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RESPIRATORY FAILURE
2 TO HCAP
Aramburo, Cristina
Binag, Lady Vi
Cabaldo, Jeanette
Diron, Anne
Kit, Alyssa
Lai, Kierstein
Largo, Nicole
Ledda, Richan
Tomacruz, Samantha
INTRODUCTION:
Degenerative disc disease in the lumbar spine, or lower back particularly in the L4
-L5 refers to a syndrome in which a compromised disc causes low back pain (referred
to as lumbago) or irritation of a spinal nerve to cause pain radiating down the leg
(sciatica), numbness in dermatomes distribution and positive straight leg raising test.
Sciatic pain aggravates on standing, walking, bending, straining and coughing. Other
symptoms of lumbar disc degeneration are sensory disturbances in legs, claudication,
relief of pain when bending forward and weakness.
As we age, the water and protein content of the cartilage of the body changes. This
change results in weaker, more fragile, and thin cartilage. Because both the discs and
the joints that stack the vertebrae (facet joints) are partly composed of cartilage, these
areas are subject to wear and tear over time (degenerative changes).
The disc itself does not have a blood supply, so if it sustains an injury it
cannot repair itself the way other tissues in the body can. An otherwise
insignificant injury to the disc can start a degenerative cascade whereby the
disc wears out thus causes various complications such as immobility leading
to respiratory complications as lungs are unable to expand properly.
The lungs can be affected after very short periods of immobility leading to
respiratory complications. Even a day or two the chest muscles become
weakened resulting in decreased lung expansion and shallow breathing.
Coughing an important protective function to clear the airways, becomes
weaker and less effective.
Secretions build up in the lungs, increasing the risk of pneumonia and later on will lead to
respiratory failure which results from inadequate gas exchange by the respiratory system, meaning
that the arterial oxygen, carbon dioxide or both cannot be kept at normal levels. A drop in the oxygen
carried in blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia
The prevalence of Degenerative Disk disease related respiratory complications is higher in men with
the percentage of 77% and 71 % in women ages from 50 years old and above. The highest
prevalence of an intervertebral space with degenerative disc disease is in L4 L5 about 75.8%. Age
and obesity were associated with the presence of degenerative disc disease in all regions.
In the case of the patient D.A, 74 years old, male, chief complain difficulty of breathing of two days
duration and admitted due to sepsis secondary to hospital acquired pneumonia and complicated UTI.
Patient was diagnosed with degenerative disc disease particularly in L4 and L5 and
experienced symptoms such as bilateral knee pain, and general body weakness,
leading to immobilization. Due to immobilization, the patient had a community
acquired pneumonia then was admitted to UERM hospital and it was resolved. Later
on, the patient had hospital acquired pneumonia at the same time with complicated
UTI. From complicated UTI, and the destruction of L4 and L5 it results to ascending
infection leading to the acute kidney injury then going to systemic circulation which
results to sepsis.
DEMOGRAPHIC DATA
Name: D.A
Gender: Male
Age: 74 years old
Status: Single
Occupation: Retired MMDA Officer
Nationality: Filipino
Address: Cubao, Quezon City
Religion: Catholic
Date of Birth: 08/01/1941
Admission Date and Time: 3/18/2016; 5:38PM
Chief Complaint: Difficulty of breathing for two days.
DEMOGRAPHIC DATA
Admitting Diagnosis: Sepsis secondary to hospital acquired pneumonia and complicated
UTI.
Past Health History:
Status post renal stones 1990s, AKI secondary post renal (BPH), sacral ulcer grade II; to
consider herniated disc L4-L5; sepsis secondary to complicated UTI.
Family History:
Patient D.A has a familial history of Hypertension, Diabetes Mellitus and Asthma.
Present Health History:
2 days prior to admission, patient was noted to have halak associated with shortness of
breath, decreased sensorium, and undocumented fever relieved by TSB. Persistence of
symptoms prompted consult at UERM.
Figure A shows the location of the respiratory structures in the body. Figure B is an
enlarged view of the airways, alveoli (air sacs), and capillaries (tiny blood vessels). Figure
C is a closeup view of gas exchange between the capillaries and alveoli. CO2 is carbon
dioxide, and O2 is oxygen.
Mouth
Air first enters your body through your nose or mouth, which wets and warms the air. (Cold, dry
air can irritate your lungs.) The air then travels through your voice box and down your
windpipe. The windpipe splits into two bronchial tubes that enter your lungs.
A thin flap of tissue called the epiglottis (ep-ih-GLOT-is) covers your windpipe when you
swallow. This prevents food and drink from entering the air passages that lead to your lungs.
Diaphragm (DI-ah-fram)
Intercostal muscles
Abdominal muscles
Every day, the two kidneys filter about 120 to 150 quarts of blood
to produce about 1 to 2 quarts of urine, composed of wastes and
extra fluid.
