Nursing management of patient with Respiratory DO.pptx

4/10/2024
By Abdi Wakjira( Bsc, Msc)
1
NEKEMTE HEALTH
SCIENCE COLLEGE
Department of
Nursing
For Post Basic BSc Nursing
Students

Objectives
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 At the end of this chapter students will able to:-
Conduct the assessment of respiratory system
Air way patency care in respiratory system disorder
Describe upper respiratory system disorders and
their managements
Describe upper lower system disorders and their
managements

Respiratory systems disorder
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Anatomic and Physiologic Overview
The respiratory system is composed of the upper and lower
respiratory tracts.
Upper Respiratory Tract consist of the nose, sinuses and
nasal passages, pharynx, tonsils and adenoids, larynx, and
trachea. warms and filters inspired air.
Lower Respiratory Tract consists of the lungs, which
contain the bronchial and alveolar structures needed for gas
exchange. accomplish gas exchange.
Together, the two tracts are responsible for ventilation
(movement of air in and out of the airways).

Function of the Respiratory System
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Provides oxygen to the blood stream and
removes carbon dioxide
Enables sound production or vocalization as
expired air passes over the vocal chords
Enables protective and reflexive non-breathing air
movements such as coughing and sneezing, to
keep the air passages clear
Control of acid-base balance
Control of blood ph

Diagnostic procedures Of Respiratory systems
disorder
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Pulmonary Function Tests: used in patients with
chronic respiratory disorders.
Complete blood count. Measurement of red blood
cells and hemoglobin can give information about the
oxygen-carrying capacity of the blood.
Arterial Blood Gas Studies:- Measurements of blood
pH and of arterial oxygen and carbon dioxide tensions
 The arterial oxygen tension (PaO2) indicates the
degree of oxygenation of the blood.
 The arterial carbon dioxide tension (PaCO2) indicates
the adequacy of alveolar ventilation.

Diagnostic ….
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Sputum Studies used to:
 Identify pathogenic organisms
 Determine whether malignant cells are present.
 Assess for hypersensitivity states (in which there is an
increase in eosinophils).
Pulse Oximetry:-is a noninvasive method of continuously
monitoring the oxygen saturation of hemoglobin (SaO2).
Chest x-ray:_ ordered to help diagnose a variety of
pulmonary disorders.
Usually, posterior-anterior and side views (lateral) are taken.

Diagnostic….
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Computed Tomography is an imaging method in which
the lungs are scanned in successive layers by a narrow-
beam x-ray.
Bronchoscopy:- is the direct inspection and
examination of the larynx, trachea, and bronchi through
either a flexible fiberoptic bronchoscope or a rigid
bronchoscope.
Thoracoscopy:- is a diagnostic procedure in which the
pleural cavity is examined with an endoscope.
Thoracentesis (aspiration of fluid or air from the pleural
space) is performed for diagnostic or therapeutic reasons.

Chest Examination
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 Physical Examination. Vital signs,
including temperature, pulse, respirations,
blood pressure, and SpO2 (oxygen
saturation obtained by pulse oximetry), are
important data to collect before
examination of the respiratory system.

FOUR COMPONENTS OF A
RESPIRATORY ASSESSMENT
 INSPECTION
 PALPATION
 PERCUSSION
 AUSCULTATION

INSPECTION
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 Nose. Inspect the nose for patency,
inflammation, deformities, symmetry, and
discharge.
 Check each naris for air patency with
respiration while the other naris is briefly
occluded.
 Tilt the patient’s head backward and push
the tip of the nose upward gently. With a
nasal speculum and a good light, inspect
the interior of the nose.

Cont …d
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 Mouth and Pharynx. Using a good light source,
inspect the interior of the mouth for color, lesions,
masses, gum retraction, bleeding, and poor
dentition.
 Inspect the tongue for symmetry and lesions.
 Observe the pharynx by pressing a tongue blade
against the middle of the back of the tongue.
 A normal response (gagging) indicates that
cranial nerves IX (glossopharyngeal) and X
(vagus) are intact and that the airway is
protected

Cont ..d
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 Neck. Inspect the neck for symmetry and tender
or swollen areas.
 Palpate the lymph nodes while the patient is
sitting erect with the neck slightly flexed.
 Progression of palpation is from the nodes
around the ears, to the nodes at the base of the
skull, and then to those located under the angles
of the mandible to the midline.
 The patient may have small, mobile, nontender
nodes (shotty nodes), which are not a sign of a
pathologic condition.
 Tender, hard, or fixed nodes indicate disease.

Cont …d
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 Thorax and Lungs. Picture imaginary lines on the
chest to help identify abnormalities.
 Describe abnormalities in terms of their location
relative to these lines (e.g., 2 cm from the right mid
clavicular line).
 Chest examination is best performed in a well-
lighted, warm room with measures taken to ensure
the patient’s privacy.
 Perform all physical assessment maneuvers
(inspection, palpation, percussion, auscultation) on
either the anterior or the posterior chest rather than
moving from anterior to posterior or vice versa with
each maneuver.

Cont…d
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 Inspection- When inspecting the anterior chest,
have the patient sit upright or with the head of the
bed upright.
 The patient may need to lean forward for support on
the bedside table to facilitate breathing.
 First, observe the patient’s appearance and note any
evidence of respiratory distress, such as tachypnea
or use of accessory muscles.
 Next, determine the shape and symmetry of the
chest.

Inspection Cont ..d
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 Chest movement should be equal on both
sides, and the AP diameter should be less
than the side-to-side or transverse diameter
by a ratio of 1:2.
 An increase in AP diameter (e.g., barrel
chest) may be a normal aging change or
result from lung hyperinflation.
 Observe for abnormalities in the sternum
(e.g., pectus carinatum [a prominent
protrusion of the sternum] and pectus
excavatum [an indentation of the lower
sternum above the xiphoid process]).

Inspection Cont ..d
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 Next observe the respiratory rate, depth, and
rhythm.
 The normal rate is 12 to 20 breaths/minute; in
the older adult, it is 16 to 25 breaths/minute.
Inspiration (I) should take half as long as
expiration (E) (I:E ratio = 1:2).

Inspection Cont ..d
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 Observe for abnormal breathing patterns, such
as Kussmaul (rapid, deep breathing),
CheyneStokes (abnormal respirations
characterized by alternating periods of apnea
and deep, rapid breathing), or Biot’s (irregular
breathing with apnea every four to five cycles)
respirations.
 Skin color provides clues to respiratory status.
Cyanosis, a late sign of hypoxemia, is best
observed in a dark-skinned patient in the
conjunctivae, lips, and palms and under the
tongue.

