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INITIAL EVALUATION

S:
Pt. name: L.J
Age: 65y.o
Sex: Male
Address: San Martin, Bacnotan La Union
Civil status: Married
Handedness: Right
Occupation: Retired Teacher
Religion: Baptist
Referral unit: IPD
Referral Dr: Dr.M
Rehab. Dr: Dr. C
Date of IE: October 4, 2016
Date of Referral: October 4, 2016
Date of consultation: October 4, 2016
Diagnosis: Community-acquired pneumonia
C/c: "marigatan nak met aganges ken aggorigor ak metten ken kumarkaro toy
uyek ko"
PT Translation: Pt. states that he has difficulty in breathing, sudden fever, and
productive cough.
HPI:
Pt. States that condition started 2wks ago when he felt difficulty in breathing
and experienced productive cough c yellowish expectorate associated c
undocumented febrile episodes. 1wk ago pt. was confined at LMC and was
consulted by Dr. M who requested a radiologic examination. Pt was diagnosed of
CAP and he took hydrocortisone 100mg (every 4hrs), sultacillin 1.5g (every
6hrs), azithromycin 500mg (1 tab/day), and fluimucil 600mg (2xday) for his
condition. Dr. M referred the pt. to Dr. C for further evaluation and management.
PMHx:
(+) Htn
(+) COPD

(+) cataract (R) eye


(-) allergies
FMHx:
HTN
COPD
Asthma
Heart

M
+
-

F
+
-

Disease
PSHx:
L.J is a 65 y/o male living a sedentary lifestyle who used to work as a teacher in
DMMSU N-LUC. Pt has a hx of smoking (40 packs/yr) but stopped 1 yr ago. He is
a non-alcoholic beverage drinker and not abusing any substance. He lives in a
2-storey building with his wife, daughter and son-in-law. Main door to Living
room: 3 steps; Living room to Bed room: 12 steps; Main door to Kitchen: 7 steps;
Comfort room to Bed room: 6 steps.
Ancillary procedure:
Date/Procedure
X-ray: 9/29/16LMC

Results
(+) bilateral
pneumonia c slight
regression in the (L)

Pt. Goal:
Gusto kong makahinga ng maayos ng hindi nahihirapan at matanggal itong
ubo ko.
O:
V.S:
BP: 120/70mmhg
HR: 119bpm
RR: 32cpm
To: 37.3 oC
O.I
Manner of arrival: ambulatory s AD

Mental status: coherent/conscious


Physique: ectomorph
Attachments: (-)
Swelling: (-)
Redness: (-)
Pallor: (-)
Jaundice: (-)
Palpation:
Thermal assessment: hyperthermic on all exposed body parts 2o to fever
Tone assessment: normotonic on all muscles
Tropic skin changes: (-)
Muscle spasm: (-)
Edema: (-)
Muscle tightness: (-)
PA:
Anterior view: (B) sh. is elevated
Lateral view: slight forward head
Posterior view: round back
ROM:
Findings: all major jts on (B) UE & LE are WNL actively and passively done c
normal end feel.
Sig: for base line data
MMT:
All major muscle groups of (B) UE and LE are grossly graded 4-5/5
Significance: for base line data
Neurologic Evaluation:
Sensory testing:
Device used: pin for pain, brush for light touch and thumb for pressure
Findings: 100% sensory intact on (b) UE/LE
Sig.: intact sensory pathway
DTR:
R

++ ++
++
++

++ ++
++
++

++

Legend:
areflexia
+ hyporeflexia
++
normoreflexia
+++ hyperreflexia
++++ clonus
0

++

Findings: All reflexes are normal


Significance: For baseline purposes
Functional analysis:
ADL
GRADE
Self care
7
Feeding
7
Grooming
5
Bathing
6
Upper
Garment
5
Dressing
Lower
Garment
7
Dressing
7
Sphincter Control
Bladder Mx
7
Bowel Mx
7
Mobility
6
Bed mobility
7
Chair mobility
7
Toileting
Transfer
Locomotion
Gait
6-minute Walk Test
Pt was able to walk 300 m
Findings: Pt was able to do the test without any problems
12-minute Walk Test
Pt was able to walk 600 m
Findings: Pt SOB p walking 380 m
A:
PT impression: Pt has decrease endurance d/t CAP and sedentary lifestyle.

