ATENEO de ZAMBOANGA UNIVERSITY

SCHOOL OF MEDICINE
BEDSIDE OUTPUT

LARDEL KENT D. CARAY (LEVEL III)

GENERAL DATA
Patient S.S is a 43 year old, married man, from Putik, Zamboanga City. He’s a
carpenter and a practicing Roman Catholic.

CHIEF COMPLAINT: Difficulty of Breathing

HISTORY OF PRESENT ILLNESS:

Patient is a known case of Bronchial Asthma and was diagnosed since he was
20 years old. Accordingly, he was advised on home mediations, Prednisone and Salbutamol but
was non-compliant.

1 day PTA, patient had sudden onset of difficulty of breathing, shortness of

breath and was initially nebulized and given Guafenesin, however there was no relief of
symptoms.

Few hours PTA, the symptoms wordened which promted the patient to seek
consult at the ZCMC ER-IM.

PAST MEDICAL HISTORY:

Known asthmatic, non-compliant to medications. No other diagnosed diaseases such as
hypertension, DM, or CA
FAMILY MEDICAL HISTORY:
There are no other known heredofamilial diseases such Hypertension, Diabetes
Mellitus, or Cardiovascular diseases.

PERSONAL AND SOCIAL HISTORY

S.S. works as a freelance carpenter. He is a smoker of 15 pack years and an
occasional alcoholic beverage drinker of about 1-2 bottles a week. He denies any illicit drug use
and his usual diet consists of rice, fish and vegetables.

REVIEW OF SYSTEMS
GENERAL: Patient has weight loss
HEENT:
Head: No dizziness, headache or lightheadedness
Eyes: No blurred vision, no itchiness
Ears: No tinnitus, no ear pain
Nose: No colds, No epistaxis
Throat/mouth: No neck mass, no pain

NECK: no neck pain

RESPIRATORY: (+) difficulty of breathing, (+) shortness of breath, (-) cough, (-) orthopnea

CARDIOVASCULAR: (-) palpitations, (-) chest pain

GASTROINTESTINAL: (-) abdominal pain, (-) diarrhea, (-) constipation, (-) changes in stool
color, (-) loss of appetite

GENITOURINARY: (-) frequent urination, (-) dysuria, (-) hematuria, (-) flank pain

PERIPHERAL VASCULAR: (-) claudication, (-) leg cramps, (-) tenderness

MUSCULOSKELETAL: (-) joint pain. (-) muscle pain, (-) stiffness, (-) strain/sprain, (-)
limitation of motion or action
PHYSICAL EXAMINATION
General: Patient is awake, coherent and not in respiratory distress;

Vital Signs: BP: 180/70 mmHg Temp. : 36.7C PR: 116 bpm RR: 35 cpm O2 sat: 69%

Skin: No jaundice or pallor.

HEENT: Head: Atraumatic head, no scars or lesions

Eyes: Anicteric sclera, pale palpebral conjunctivae, Pupils are equal and reactive to
light and accommodation.
Ears: No lesions, no discharges, nontender

Nose: No discharges, nontender

Throat and Mouth: Moist lips and oral mucosa

CHEST and LUNGS: No scars or lesions, Equal chest expansion, (+) wheezing on bilateral
lung fields, (+) tachypneic

CARDIOVASCULAR: Adynamic precordium, tachycardic, regular rhythm, no heaves or thrills,

no murmur, PMI at the 5th ICS midclavicular line

ABDOMEN: No scars or lesions, normoactive bowel sounds, tympanitic, nontender abdomen

PERIPHERAL VASCULAR: Good peripheral pulses, no edema, CRT <2 seconds

CASE DISCUSSION

I. CLINICAL DIAGNOSIS :
Primary Diagnosis: Respiratory Failure sec to Bronchial Asthma in Acute
Exacerbation
Secondary Diagnosis: Chronic Obstructive Pulmonary Disease in Acute
Exacerbation

Basis:

1. For this case, we are entertaining BA in AE and COPD in AE as our primary and
secondary basis, respectively. First, for Bronchial Asthma in Acute Exacerbation, we
consider the patient’s history, chief complaint, symptoms and his PE findings. These
include:
 Known case of Bronchial asthma but was non-compliant to medication
 Symptoms of worsening difficulty of breathing
 Presence of wheezes on bilateral lung fields

Asthma is a syndrome characterized by airflow obstruction that varies markedly,

both spontaneously and with treatment. Asthmatics harbor a special type of inflammation in the
airways that makes them more responsive than nonasthmatics to a wide range of triggers, leading
to excessive narrowing with consequent reduced airflow and symptomatic wheezing and
dyspnea. Narrowing of the airways is usually reversible, but in some patients with chronic
asthma there may be an element of irreversible airflow obstruction. Asthma is a heterogeneous
disease with interplay between genetic and environmental factors. Several risk factors that
predispose to asthma have been identified such as genetic predisposition, atopy, environmental
allergens, and many others.