Inspection Cont ..d
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 Inspect the fingers for evidence of long-
standing hypoxemia known as clubbing (an
increase in the angle between the base of
the nail and the fingernail to 180 degrees
or more, usually accompanied by an
increase in the depth, bulk, and
sponginess of the end of the finger)

Palpation
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 Palpation. Determine tracheal position by
gently placing the index fingers on either
side of the trachea just above the
suprasternal notch and gently pressing
backward. Normal tracheal position is
midline; deviation to the left or right is
abnormal.
 Tracheal deviation occurs away from the
side of a tension pneumothorax or a neck
mass, but toward the side of a
pneumonectomy or lobar atelectasis.

Palpation cont…d
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 Symmetry of chest expansion and extent of movement
are determined at the level of the diaphragm.
 Place your hands over the lower anterior chest wall
along the costal margin and move them inward until
the thumbs meet at midline.
 Ask the patient to breathe deeply.
 Observe the movement of the thumbs away from each
other. Normal expansion is 1 in (2.5 cm).
 Hand placement on the posterior side of the chest is at
the level of the tenth rib.
 Move the thumbs until they meet over the spine.
 Check expansion anteriorly or posteriorly, but it is
not necessary to check both.

Palpation cont…d
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 Normal chest movement is equal.
 Unequal expansion occurs when air entry is limited
by conditions involving the lung (e.g., atelectasis,
pneumothorax) or the chest wall (e.g., incisional
pain).
 Equal but diminished expansion occurs in conditions
that produce a hyperinflated or barrel chest or in
neuromuscular diseases (e.g., amyotrophic lateral
sclerosis, spinal cord lesions).
 Movement may be absent or unequal over a pleural
effusion, an atelectasis, or a pneumothorax.

Cont …d
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 Fremitus is the vibration of the chest wall
produced by vocalization.
 Tactile fremitus can be felt by placing the palmar
surface of the hands with hyperextended fingers
against the patient’s chest.
 Ask the patient to repeat a phrase such as
“ninety-nine” in a deeper, louder than normal
voice.
 Move your hands from side to side at the same
time from top to bottom on the patient’s chest.
 Fremitus is less intense farther away from these
areas

Fremitus Cont …d
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 When performing percussion, palpate all
areas of the chest and compare vibrations
from similar areas.
 Tactile fremitus is most intense adjacent to
the sternum and between the scapulae
because these areas are closest to the
major bronchi.
 Fremitus is less intense farther away from
these areas

Fremitus Cont …d
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 Increased fremitus occurs when the lung becomes
filled with fluid or is denser.
 As the patient’s voice moves through a dense tissue
or fluid, you can feel that the vibration is increased.
 This is found in pneumonia, in lung tumors, with
thick bronchial secretions, and above a pleural
effusion (the lung is compressed upward).
 Fremitus is decreased if the hand is farther from the
lung (e.g., pleural effusion) or the lung is
hyperinflated (e.g., barrel chest).Absent fremitus
may be noted with pneumothorax or atelectasis.

Percussion
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 Percussion. Percussion is performed to assess the
density or aeration of the lungs.
 The anterior chest is usually percussed with the patient
in a semi-sitting or supine position.
 Starting above the clavicles, percuss downward,
interspace by interspace
 The area over lung tissue should be resonant, with the
exception of the area of cardiac dullness.
 For percussion of the posterior chest, have the patient sit
leaning forward with arms folded.
 The posterior chest should be resonant over lung tissue
to the level of the diaphragm

Percussion Cont …d
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 Sound Description
Resonance Low-pitched sound heard over normal lungs
Hyperresonance
Loud, lower-pitched sound than normal
resonance heard over hyperinflated lungs,
such as in chronic obstructive pulmonary
disease and acute asthma
Tympany
Sound with drumlike, loud, empty quality
heard over gas-filled stomach or intestine, or
pneumothorax
Dull
Sound with medium-intensity pitch and
duration heard over areas of “mixed” solid
and lung tissue, such as over top area of
liver, partially consolidated lung tissue
(pneumonia), or fluid-filled pleural space
Flat
Soft, high-pitched sound of short duration
heard over very dense tissue where air is
not present, such as posterior chest below
level of diaphragm

Auscultation
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 Auscultation. During chest auscultation, instruct the
patient to breathe slowly and a little more deeply
than normal through the mouth.
 Auscultation should proceed from the lung apices to
the bases, comparing opposite areas of the chest,
unless the patient is in respiratory distress or will tire
easily; if so, start at the bases
 Place the stethoscope over lung tissue, not over
bony prominences.
 At each placement of the stethoscope, listen to at
least one cycle of inspiration and expiration.
 Note the pitch (e.g., high, low), duration of sound,
and presence of adventitious or abnormal sounds.

Auscultation Cont …d
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 At each placement of the stethoscope, listen to at
least one cycle of inspiration and expiration.
 Note the pitch (e.g., high, low), duration of sound,
and presence of adventitious or abnormal sounds.
 The lung sounds are heard anteriorly from a line
drawn
perpendicular to the xiphoid process lateral to the
midclavicular line.
 Palpate inferiorly (down) two ribs in the midaxillary
line and around to the posterior chest. .

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 This gives you a fairly accurate and easy
way to determine the lung fields to be
auscultated
 When documenting the location of the lung
sounds, divide the anterior and posterior
lung into thirds (upper, middle, and lower)
and note, for example, “crackles posterior
right lower lung field.”
 You are not expected to define which lobe
of the lung has particular lung sounds

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 The three normal breath sounds are vesicular,
bronchovesicular, and bronchial.
 Vesicular sounds are relatively soft, lowpitched, gentle,
rustling sounds.
 They are heard over all lung areas except the major
bronchi. Vesicular sounds have a 3:1 ratio, with
inspiration three times longer than expiration.
 Bronchovesicular sounds have a medium pitch and
intensity and are heard anteriorly over the mainstem
bronchi on either side of the sternum and posteriorly
between the scapulae.
 Bronchovesicular sounds have a 1:1 ratio, with
inspiration equal to expiration.

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 Bronchial sounds are louder and higher pitched and
resemble air blowing through a hollow pipe.
 Bronchial sounds have a 2:3 ratio with a gap between
inspiration and expiration.
 This reflects the short pause between the respiratory
cycles.
 To hear the likeness of bronchial breath sounds, place
the stethoscope alongside the trachea in the neck.
 The term abnormal breath sounds describes bronchial or
bronchovesicular sounds heard in the peripheral lung
fields.

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 Adventitious sounds are extra breath
sounds that are abnormal. Adventitious
breath sounds include crackles, rhonchi,
wheezes, and pleural friction rub
(described in Table 26-7).
 A variety of terms are used to describe
breath sounds. The spoken voice can be
auscultated over the thorax just as it can
be palpated for fremitus.
 Egophony is positive (abnormal) when the
person says “E” but it is heard as “A.”

