ATENEO de ZAMBOANGA UNIVERSITY

SCHOOL OF MEDICINE
BEDSIDE OUTPUT

LARDEL KENT D. CARAY (LEVEL III)

GENERAL DATA
Patient JM is a 22 year old, single man, from Camino Nuevo, Zamboanga City.
He works as a laborer at a grocery store and a practicing Roman Catholic.

CHIEF COMPLAINT: Cough

HISTORY OF PRESENT ILLNESS:

9 days PTC, patient had an onset of productive cough, with whitish to yellowish
sputum. This was associated with intermittent, undocumented fever. Patient took Paracetamol
which provided temporary relief of the fever. No consult was done. Patient tolerated his
symptoms.

Hours PTC, patient noted persistence of symptoms and now with associated
body malaise which prompted him to seek consult at the IM-OPD.

PAST MEDICAL HISTORY:

Patient has no previous hospitalizations or surgeries. He denies to be diagnosed with

diseases such as Hypertension, DM, or Asthma. Denies any allergies to any food or medications.
FAMILY MEDICAL HISTORY:
Patient has a family history of Hypertension on both maternal and paternal side.
There are no other known heredofamilial diseases such Diabetes Mellitus, Cardiovascular
diseases or Asthma.

PERSONAL AND SOCIAL HISTORY

JM is the eldest of five siblings. He works as a laborer at a grocery store. He is a
smoker of 5 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 had body malaise but no 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 lymphadenopathies
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: 100/70 mmHg Temp. : 37.8 ˚C PR: 115 bpm RR: 22 cpm O2 sat: 95%

Skin: No jaundice, cyanosis or skin pallor. With good skin turgor.

HEENT: Head: Atraumatic head, no scars or lesions

Eyes: Anicteric sclera, pink 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, Tactile fremitus, Resonant on
percussion, (+) Fine crackles on bilateral mid lung field

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: Community-Acquired Pneumonia Low Risk (CAP-LR)
Secondary Diagnosis: Hypersensitivity pneumonitis

Basis:

1. For this case, we are entertaining CAP-LR and Acute Bronchitis as our primary and
secondary basis, respectively. First, for community-acquired pneumonia low risk, we
consider the patient’s history, chief complaint, symptoms and his PE findings. These
include:
 acute onset of cough for less than 2 weeks,
 productive sputum of whitish to yellowish in color
 presence of fever
 body malaise
 tachycardia
 presence of fine crackles on bilateral mid lung fields

Worldwide, pneumonia remains the leading cause of death from an infectious diseases,
while it being the 6th leading cause of death in overall (1). In studies in China and other Asian
countries, M. pneumoniae was detected at high rates among adult pneumonia cases while
Klebsiella pneumoniae has been detected frequently in patients with severe pneumonia (2).

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 in several ways. The most common is by aspiration from the oropharynx. Mechanical
factors are critically important in host defense including the hairs and turbinates of the nares,
the branching architecture of the tracheobronchial tree, the gag and cough reflexes. When
these barriers are overcome or when microorganisms are small enough to be inhaled to the
alveolar level, resident alveolar macrophages are extremely efficient at clearing and killing
pathogens.
 Once engulfed by the macrophage, the pathogens—even if they are not killed—are
eliminated via either the mucociliary elevator or the lymphatics and no longer represent an
infectious challenge.

Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms
is exceeded does clinical pneumonia become manifest. In that situation, the alveolar
macrophages initiate the inflammatory response to bolster lower respiratory tract defenses.
The host inflammatory response, rather than proliferation of microorganisms, triggers the
clinical syndrome of pneumonia. The release of inflammatory mediators, such as interleukin
1 and tumor necrosis factor, results in fever. Chemokines, such as interleukin 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. The
capillary leak results in a radiographic infiltrate and rales detectable on auscultation, and
hypoxemia results from alveolar filling. Decreased compliance due to capillary leak,
hypoxemia, increased respiratory drive, increased secretions, and occasionally infection-
related bronchospasm all lead to dyspnea.
 ALGORITHM

Precipitating factor: Predisposing factor:

Exposure to causative Microorganism
agents Age, work-related stress

Enters the nose

Passes through larynx, pharynx

and trachea

Microorganism enters and affects both lung

parenchyma

Airway damage Lung invasion

Flattening of epith.
Infiltration of
cells
bronchi

Decreased Macrophages and leukocytes

Infectious organism lodges compliance, release chemokines
Stimulation in bronchioles hypoxemia, increased
respiratory drive,
increased
secretions
Increased purulent
Release of secretions
inflammatory Narrowing of air
mediators passage