Rehab Potential: Pt. has good rehab potential because he adhere to all task
given to him and has support from his family.
Problem list:
Problem Lists

STG (2 weeks Tx

LTG (4 weeks Tx

1. Difficulty in breathing

Session)
To increase

Session)
To increase

during long distance walk

cardiopulmonary

cardiopulmonary

endurance to be able to

endurance to be able to

do 15 continuous aerobic

do 20 continuous aerobic

2. Productive cough d/t

exercises
To stop the productivity of

exercises
To eliminate the cough of

present condition
3. Postural deviation

the cough
Pt will correct the body

the pt
Pt will demonstrate proper

posture every p tx session

body mechanics and


observe proper posture p

4. Pt has min. difficulty in

Pt will perform ADL's c

tx session
Pt will perform ADL's s

doing ADL's such as

mod-complete

difficulty every p tx

bathing, doffing& donning

independence every p tx

session

of clothes & toileting

session

P:
PTMx:
1. Breathing exercise to inc. pulmonary endurance
Positive Expiratory Pressure Breathing x2 sec hold x 10 cycles
2. Percussion x15' to inc. the amount of secretions of phlegm
3. Aerobic Exercises (20 mins non-continuous) to inc cardiopulmonary
endurance

Ergobike UE & LE x6 min

4. Strengthening exercises
Biceps curls x3 lbs DB on (B) sh AP x7 reps x 2sets
Home instructions:
1. Exercises to mobilize the chest
Mobilization of upper chest and stretch of pectoralis muscles x
10reps x 2sets

Mobilization of upper chest and shoulders x 10reps x 2sets

Precautions:
BP
RR

LORMA COLLEGES
College of Physical and Respiratory Therapy

Clinical Education 2

COMMUNITY-ACQUIRED PNEUMONIA
October 6, 2016

Submitted to:
Ms. Teresa Rose Combalicer, PTRP

Submitted by:
Flores, Paul John
Floresca, Denise Dawn
Garcia, Jennie Ross
Gurtiza, Joanna Eden
PATHOPHYSIOLOGY:
Pneumonia results from the proliferation of microbial pathogens at the alveolar level and
the hosts response to those pathogens.
Microorganisms gain access to the lower respiratory tract in several ways. The most common is
by aspiration from the oropharynx. Small-volume aspiration occurs frequently during sleep

(especially in the elderly) and in patients with decreased levels of consciousness. Many
pathogens are inhaled as contaminated droplets. Rarely, pneumonia occurs via hematogenous
spread (e.g., from tricuspid endocarditis) or by contiguous extension from an infected pleural or
mediastinal space.
Mechanical factors are critically important in host defense.
The hairs and turbinates of the nares capture larger inhaled particles before they reach the
lower respiratory tract.
The branching architecture of the tracheobronchial tree traps microbes on the airway lining,
where mucociliary clearance and local antibacterial factors either clear or kill the potential
pathogen.
The gag reflex and the cough mechanism offer critical protection from aspiration.
In addition, the normal flora adhering to mucosal cells of the oropharynx, whose components
are remarkably constant, prevents pathogenic bacteria from binding and thereby decreases the
risk of pneumonia caused by these more virulent bacteria.
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. Macrophages are assisted by proteins that are produced by the alveolar epithelial
cells (e.g., surfactant proteins A and D) and that have intrinsic opsonizing properties or
antibacterial or antiviral activity. Once engulfed by the macrophage, the pathogenseven if they
are not killedare 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. Inflammatory mediators released by macrophages and the newly recruited
neutrophils create an alveolar capillary leak equivalent to that seen in the acute respiratory
distress syndrome, although in pneumonia this leak is localized (at least initially). Even
erythrocytes can cross the alveolar-capillary membrane, with consequent hemoptysis. The
capillary leak results in a radiographic infiltrate and rales detectable on auscultation, and
hypoxemia results from alveolar filling. Moreover, some bacterial pathogens appear to interfere
with the hypoxemic vasoconstriction that would normally occur with fluid filled alveoli, and this
interference can result in severe hypoxemia. Increased respiratory drive in the systemic
inflammatory response syndrome leads to respiratory alkalosis. Decreased compliance due to
capillary leak, hypoxemia, increased respiratory drive, increased secretions, and occasionally
infection-related bronchospasm all lead to dyspnea. If severe enough, the changes in lung

mechanics secondary to reductions in lung volume and compliance and the intrapulmonary
shunting of blood may cause respiratory failure and the patients death.