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Palpation
Description Possible Etiology and
Significance
Tracheal deviation
Leftward or rightward
movement of trachea
from normal midline
position.
Nonspecific indicator of change in
position of mediastinal structures.
Medical emergency if caused by
tension
pneumothorax. Trachea deviates
to the side opposite the collapsed
lung.
Altered tactile
fremitus
Increase or decrease in
vibrations.
↑ In pneumonia, pulmonary
edema. ↓ In pleural effusion, lung
hyperinflation. Absent in
pneumothorax, atelectasis.
Altered chest
movement
Unequal or equal but
diminished movement of
two sides of chest with
inspiration.
Unequal movement caused by
atelectasis, pneumothorax,
pleural effusion, splinting. Equal
but diminished movement caused
by barrel chest, restrictive
disease, neuromuscular disease.

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Palpation
Description Possible Etiology
and Significance
Percussion
Hyperresonance
Loud, lower-pitched
sound over areas that
normally produce
a resonant sound.
Lung hyperinflation
(COPD), lung collapse
(pneumothorax),
air trapping (asthma).
Dullness
Medium-pitched
sound over areas that
normally produce a
resonant sound.
↑ Density (pneumonia,
large atelectasis), ↑
fluid in pleural
space (pleural
effusion).

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Auscultation
and Significance
Fine crackles
Series of short-duration, discontinuous,
high-pitched sounds heard just before the
end of inspiration. Result of rapid
equalization of gas pressure when
collapsed alveoli or terminal bronchioles
suddenly snap open. Similar sound to
that made by rolling hair between fingers
just behind ear.
Idiopathic pulmonary fibrosis,
interstitial edema (early
pulmonary edema), alveolar
filling (pneumonia), loss of lung
volume (atelectasis), early
phase of heart failure.
Coarse crackles
Series of long-duration, discontinuous,
low-pitched sounds caused by air
passing through airway intermittently
occluded by mucus, unstable bronchial
wall, or fold of mucosa. Evident on
inspiration and, at times, expiration.
Similar sound to blowing through straw
under water. Increase in bubbling quality
with more fluid.
Heart failure, pulmonary
edema, pneumonia with
severe congestion, COPD.
Rhonchi
Continuous rumbling, snoring, or rattling
sounds from obstruction of large airways
with secretions. Most prominent on
expiration. Change often evident after
coughing or suctioning.
COPD, cystic fibrosis,
pneumonia, bronchiectasis.

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Auscultation
and Significance
Wheezes
Continuous high-pitched
squeaking or musical sound
caused by rapid vibration of
bronchial walls. First evident
on expiration but possibly
evident on inspiration as
obstruction
of airway increases. Possibly
audible without stethoscope.
Bronchospasm (caused by
asthma), airway obstruction
(caused by foreign body,
tumor), COPD.
Stridor
Continuous musical or crowing
sound of constant pitch. Result
of partial obstruction of larynx
or trachea.
Croup, epiglottitis, vocal cord
edema after extubation,
foreign body.
Absent breath sounds
No sound evident over entire
lung or area of lung.
Pleural effusion, mainstem
bronchi obstruction, large
atelectasis, pneumonectomy,
lobectomy.

Sequence for examination of chest
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 Sequence for examination of the chest. A, Anterior sequence. B, Lateral sequence. C,
Posterior sequence. For palpation, place the palms of the hands in the position
designated as “1” on the right and left sides of the chest. Compare the intensity of
vibrations. Continue for all positions in each sequence. For percussion, tap the chest at
each designated position, moving downward from side to side. Compare percussion
sounds at all positions. For auscultation, place the stethoscope at each position and
listen to at least one complete inspiratory and expiratory cycle. Keep in mind that, with a
female patient, the breast tissue will modify the completeness of
the anterior examination.

Auscultation Cont..d
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 Bronchophony is positive (abnormal) when a person
repeats “ninety-nine” and the words are easily
understood and are clear and loud.
 Whispered pectoriloquy is positive (abnormal) when
the patient whispers “one-two-three” and the almost
inaudible voice is transmitted clearly and distinctly.
 Conditions that increase lung density or a
consolidated lung (e.g., pneumonia) have positive
(abnormal) voice sounds.

4/10/2024 By Abdi Wakjira( Bsc, Msc) 39
UPPER RESPIRATORY
DISORDERS

Types of Rhinitis
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1. Allergic Rhinitis - is the reaction of the
nasal mucosa to a specific allergen.
Allergic rhinitis can be classified according to
the causative allergen (seasonal or perennial)
or,
 the frequency of symptoms (episodic,
intermittent, or persistent).
 Episodic refers to symptoms related to
sporadic exposure to allergens that are not
typically encountered in the patient’s normal
environment, such as exposure to animal

Allergic Rhinitis …
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Intermittent means that the symptoms are
present less than 4 days a week or less than 4
weeks per year.
Persistent means that the symptoms are
present more than 4 days a week and for
more than 4 weeks per year

Pathophysiology
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 Sensitization to an allergen occurs with initial allergen exposure,
which results in the production of antigen-specific immunoglobulin
E (IgE).
 After exposure, mast cells and basophils release histamine,
cytokines, prostaglandins, and leukotrienes.
 These cause the early symptoms of sneezing, itching,
rhinorrhea, and congestion.
 Four to 8 hours after exposure, inflammatory cells infiltrate
the nasal tissues, causing and maintaining the inflammatory
response.
 Because symptoms of rhinitis resemble those of the common
cold, the patient may believe the condition is a continuous or
repeated cold.

Clinical Manifestations
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 Manifestations of allergic rhinitis are initially
sneezing; watery, itchy eyes and nose; altered
sense of smell; and thin, watery nasal discharge that
can lead to a more sustained mucus production and
nasal congestion.
 The nasal turbinates appear pale,boggy, and
swollen.
 C/M is characterized by 4 cardinal symptoms of
watery Rhinorrhoea, nasal obstruction, nasal itching
and sneezing.

Clinical Manifestations Cont…d
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 The posterior ends of the turbinates can become so
enlarged that they obstruct sinus aeration or
drainage and result in sinusitis.
 With chronic exposure to allergens, the patient’s
responses include headache, congestion, pressure,
nasal polyps, and postnasal drip as the most
common cause of cough.
 The patient may complain of cough, hoarseness,
and the recurrent need to clear the throat.
Congestion may cause snoring

DIAGNOSIS OF Allergic Rhinitis
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The diagnosis of AR is based on a typical history of
allergic symptoms and diagnostic tests.
When 2 or more symptoms out of watery Rhinorrhoea,
sneezing, nasal obstruction and nasal pruritus persist for
≥1 hour on most days, Allergic Rhinitis is strongly
suspected
Skin testing
Skin testing is the most important to find offending
allergens.
There are various testing methods including the scratch,
prick/
puncture, intradermal and patch tests.
 The radioallergosorbent test (RAST);Serum specific
IgE level

TREATMENT OF ALLERGIC RHINITIS
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 Requires a stepwise approach depending on the
severity and duration of symptoms.
 Treatment options for AR consist of
a) Allergen avoidance,
b) Pharmacotherapy,
c) Immunotherapy and
d) Surgery.
The four major categories of medications used to
manage cold symptoms are antihistamines,
decongestants, antitussives, and expectorants.