Asthma is associated with a specific chronic inflammation of the mucosa of the

lower airways. One of the main aims of treatment is to reduce this inflammation. There is
inflammation in the respiratory
mucosa from the trachea to terminal bronchioles, but with a predominance in the bronchi
(cartilaginous airways), but it is still uncertain how inflammatory cells interact and how
inflammation translates into the symptoms of asthma (Fig. 281-2). There is good evidence that
the

specific pattern of airway inflammation in asthma is associated with airway hyperresponsiveness

(AHR), the physiologic abnormality of asthma, which is correlated with variable airflow
obstruction. The pattern of inflammation in asthma is characteristic of allergic diseases, with
similar inflammatory cells seen in the nasal mucosa in rhinitis. However, an indistinguishable
pattern of inflammation is found in intrinsic asthma, and this may reflect local rather than
systemic IgE production. (Harrison’s, 20th edition)

The characteristic symptoms of asthma are wheezing, dyspnea, and coughing, which are
variable, both spontaneously and with therapy. Symptoms may be worse at night and patients
typically awake in the early morning hours. Patients may report difficulty in filling their lungs
with air. There is increased mucus production in some patients, with typically tenacious mucus
that is difficult to expectorate. There may be increased ventilation and use of accessory muscles
of ventilation. Prodromal symptoms may precede an attack, with itching under the chin,
discomfort between the scapulae, or inexplicable fear (impending doom). Typical physical signs
are inspiratory, and to a greater extent expiratory, rhonchi throughout the chest, and there may be
hyperinflation.
 In our case since the patient is non-compliant to his medications, we see the worsening of
his dyspnea as well as evidence of respiratory failure.

2. COPD in AE
Chronic obstructive pulmonary disease (COPD) is defined as a disease state
characterized by persistent respiratory symptoms and airflow limitation that is not fully
reversible (http://www.goldcopd.com/). COPD includes emphysema, an anatomically
defined condition characterized by destruction of the lung alveoli with air space
enlargement; chronic bronchitis, a clinically defined condition with chronic cough and
phlegm; and small airway disease, a condition in which small bronchioles are narrowed
and reduced in number. The classic definition of COPD requires the presence of chronic
airflow obstruction, determined by spirometry, that usually occurs in the setting of
noxious environmental exposures—most commonly cigarette smoking. Emphysema,
chronic bronchitis, and small airway disease are present in varying degrees in different
COPD patients. Patients with a history of cigarette smoking without chronic airflow
obstruction may have chronic bronchitis, emphysema, and dyspnea.
In this case, since the patient also has a smoking history of 15 pack years, we
cannot totally rule out COPD. Symptoms of dyspnea can also be seen in patients with
COPD.

II. PARACLINICAL DIAGNOSTIC PROCEDURES

Since we are considering BA in AE and COPD, we can order some paraclinicals in order to
solidify our diagnosis, as well as to see the extent of the disease and the possible concomitant
findings.

Certainty Treatment modality

1. BA in AE 60% Bronchidilators and anticholinergics
2. COPD in AE 40% Brochodilators

Benefit Risk Cost Availability

1. Lung Quantify the decrease in expiratory No risk ?? available
 Function airflow during exacerbations
test (e.g.
PEF or
FEV1)
2. Chest x ray Check for infiltrates or Radiation 150 available
hyperinflation of lungs risk

Both of these paraclinicals are available in ZCMC and since Lunf unction test is very
vital to the assessment and management of both, then we can order this. For bronchial
asthma, if Pre-treatment PEF or FEV1 is < 25% of predicted or personal best then we can
admit the patient; Or if Post treatment PEF or FEV1 is 40-60% then we can continue
treatment and reassess frequently.

III. TREATMENT
After the all that we have done, we are now committing our clinical
diagnosis as Bronchial Asthma in Acute Exacerbation (severe), so that we may be able to
accurately address the problem with on point treatment also. For this case , the
appropriate treatment should include:
 Admission to ward or ICU
 Give inhaled SABA and ipratropium bromide
 O2 support, maintain saturation at 93-95%
 Systemic corticosteroids
 Consider high dose ICS
 And consider referral to specialists

IV. PREVENTION AND HEALTH PROMOTION

FINAL DIAGNOSIS: BRONCHIAL ASTHMA IN ACUTE EXACERBATION

(SEVERE)

In order to prevent future recurrence, patient should be advised on:

 Compliance of medications
 Proper use of inhalers
  Smoking cessation
 Balanced diet

V. REFERENCES
1. Global Initiative for Asthma, 201. Rai CSP, et al, MJAFI 2007
2. GOLD 201 COPD guidelines. www.goldcopd.org
3. Harrison’s Principle of Internal Medicine. 20th Edition