PHYSICAL ASSESSMENT
SKIN and
NAILS
ASSESSMENT
Evenly colored skin tone, dry and warm to
touch. There is presence of peeling of the
skin on both upper and lower extremities
with poor skin tugor, presence of grade four
pitting edema, both upper and lower
extremities. There are four pressure sores
that are present. Pressure sore #1 is on
sacral medial; grade 3 with measurement of
5.6 x 3.7 cm. Pressure sore #2 is on gluteal
left side; grade 2 with measurement of 1.5 x
0.6 cm. Pressure sore #3 on malleolus
(right); necrotic and dry with measurement
of 1.5 x 1 cm and pressure sore #4 on
malleolus (left); grade 2 with measurement
of 2 x 2 cm. Nails are clean and intact.
ANALYSIS
A dry skin and
pressure sore are
present due to
prolonged
immobility.
Capilliary refill of
more than two
seconds and poor
skin tugor indicates
decrease
oxygenation in the
body system.
Presence of grade
four pitting edema
is due to decrease
PHYSICAL ASSESSMENT
HEAD AND
NECK
ASSESSMENT
ANALYSIS
PHYSICAL ASSESSMENT
ASSESSMENT
ANALYSIS
PHYSICAL ASSESSMENT
MOUTH
ASSESSMENT
ANALYSIS
NORMAL
PHYSICAL ASSESSMENT
RESPIRATORY
ASSESSMENT
ANALYSIS
PHYSICAL ASSESSMENT
CARDIOVASCULAR
GASTROINTESTINAL
ASSESSMENT
ANALYSIS
No lesions, scars
NORMAL
observed on the
abdomen. Abdomen is
symmetric and flat.
Normo active bowel
sounds. Empty bladder is
not palpable or
PHYSICAL ASSESSMENT
RESPIRATORY
ASSESSMENT
ANALYSIS
PHYSICAL ASSESSMENT
URINARY
EXTREMITIES
ASSESSMENT
ANALYSIS
PHYSICAL ASSESSMENT
ASSESSMENT
ANALYSIS
PATHOPHYSIOLOGY
LABORATORY RESULTS
TEST
RESULT
REFERENCE
75 umol/L
22 g/L
44 106 umol/L
38 50 g/L
55 g/L
74 88 g/L
Globulin Mass C
33 g/L
36 38 g/L
Creatinine
Albmin Mass C
INTERPRETATION AND
ANALYSIS
NORMAL
Reflects selective loss of
albumin from circulation,
as may occur with kidney
disease
Low total protein level
suggests a kidney
disorder
May reflect
overproduction of
globulins
LABORATORY RESULTS
TEST
RESULT
REFERENCE
INTERPRETATIO
N AND ANALYSIS
Sodium
136 mmol/L
NORMAL
Potassium
3.6 mmol/L
NORMAL
LABORATORY RESULTS
TEST
RESULT
Hemoglob
in Mass C
105
REFEREN
CE
140-160
TEST
WBC
Differential
Count
Neutrophils
Lymphocytes
Eosinophils
Monocytes
Platelet
MPV
RESULT
REFERENCE
11.0
5-10
52
30
15
40-75
20-45
1-4
3
Normal
8.0
2-6
150-440
7.5-11.5
INTERPRETATION
AND ANALYSIS
Indicates presence
of infection
NORMAL
NORMAL
Indicates allergic
disorders /
infections / skin
diseases
NORMAL
NORMAL
NORMAL
DRUG ANALYSIS
Drug
MOA
weight heparin
patients with
-anemia
Classifica derivative that
acute illness
tion:
acceleratesformat who are at
Anticoag ion of antiincreased risk
ulants
thrombin IIIbecause of
thrombin complex decreased
and deactivates
mobility.
thrombin,
preventing
CI:
conversion of
Conditions with
fibrinogen to
high risk of
fibrin. Has higher uncontrolled
anti-factor Xa
hemorrhage
toantifactor IIa
including major
activity ratio.
bleeding
Nursing Responsibility:
- Monitor VS and assess for signs
of bleeding
-Give only by deep SC while lying
down
-Do not give IM
-Assess for Heparin product
hypersensitivity
-Document baseline hematologic
parameters, liver function, and
coagulation studies
-Report unusual bleeding, or
weakness
-Avoid OTC agents containing
aspirin
-Use an electronic razor to shave
-Use a bandage to prevent DVT
Drugs
Metropolol
Classificatio
n:
Beta2
Blocker
MOA
A selective
beta blocker
that
selectively
blocks beta1
receptors;
decreases
cardiac
output,
peripheral
resistance,
and cardiac
oxygen
consumption;
and
depresses
rennin
secretion.
I and CI
I:
-hypertension
CI:
-right
ventricular
failure
secondary to
pulmonary
hypertension.
SE
Dry skin,
pruritus, skin
eruptions.
Special
Senses: Dry
mouth and
mucous
membranes.