Pharmacotherapy
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An over-the-counter (OTC), non-sedating
antihistamine
Competitively inhibit the interaction of histamine
with H1 receptors.
They prevent and relieve nasal itching,
sneezing, and Rhinorrhoea, and ocular
symptoms,
e.g.
Loratadine 10 mg once daily
Desloratadine 5 mg once daily
Cetirizine 10 mg once daily or divided BID
Levocetirizine 5 mg once daily in the

Intranasal corticosteroids
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Are potent inhibitors of the late-phase allergic
reaction in Allergic Rhinitis.
They inhibit recruitment of Langerhans cells,
macrophages, mast cells, T cells, and
eosinophils into the nasal mucosa
They control itching, sneezing, Rhinorrhoea, and
stuffiness
E.g.
Beclomethasone dipropionate 2 sprays
EN/day
Fluticasone (Flonase), 1–2 sprays EN /day

Decongestants
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Decrease swelling of the nasal mucosa which, in
turn, alleviates nasal congestion
e.g. Oxymetazoline nasal spray
60 mg every 4-6 h
120mg ER every 12h
240mg ER once daily
Pseudoephedr
ine pills

NURSING AND COLLABORATIVE
MANAGEMENT
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 The most important step in managing allergic rhinitis
is identifying and avoiding triggers of allergic
reactions
 The goal of medications is to reduce inflammation
associated with allergic rhinitis, reduce nasal
symptoms, minimize associated complications, and
maximize quality of life.
 Appropriate oral medication options include:
H1-antihistamines, corticosteroids, decongestants, and
leukotriene receptor antagonists (LTRAs).

NURSING AND COLLABORATIVE
MANAGEMENT Cont …d
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 Second-generation antihistamines are
preferred over first generation antihistamines
because of their nonsedating effects.
 Remind patients who are taking
antihistamines to have adequate fluid intake to
reduce adverse symptoms.
 Nasal corticosteroid sprays are used to
decrease inflammation locally with little
absorption in the systemic circulation.
 Therefore systemic side effects are rare.

2. Non-Allergic Rhinitis
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This form of rhinitis does not depend on the
presence of IgE and is not due to an allergic
reaction.
The symptoms can be triggered by cigarette
smoke and other pollutants as well as strong
odors, alcoholic beverages, and cold.
Other causes may include blockages in the nose,
a deviated septum, infections, and over-use of
medications such as decongestants.

3. Acute viral Rhinitis
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 Acute viral rhinitis (common cold or acute
coryza) is an infection of the upper respiratory
tract that can be caused by more than 200
different viruses.
 The majority of colds, which are caused by
rhinoviruses, are mild and self-limiting.
 Cold symptoms may last 2 to 14 days, with
typical recovery in 7 to 10 days.
 Caution patients to use the intranasal
decongestant sprays for no more than 3 days
to prevent rebound congestion from occurring.
 Cough suppressants may be used.

3. Acute viral Rhinitis Cont…d
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 Complications of acute viral rhinitis include pharyngitis,
sinusitis, otitis media, tonsillitis, and lung infections.
 Unless symptoms of complications are present,
antibiotic therapy is not indicated.
 If symptoms remain for 10 to 14 days with no
improvement, acute bacterial sinusitis may be present,
and antibiotics will be prescribed.
 Teach the patient to recognize the symptoms of
secondary bacterial infection, such as a temperature
higher than 100.4° F (38° C); tender, swollen glands;
severe sinus or ear pain; or significantly worsening
symptoms.

Nasal polyp
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 Def: is a non cancerous growth(benign) develop on
the lining of the passage at sinuses.
 Small growth may cause no problem,
 Big growth may cause complications.
 It may come in many sizes & shapes.
Causes - exact cause is unknown
Risk factors – person with chronic viral or bacterial
infections have a higher incidence of nasal polyps.
Allergies, asthma, chronic rhinitis, and chronic sinusitis

Cont …d
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Incidence
Common in adult
Rare in children
 4 times are common in men than in women.

Clinical Manifestation
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 Bluish, glossy projections in the nares –
can exceed the size of grape
 Nasal congestion, nasal discharges
(usually clear mucus), speech distortion
 Reduced ability to smell (hyposmia)
 Loss of smell (anosmia)

Types
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 Antrochoanal polyps – single, unilateral and usually
found in children, originate from maxillary sinus
 Ethmoidal polyps – multiple, bilateral and usually found
in adults, originating form ethmoidal air cells

Medical management
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 Corticosteroid sprays or local injection of a
steroid into the polyp
 Steroid used to reduce the size, prevention
of recurrence and reduction of
inflammation thus reducing swelling
 Antibiotics (amoxicillin or erythromycin) if
infection present.

Surgical Management
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 Polypectomy – removal of polyps after nose is
anesthetized, NASAL SNARE is slipped around polyp,
which is transected and removed with forceps.
 Removal of polyp via CALDWELL- LUC OPERATION,
 Procedure named after George Caldwell & Guy
Luc,who desgined an operation to remove infected
polypoid tissue

Epistaxis
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Def:
Epistaxis (nosebleed) occurs in a bimodal distribution,
with children 2 to 10 years of age and adults over age
50 most affected.
Epistaxis can be caused by:
 low humidity, allergies,
 upper respiratory tract infections,
 sinusitis, trauma, foreign bodies,
 hypertension,
 chemical irritants such as street drugs, overuse of
decongestant nasal sprays, facial or nasal surgery,

Epistaxis Cont…d
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Epistaxis can be caused by ….
 Anatomic malformation, and tumors.
 Any condition that prolongs bleeding time or
alters platelet counts will predispose the
patient to epistaxis.
 Bleeding time may also be prolonged if the
patient takes aspirin, NSAIDs, warfarin, or
other anticoagulant drugs.

Nursing and collaborative management
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 Use simple first aid measures to control
epistaxis:
 (1) keep the patient quiet;
 (2) place the patient in a sitting position,
leaning slightly forward with head tilted
forward; and
 (3) apply direct pressure by pinching the
entire soft lower portion of the nose against
the nasal septum for 10 to 15 minutes.
 If bleeding does not stop within 15 to 20
minutes, seek medical assistance.

Nursing and collaborative …
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 Medical management involves identifying the bleeding
site and applying a vasoconstrictive agent,
 Cauterization, or anterior packing.
 Pledgets (nasal tampon) impregnated with anesthetic
solution (lidocaine) and/or
 Vasoconstrictive agents such as cocaine or epinephrine
are placed into the nasal cavity and left in place for 10 to
15 minutes.
 Silver nitrate may be used to chemically cauterize an
identified bleeding point after epistaxis is controlled.
 Thermal cauterization is reserved for more severe
bleeding and requires the use of local or general
anesthesia.