PRODUCTIVE
DIFFICULTY OF COUGH
Increase pyrogen in
BREATHING
the body

FEVER
 2. On the other hand, Hypersensitivity pneumonitis is an inflammatory syndrome of
the lung cause by repetitive inhalation of antigenic agents in a susceptible host. Although
offending agents are ubiquitous, the incidence is relatively small. For our patient, we
consider this as our secondary diagnosis, since the patient has a possible exposure of
unknown allergens in his nature of work. Symptoms of cough, fever and body malaise
were also present. On physical examination, patient also exhibited bibasilar crackles upon
auscultation .Although for this disease, the symptoms usually develop within hours
following significant exposure and typically resolves gradually within 12 hours to several
days after exposure removal.

II. PARACLINICAL DIAGNOSTIC PROCEDURES

Since we are considering CAP-LR and Hypersensitivity pneumonitis, 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. CAP- LR 80% Antibiotics, cough expectorants
2. Hypersensitivity pnemonitis 20% Exposure removal; steroids if subacute

Benefit Risk Cost Availability

1. Chest Xray To assess possible lung infiltrates, Radiation 150 available
or consolidation risk
2. CBC For assessment of possible increase No risk 175 available
in WBC specifically in Neutrophils
pointing towards infection

For this case Chest X-ray would be more ideal and beneficial. A chest x ray is a procedure done
to evaluate the lungs, heart and chest wall. Since we are suspecting CAPLR as our primary
diagnosis, then we can possible see abnormalities in the lung parenchyma such as pulmonary
infiltrates and consolidations seen on the chest x ray.

Patient JM undergone both Chest X ray and CBC. For the chest xray result, the xray was taken at
PA view, well taken as to position and exposure. There was no tracheal deviation, and no
atelectatasis or fluid leveling. Abnormal finding includes a pulmonary infiltrates on the bilateral
mid lung fields.

For the complete blood count, the only pertinent was an increased in the WBC of 15,000/ uL and
an increased in the neutrophil count, which gives us a more strong consideration that the
underlying disease is caused by an infection.

Furthermore, our paraclinicals are correlated with our history and physical examination which
gives us a clearer picture of the case.

III. TREATMENT
After the all that we have done, we are now committing our clinical diagnosis as
Community-Acquired Pneumonia Low Risk, so that we may be able to accurately address the
problem with on point treatment also. For this case, the appropriate antibiotics should be
administered. Based on the Philippine Clinical Practice Guidelines (PCPG) for the management
of Community-Acquired Penumonia, we catergorized this as Low risk since the patient has an:

 RR <30/ minute
 PR <125/minute
 SBP >90mmHg
 DBP >60mmHg
 Temp. >36C or <40C
 No presence of altered mental status, suspected aspiration or stable co-morbid conditions
 And on Chest X ray, only localized infiltrates are present, and no evidence of pleural
effusion

And for the treatment, the recommended antibiotics include:

 Amoxicillin 1 gm, three times a day for 5-7 days OR

 Extended macrolides (Azithromycin 500 mg OD) for 3-5 days

We can also give N-acetylcysteine 600mg tab mix with 30 ml water as mucolytic

IV. PREVENTION AND HEALTH PROMOTION

Final Diagnosis: Community Acquired Pneumonia- Low Risk

In order to prevent future recurrence of CAP, patient is advised on :

 Proper hygiene such as handwashing, coughing etiquette and proper protective equipment
at work
 A healthy and balanced diet
 Cessation of smoking and alcoholic beverage drinking
 Proper exercise

V. References
1. Philippine Clinical Practice Guidelines: Diagnosis, Emperic Treatment, Management and
Prevention of Community- Acquired Pneumonia in Immunocompetent Adults. 2016
Update
2. Lupisan S, Suzuki A, Macalalad et al., Etiology and epidemiology of Community-
acquired pneumonia in adults requiring hospital admission: A prospective study in rural
Central Philippines. Int J Infect Dis. 2013;80: 46-53, doi: 10.1016/j.ijid.2018.12.005
3. Harrison’s Principles of Internal Medicine. 20th Edition