NI
Take apical pulse and BP before
administering drug. Report to
physician significant changes in
rate, rhythm, or quality of pulse
or variations in BP prior to
administration.
Monitor BP, HR, and ECG
carefully during IV
administration..
DRUGS
MOA
CONTRAININDICATION DICATIONS
S
- To treat
- Contraindi
Clindamy Inhibits
serious
cated to
cin
protein
respirator
patient
synthesis in
y tract
hypersens
Classificat susceptible
infection
itive to
ion:
bacteria at the
caused by
drugs
Anti
level of 50S
pneumon - Use
Ineffectiv ribosomes
ococci
cautiously
e
- Infection
in patient
Bactericidal;
in skin
with renal
hinders or kills
and soft
or hepatic
susceptible
tissue
dse.
bacteria
injury
SIDE
EFFECTS
NURSING
RESPONSIBILITY
Assess for
patients
condition (V.S,
appearance of
the wound,
sputum)
Obtain specimen
for culture and
sensitivity prior
to initiating
therapy
Monitor peak
and through of
antibiotic
treatment
Assess patient
for
hypersensitivity
DRUGS
MOA
CONTRAIN
INDICATIO NS
DICATIONS
Lansopra Bind enzyme - Active
Hypersens
benign
zole
in presence
itivity to
hastric
of acidic
the drug
ulcer
Classifica gastric PH
- Prolonge
tion:
d ET and
PPI
Preventing
NGT
final
tube
transport of
hydrogen
ions to
gastric
lumen
SIDE
EFFECTS
NURSING
RESPONSIBILIT
Y
Dry mouth - Assess patient
routinely for
Peripheral
epigastric or
edema
abdominal
pain
- Administer
drug before
meals
- Report
headache and
worsening of
symptoms
- Oral care and
ice chips to
prevent
dryness of
Planni
Interventi
ng
on
Diagnosi
Rationale
Evaluation
Objective:
Ineffectiv After
Independe
Independent:
After 4hrs of
e airway
4hrs of
nt:
to take
nursing
clearanc
nursing
elevate
advantage of
intervention
e r/t
interven
head of
gravity
the client
retained
tion the
bed
decreasing
was able to
and
will be
change
diaphragm and
airway
able to
position
enhancing
patency
maintai
Q2/PRN
drainage
airway
patency
consistency.
Intervention
Dependent:
Give expectorants/ bronchodilators as ordered
Collaborative:
Assist with procedure (endotracheostomy)
Rationale
to maximize comfort
Collaborative:
to clear/maintain open airway
Diagnosis
Ineffective
Planning
Short term:
related to
hypoventilation as
be able to improve
manifested by RR
of 28 bpm and
oxygenation.
crackles upon
auscultation
Long term:
maintain as normal
respiratory rate.
Rationale
Independent:
Independent:
lung
Provided physiotherapy
Dependent:
Collaborative:
Long term:
After 2-3days of nursing intervention the client breathing pattern was
maintain into normal respiratory rate .
JOURNAL: RESPIRATORY
FAILURE
Respiratory failure occurs due mainly either to lung failure resulting in
hypoxemia or pump failure resulting in alveolar hypoventilation and
hypercapnia. Hypercapnic respiratory failure may be the result of
mechanical defects, central nervous system depression, imbalance of
energy demands and supplies and/or adaptation of central controllers.
Hypercapnic respiratory failure may occur either acutely, insidiously or
acutely upon chronic carbon dioxide retention. In all these conditions,
pathophyisiogically, the common denominator is reduced alveolar
ventilation for a given carbon dioxide production.
Acute hypercapnic respiratory failure is usually caused by defects in the
central nervous system, impairment of neuromuscular transmission,
mechanical defect of the ribcage and fatigue of the respiratory muscles.
JOURNAL: RESPIRATORY
FAILURE
The pathophysiological mechanisms responsible for chronic carbon dioxide retention are not
yet clear. The most attractive hypothesis for this disorder is the theory of natural wisdom.
Patients facing a load have two options, either to push hard in order to maintain normal
arterial carbon dioxide and oxygen tensions at the cost of eventually becoming fatigued and
exhausted or to breathe at lower minute ventilation, avoiding dyspnea, fatigue and
exhaustion but at the expense of reduced alveolar ventilation. Based on most recent work,
the favored hypothesis is that a threshold inspiratory load may exist, which, when exceeded,
results in injury to the muscles and, consequently, an adaptive response is elicited to
prevent and/or reduced this damage. This consists of cytokine production, which, in turn,
modulates the respiratory the respiratory controllers, either directly through the blood or
probably the small afferents or via the hypothalamic-pituitary-adrenal axis. Modulation of the
pattern of breathing, however, ultimately results in alveolar hypoventilation and carbon
dioxide retention.
REFERENCE:
Roussos, C., & Koutsoukou, A. (2003). Respiratory failure [Abstract]. European Respiratory
Journal, 3-14. Retrieved May 02, 2016.