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 If bleeding does not stop, packing may be used. Packing with
compressed sponges (e.g., Merocel) or epistaxis balloons
(e.g., Rapid Rhino) is preferred over the use of traditional
Vaseline ribbon gauze
 The balloon is inflated with air to achieve the same pressure
effect.
 Closely monitor respiratory rate, heart rate and
rhythm,
 Oxygen saturation using pulse oximetry (SpO2), and
 Level of consciousness, and observe for signs of aspiration.
 Because of the risk of complications, all patients with
posterior packing should be admitted to a monitored unit to
permit closer observation.

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 Nasal packing may be left in place for a few days.
 Before removal, medicate the patient for pain because
this procedure is very uncomfortable.
 After removal, cleanse the nares gently and lubricate
them with water-soluble jelly.
 Instruct the patient to avoid vigorous nose blowing,
engaging in strenuous activity, lifting, and straining for 4
to 6 weeks.
 Teach the patient to use saline nasal spray and/or a
humidifier, to sneeze with the mouth open, and to avoid
the use of aspirin-containing products or NSAIDs.

Sinusitis
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Four pairs of paranasal
sinuses
1. Frontal-above eyes in
forehead bone
2. Maxillary-in cheekbones,
under eyes
3. Ethmoid-between eyes and
nose
4. Sphenoid-in center of skull,
behind nose and eyes

Sinusitis---
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An acute inflammatory process
involving one or more of the
paranasal sinuses.
A complication of 5%-10% of
URIs in children.
Persistence of URI symptoms
>10 days without improvement.
Maxillary and ethmoid sinuses
are most frequently involved.

Types of Sinusitis
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It is typically classified by:_
Duration of illness (acute vs. Chronic)
Etiology (infectious vs. Noninfectious)
 Pathogen type (viral, bacterial, or fungal)
1. Acute Sinusitis – respiratory symptoms last longer than
10 days but less than 30 days.
2. Sub acute sinusitis – respiratory symptoms persist longer
than 30 days without improvement.
3. Chronic sinusitis – respiratory symptoms last longer than
120 days.

Pathophysiology of sinusitis
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If the sinus orifices are blocked by swollen mucosal lining,
the pus cannot enter the nose and builds up pressure
inside the sinus cavities
Postnasal drainage causes obstruction of nasal passages
and an inflamed throat.
With inflammation, the mucosal lining of the sinuses
produce mucoid drainage. Bacteria invade and pus
accumulates inside the sinus cavities.
Inflammation and edema of mucous
membranes lining the sinuses cause
obstruction.
Rhinitis or abrupt pressure changes (air planes,
diving) or dental extractions or infections.

Predisposing Factors
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Allergies,
Cold weather
High pollen counts
Day care attendance
Smoking in the home
Reinfection from siblings
Anatomical: septal deviation, nasal
deformities, nasal polyps
Mucociliary functions: cystic fibrosis, immotile
cilia syndrome.
Systemic disease: immune deficiency.: DM,
AIDS,

Etiology
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Acute sinusitis
Str. pneumoniae %41
H. influenzae %35
M. catarrhalis %8
Others %16
 Strep. pyogenes
 S. aureus
 Rhinovirus
 Parainfluenzae
 Veilonella,
peptococcus
Chronic sinusitis
Anaerob bacteria:
 Bactroides,
fusobacterium
 S. Aureus
 Strep. Pyogenes
 Str. Pneumoniae
 Gram (-) bacteria
fungi

Signs and Symptoms
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Headache, congestion, facial pain, fatigue, and
cough,
Purulent nasal discharge.
Pain over the region of the affected sinuses
If a maxillary sinus is affected, the patient
experiences pain over the cheek and upper
teeth.
In ethmoid sinusitis, pain occurs between and
behind the eyes.
Pain in the forehead typically indicates
frontal sinusitis.
Fever may be present in acute infection, with or

Diagnosis of sinusitis
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History ;persistent symptom of URI and physical findings
Radiographic studies
Opacification and mucosal thickening air filled level
Others :
Translumination of sinus cavity
Sinus aspirate culture
Nasal endoscopy
If repeated episodes occur:-
 x-ray examination
 computed tomography (CT) scan
 magnetic resonance imaging (MRI)

Treatment of Sinusitis
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Nondrug measures :
Maintain adequate hydration(drink 6-10glasses of
liquid )
Personal Steam vaporizer
Apply warm facial packs (warm wash cloth, hot
water bottle)
Saline irrigation lavage or sniff (1/4 teaspoon salt
dissolved in 1cup of water )
Sleep ahead of bed elevated
Adequate rest
Avoid cigarette smoke and extremely dry or cool air

Drug Treatment
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Antibiotics
First-line:
 Amoxicillin, 1.5 to 3.5 g/d divided 2 or 3 times daily)
 Trimethoprim–sulfamethoxazole 800/160 mg twice
daily
Second-line:
 Amoxicillin–Clavulanate (500/125 mg 3 times daily)
Second- or third-generation cephalosporin
 Cefuroxime, 250 or 500 mg twice daily,
Doxycycline 200 mg on first day then 100 mg twice
daily for 2 to 10 days

Antibiotics----
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Macrolides :
Clarithromycin, 500 mg twice daily or
Azithromycin, 500 mg daily for 5 days
Fluoroquinolones :
Ciprofloxacin, 500 twice a day or
Levofloxacin, 500 mg once daily
Oral antihistamines :Loratadine, 10 mg daily
Nasal decongestant: Xylometazoline intranasally, 2 to 3
sprays every 8 to 10 hr.
Nasal steriods :Fluticasone, 2 puffs) intranasally [200 µg]
daily
Acetaminophen or ibuprofen is given for pain and fever.

Nursing management
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Patient teaching self care
 Instruct patient to blow the nose gently and to use tissue to
remove the nasal drainage.
 Increasing fluid intake,
 Applying local heat (hot wet packs), and
 Elevating the head of the bed promote drainage of the sinuses.
 Instructs the patient about the importance of medication
regimen.

Tonsillitis
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Tonsils are protective (lymph) glands that are
situated on both sides in the throat.
The tonsils constitute an important part of the
body's immune system and are vital defense
organs.
They protect the body from bacteria and viruses
by fighting these as soon as they enter the body
(via the oral / nasal cavity).
Inflammatory process of the mucosa and
structures of the pharyngo-tonsillar area, usually
of infectious origin
Tonsillitis is contagious.

