day or 500mg 3x per week) or Erythromycin (250mg BID) for
one year in patients prone to exacerbations reduced the risk of exacerbations
compared to usual care.
● Azithromycin use was associated with increased incidence of bacterial resistance,
prolongation of QTc interval, and impaired hearing tests.
● No fata showing the efficacy or safety of chronic azithromycin treatment to prevent
COPD exacerbation beyond one-year of treatment
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THANK YOU!
83

Case Presentation COPD

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Case Presentation COPD

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CASE MANAGEMENT

DENISE NOELLE S. GONZALES

Persistence of the above symptoms prompted consult at MMMH&MC ER

Vital Signs: BP 120/70, CR 126, RR 25, T 37.0, SpO2 80s% at RA

Anthropometrics: Ht 157 cm, Wt 42 kg, BMI: 17 kg/m2 (overweight by Asia Pacific)

Nose: No alar flaring, nasal septum midline, no blood clots

GCS GCS 15 (E4V5M6)

CEREBRUM Oriented to Time, Place and Person

CEREBELLUM Intact balance/equilibrium

CRANIAL I: Not tested

MOTOR Right upper ext: 5/5

SENSORY No sensory deficit

● 71/M Considered MOST PROBABLE diagnosis:

● 71/M Considered a primary diagnosis:

● 71/M Considered a primary diagnosis:

• Maintain O2 via FM at 5LPM to

Compensated primary metabolic alkalosis

● Globally, there are an estimated 250 million with COPD

● Passive or second-hand smoking exposure

● Genetic considerations: α1 Antitrypsin Deficiency

• Maintain O2 via FM at 5LPM to

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