Tonsillitis ---
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Throat pain, either mild or severe.
Swallowing with difficulty.
Odynophagia, pharyngeal exudate, anterior cervicolateral
lymphadenopathy, scarlet rash and headache
Chills and fever as high as 104° F (40° C) or more.
Swollen lymph glands on either side of the jaw.
Ear pain.
Cough (sometimes).
Vomiting (sometimes).
Refusal to eat in a very young child.
Erythema,
Edema,
Ulcer or vesicles

Causes of Tonsillitis
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Viruses: Rhinovirus, adenovirus, influenza virus,
Para influenza virus,Coxsackie virus and Epstein-
Barr virus
Aerobic Bacteria: GABHS and other streptococcal
species, Neisseria gonorrhoeae, Corynebacterium
diphtheriae.
Yeast :Candida species.
Spirochetes:Treponema pallidum (syphilis)

Causes ----
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Assessment and Diagnostic
Findings
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History :look at throat to see red
and swollen tonsils with spots or
sores.
Throat culture: rapid strep test
Blood test ;done to confirm
presence of infection

Medical Management
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 Bed rest, except to use the bathroom, is necessary
until fever subsides.
DIET
 Supportive measures include Increase all fluid intake.
While the throat is very sore, use liquid nourishment,
such as milk shakes, soups, and high-protein fluids
(diet or instant-breakfast milk drinks).
Viral tonsillitis is not effectively treated with antibiotic
therapy.
Tonsillectomy if complicated

Antibiotic treatment of choice
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 Penicillin V: <12 years or <27 kg: 250mg / 12h 10 days
>12 years or >27 kg: 500mg / 12h 10 days
 Penicillin G Benzathine:
<12 years or <27 kg: 600.000 UI, single dose
>12 years or >27 kg: 1.200.000 UI, single dose
 Amoxicillin: 50mg /kg/day, every 12-24 hours, 10 days,
with a maximum dose of 500mg /12h or 1g/24h.
 Mediated by IgE:
- Azithromycin: 20mg/kg /day, once a day, 3 days
(maximum 500mg/day)
- Clindamycin: 20-30mg/kg /day, every 8-12h, 10 days
(maximum 900mg/day).

Indications for tonsillectomy
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Recurrent tonsillitis (more than seven per year
Persistent, chronic tonsillitis
Recurrent peritonsillar abscess with previous
history of recurrent or persistent tonsillitis.
Unilateral tonsillar hypertrophy.
Hemorrhagic tonsillitis.
Chronic tonsillolithiasis.
Nasal obstruction with speech abnormalities,
orodental abnormalities.

Complications of tonsillitis
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 Classified into suppurative and nonsuppurative
complications.
 The nonsuppurative complications include
 Scarlet fever,
 Acute rheumatic fever, and
 Post-streptococcal glomerulonephritis.
Suppurative complications include
Peritonsillar, parapharyngeal and retropharyngeal
abscess formation.

Pharyngitis
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ACUTE PHARYNGITIS:is a sudden painful
inflammation of the pharynx, the back portion of the throat
that includes the posterior third of the tongue, soft palate,
and tonsils.
It is commonly referred to as a sore throat
Causes
 Viral infection- most common(adenovirus, influenza
virus, Epstein-Barr virus, and herpes simplex virus)
 Bacterial infection-Group A beta-hemolytic
streptococcal bacterial infection called strep throat.

Cont….d
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Pathophysiology
Viral/ strep throat infection
The body responds by triggering an inflammatory response
in the pharynx.
This results in pain, fever, vasodilation, edema, and tissue
damage, manifested by redness and swelling in the tonsillar
pillars, uvula, and soft palate.
A creamy exudate may be present in the tonsillar pillars
If caused by GA hemolytic streptococcus- it may be severe
If caused by uncomplicated virus- may be subside
promptly(3 to 10 days after the onset).

Cont….d
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Complications
Sinusitis
Otitis media
Peritonsillar abscess
Mastoiditis
Cervical adenitis
In rare cases, the infection may lead to bacteremia,
pneumonia, meningitis, rheumatic fever, and
nephritis.

Cont….d
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Clinical features
Fiery-red pharyngeal membrane and tonsils
Lymphoid follicles that are swollen and flecked with
white-purple exudate, and enlarged
Tender cervical lymph nodes
No cough
Fever
Malaise
Sore throat

Cont….d
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Cont….d
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 Assessment and dxs
Accurate diagnosis of pharyngitis is essential to determine
the cause (viral or bacterial)
Newer and more rapid diagnostic tests (eg, the rapid
streptococcal antigen test (RSAT).
Medical mgt
For virus- supportive care
For bacterial-penicillin is a drug of choice if allergic and
resistance (clarithromycin and azithromycin) may be used.
Analgesic medications, as prescribed( i.e. Aspirin or
acetaminophen)can be taken

Cont….d
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Nursing management
Instructs the patient to:_
 Stay in bed during the febrile stage of illness and
 Full course of antibiotic therapy
Preventive measures
 Not sharing eating utensils, glasses, napkins, food, or towels;
cleaning telephones after use
 Using a tissue to cough or sneeze
 Disposing of used tissues appropriately
 Avoiding exposure to tobacco and secondhand smoke.

Cont….d
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Chronic pharyngitis:- is a persistent inflammation of the
pharynx.
Types
 Hypertrophic: characterized by general thickening and
congestion of the pharyngeal mucous membrane
 Atrophic: probably a late stage of the first type (the
membrane is thin, whitish, glistening, and at times
wrinkled)
 Chronic granular (“clergyman’s sore throat”),
characterized by numerous swollen lymph follicles on the
pharyngeal wall

Cont….d
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Common in person :_
 work in dusty surroundings
 Use their voice to excess
 Suffer from chronic cough
 Habitually use alcohol and tobacco.
Clinical manifestation
 Sense of irritation or fullness in the throat,
 Mucus that collects in the throat and can be expelled by
coughing
 Difficulty swallowing.

Cont….d
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Medical management
Nasal congestion medications (ephedrine sulfate
(Kondon’s Nasal) or phenylephrine hydrochloride)
Antihistamine decongestant medications, such as
Pseudoephedrine.
For adults with chronic pharyngitis, tonsillectomy is an
effective option.
Nursing management
Avoid alcohol, tobacco, secondhand smoke, and exposure to
cold or to environmental or occupational pollutants.

LARYNGITIS
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DEFINITION
It is the inflammation
of larynx leading to
oedema of laryngeal
mucosa and
underlying
structures.

ETIOLOGY
102
INFECTIOUS:
 Viral laryngitis can be caused by rhinovirus, influenza
virus, parainfluenza virus, adenovirus, coronavirus,
and RSV.
 Bacterial laryngitis can be caused by group A
streptococcus, streptococcus pneumoniae, C.
diphtheriae, M. catarrhalis,haemophilus
influenzae, bordetella pertussis, and M. tuberculosis.
 Fungal laryngitis can be caused by Histoplasma,
Candida (especially in immunocompromised persons)

NON INFECTIOUS
 Inhaled fumes
 Acid reflux disease
 Allergies
 Excessive coughing, smoking, or alcohol
consumption.
 Inflammation due to overuse of the vocal cords
 Prolonged use of inhaled corticosteroids for asthma
treatment
 Thermal or chemical burns
 Laryngeal trauma, including iatrogenic one caused by
endotracheal intubation

Predisposing factors
 Smoking
 Psychological strain
 Physical stress
 Voice abuse misuse
 Acid reflux (GERD)
 Frequent sinus infectionsr
 Types – acute (less then 3 weeks)and
chronic (more than 3 weeks )

Pathophysiology
 Due to etiological factors
 The mucosa of the larynx becomes
congested and may become oedematous.
 A fibrinous exudate may occur on the
surface.
 Signs and symptoms
 Sometimes infection involves the
perichondrium of laryngeal cartilages
producing perichondritis.

Types of Laryngitis
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 1. Acute Laryngitis
 2. Chronic laryngitis
1. Acute laryngitis:
Def: It is the inflammation of larynx which
lasts less than a few days & leads to edema
of laryngeal mucosa & underlying structures.
Most cases of AL are temporary & improve
after the underlying causes get better.

Acute Laryn ….
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 Frequently caused by ‘Rhinovirus”
 Other causative Organisms:
 Para influenza virus
 Respiratory syncytial virus
 Adeno virus
 Measles & Mumps
 Bacterial infection- such as Diphteria,
these are rae.

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 Vocal misuse, vocal strain or yelling or
over use of the voice.
 Exposure to noxious
 Viral infections such as that cause a cold.
 Frank aphonia

Chronic Laryngitis
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 Laryngitis that lasts more than 3 weeks is
known as chronic laryngitis.
 More persistent disorder that produces
lingering hoarseness & other voice
changes
 It is usually painless & has no significant
sign of infection.

Etiology
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 Vocal misuse
 Exposure to noxious agent.
 Infectious agents leading to upper
respiratory tract infections. Most often viral
but some times bacterial
 Inhaled irritants such as chemical fumes,
allergens or smoking.
 Acid reflex, also gastro esophageal reflux
disease (GERD)

Cont …d
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 Chronic sinusitis, bronchitis
 Excessive alcohol use
 Habitual over use of the voice such as with singers
or cheerleaders.
 Smoking
Less common cause of chronic laryngitis include:
 Infections such as TB, syphilis or a fungal infections.
 Infections with certain parasites.
 Cancer
 Vocal cord paralysis, which can result from injury,
stroke or a lung tumor or other conditions.

Clinical features
 Husky, high pitched voice, Body aches, Fever, Malaise.
 Dysphonia (hoarseness) or aphonia (inability to speak)
 Dysphagia (difficulty in swallowing)
 Dyspnea (difficulty in breathing), predominantly in
children
 Dry, burning throat, Dry irritating paroxysmal cough.
 Cold or flu-like symptoms , Swollen lymph nodes in the
throat, chest, or face
 Hemoptysis (coughing out blood), Increased production
of saliva.

Clinical features Cont…d
 Signs of acute URTI.
 Dry thick sticky secretions.
 Dusky red and swollen vocal cords.
 congestion of laryngeal mucosa.

Treatment
SUPPORTIVE
 Voice rest.
 Steam inhalation.
 Cough suppressants.
 Avoid smoking and cold climate.
 Fluid intake.

Diagnosis
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 Based upon a combination of a complete
history & physical exam.
 If symptoms are severe, particularly in
children, the doctor may order an x-ray of
the neck & chest.
 CBC Some times in children rarely in
adults.

Laryngoscopy
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 Visual examination of vocal cords in a procedure
called laryngoscopy, by using a light & a tiny
mirror to look in to the back of the throat.
 Fiber optic -laryngoscopy
 Biopsy

Treatment
DEFINITIVE
 If laryngitis due to gastroesophageal reflux, an H2-
inhibitor (ranitidine) or proton-pump inhibitor
(omeprazole) is used to reduce gastric
acid secretions.
 If laryngitis is caused by thermal or chemical burns,
steroids are used.
 In viral laryngitis, drinking sufficient fluids will be
helpful.
 If laryngitis is due to a bacterial or fungal infection,
appropriate antibiotic or antifungal therapy is
given.

Supportive Therapy
 Drinking lot of fluids - Drink 7-9 glasses of water per day;
herbal tea and chicken soup also provides soothing effect.
 maintaining good general health - Exercise regularly.
 Avoiding smoking - They are bad for the heart, lungs and
vocal tract.
 Eating a balanced diet - Include vegetables, fruits and
whole grain foods.
 Avoid dry, artificial interior climates.
 Do not eat late at night - may have problems when
stomach acid backs up on the vocal cords.
 Use a humidifier to assist with hydration.

Laryngotracheal bronchitis (Viral croup)
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 Known as laryngotracheitis or
laryngotracheobronchitis
 Most common etiology is viral
Parainfluenza virus, adenovirus, RSV
 Leads to infection and inflammation of the
larynx and subglottic area
 Decreased mobility of the vocal cords
 Frequently affects children

Etiology
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 Most common etiology is viral Parainfluenza
virus, adenovirus, RSV
 Leads to infection and inflammation of the larynx
and subglottic area
 Decreased mobility of the vocal cords
 Frequently affects children

Clinical manifestation
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 Begins with respiratory symptoms
 Within 2 days progresses to:
 Hoarseness
 Barking seal like cough
 Stridor-
 Symptoms worse at night
 Fever

Viral Croup
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 Mild disease: occasional barking cough, no
strider at rest, mild to no suprasternal
retractions
 Moderate: frequent cough, audible strider at
rest, retractions,
 Severe: frequent cough, Barking type
 inspiratory/expiratory strider, retractions,
decreased air entry, distress, and agitation.

Viral Croup Cont …d
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 A/P neck x-ray: Shows subglottic
narrowing
 CBC might show lymphocytosis-
DDx:
 Diphtheria
 Epiglottitis
 Peritonsillar abscess
 Inhalation injuries

Viral Croup Management
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 Moist steam
 Exposure to out door cool air
 Adequate hydration
 Glucocorticoid
 Racemic epinephrine
 Dexamethasone for severe cases

Hospitalization Indication
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 Dehydration-
 Significant respiratory compromise
 Signs of respiratory failure
Spasmodic Croup
 No prodrome of upper respiratory
syndrome.
 Subglottic edema
 Affects individual at night.
 Affects children between 1-3 years
 Managed at home

Epiglottitis
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Def:
 The epiglottis is a cartilaginous structure covered
with mucous membrane.
 Epiglottitis is an acute inflammation of the epiglottis
and pharyngeal structures
 Can be severe life threatening disease
 Primarily affects children 2-7 years.
 Presents more acutely in young children
Etiology: H. influenzae type B, also group A S
pneumoniee, H pereintluensee, S sureus, and beta
hemolytic streptococci

C/M
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 Triad of drooling, dysphagia, and distress.
 High fever
 Positioning- tripod position
 Dyspnea/inspiratory stridor/ accessory
muscle use/muffled voice
 Brassy cough

Diagnosis
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 Lateral neck –enlarged, edematous epiglottis.
 Laryngoscopy: Direct inspection of epiglottis
under controlled conditions
 Leukocytosis
 Blood cultures positive

Differential Dx
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 Anaphylaxis
 Croup
 Retropharyngeal Abscess
 Foreign body obstruction

Epiglottitis Management
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 Secure airway with endotracheaI
intubation.
 Might need cricothyroidotomy.
 Child should sit upright
 Humidified oxygen
 Hospitalization
 No tongue blades
 IV antibiotics: Ceftriaxone (Rocephin)
cefotaxime (Ceftin), Ampicillin with
chloramphenicol

Epiglottitis Management ….
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 Evaluate for extubation 24-48 hours post
intubation.
 Rifampin prophylaxis for 4days for
household contacts if: children in
household have not been vaccinated with
the entire series

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Management of pt with respiratory disorder
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Oxygen Therapy
 Is the administration of oxygen at a concentration greater than
that found in the environmental atmosphere
 The goal of oxygen therapy is to provide adequate transport of
oxygen in the blood while decreasing the work of breathing
and reducing stress on the myocardium
Indications
 Change in the patient’s respiratory rate or pattern( hypoxemia
or hypoxia)
 Need for oxygen is assessed by arterial blood gas analysis,
pulse oximetry, and clinical evaluation.

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 Oxygen therapy is the administration of oxygen at a
concentration greater than that found in the
environmental atmosphere.
 At sea level, the concentration of oxygen in room air is
21%.
 The goal of oxygen therapy is to provide adequate
transport of oxygen in the blood while decreasing the
work of breathing and reducing stress on the
myocardium.
 Oxygen transport to the tissues depends on factors such
as cardiac output, arterial oxygen content, concentration
of hemoglobin, and metabolic requirements.
 These factors must be kept in mind when oxygen

Indications
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 A change in the patient’s respiratory rate or pattern
may be one of the earliest indicators of the need for
oxygen therapy.
 The change in respiratory rate or pattern may result
from hypoxemia or hypoxia.
 Hypoxemia - a decrease in the arterial oxygen
tension in the blood is manifested by changes in
mental status.
Such as:
 progressing through impaired judgment,
 agitation,
 disorientation,

Indications Cont …d
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 Sign & symptoms of hypoxemia include:
 confusion,
 lethargy, and coma,
 dyspnea,
 increase in blood pressure,
 changes in heart rate,
 dysrhythmias,
 central cyanosis (late sign),
 diaphoresis, and cool extremities.
 Hypoxemia usually leads to hypoxia, which is a
decrease in oxygen supply to the tissues.
Hypoxia, if severe enough, can be life-
threatening.

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 The signs and symptoms signaling the need for
oxygen may depend on how suddenly this need
develops.
 With rapidly developing hypoxia, changes occur in
the central nervous system because the higher
neurologic centers are very sensitive to oxygen
deprivation.
 The clinical picture may resemble that of alcohol
intoxication, with the patient exhibiting lack of
coordination and impaired judgment.

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 Longstanding hypoxia (as seen in chronic obstructive
pulmonary disease [COPD] and chronic heart failure)
may produce fatigue, drowsiness, apathy,
inattentiveness, and delayed reaction time.
 The need for oxygen is assessed by arterial blood gas
analysis and pulse oximetry as well as by clinical
evaluation.
Cautions in Oxygen Therapy
As with other medications, the nurse administers oxygen
with
caution and carefully assesses its effects on each patient.
Oxygen is a medication and except in emergency
situations is administered only when prescribed by a

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 In general, patients with respiratory conditions are
given oxygen therapy only to raise the arterial
oxygen pressure (PaO2) back to the patient’s normal
baseline, which may vary from 60 to 95 mm Hg.
 In terms of the oxyhemoglobin dissociation curve the
blood at these levels is 80% to 98% saturated with
oxygen; higher inspired oxygen flow (FiO2) values
add no further significant amounts of oxygen to the
red blood cells or plasma.

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Types of Hypoxia:
Hypoxia can occur from either severe
pulmonary disease (inadequate oxygen
supply) or from extrapulmonary disease
(inadequate oxygen delivery) affecting gas
exchange at the cellular level.
The four general types of hypoxia are
hypoxemic hypoxia, circulatory hypoxia,
anemic hypoxia, and histotoxic hypoxia.

Types of Hypoxia Cont …d
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1. Hypoxemic Hypoxia
 Hypoxemic hypoxia is a decreased oxygen level in
the blood resulting in decreased oxygen diffusion
into the tissues.
 It may be caused by hypoventilation, high altitudes,
ventilation–perfusion mismatch (as in pulmonary
embolism), shunts in which the alveoli are collapsed
and cannot provide oxygen to the blood (commonly
caused by atelectasis), and pulmonary diffusion
defects.
 It is corrected by increasing alveolar ventilation or
providing supplemental oxygen

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2. Circulatory Hypoxia
 Circulatory hypoxia is hypoxia resulting from inadequate
capillary circulation.
 It may be caused by decreased cardiac output, local
vascular obstruction, low-flow states such as shock, or
cardiac arrest.
 Although tissue partial pressure of oxygen (PO2) is
reduced, arterial oxygen (PaO2) remains normal.
 Circulatory hypoxia is corrected by identifying and
treating the underlying cause.

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3. Anemic Hypoxia
Anemic hypoxia is a result of decreased effective
hemoglobin concentration, which causes a
decrease in the oxygen-carrying capacity of the
blood. It is rarely accompanied by hypoxemia.
Carbon monoxide poisoning, because it reduces
the oxygen-carrying capacity of hemoglobin,
produces similar effects but is not strictly anemic
hypoxia because hemoglobin levels may be
normal

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4. Histotoxic Hypoxia
Histotoxic hypoxia occurs when a toxic substance,
such as cyanide, interferes with the ability of
tissues to use available oxygen

OXYGEN TOXICITY
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 Oxygen toxicity may occur when too high a
concentration of oxygen (greater than 50%) is
administered for an extended period (longer than 48
hours).
 It is caused by overproduction of oxygen free
radicals, which are byproducts of cell metabolism.
 If oxygen toxicity is untreated, these radicals can
severely damage or kill cells.
Antioxidants such as vitamin E, vitamin C, and beta-
carotene may help defend against oxygen free
radicals. (Scanlan, Wilkins & Stoller, 1999).

OXYGEN TOXICITY Cont…d
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Signs and symptoms of oxygen toxicity
include:
 substernal discomfort,
 paresthesias,
 dyspnea,
 restlessness,
 fatigue,
 malaise,
 progressive respiratory difficulty, and
 alveolar infiltrates evident on chest x-rays.

SUPPRESSION OF VENTILATION
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 In patients with COPD, the stimulus for respiration is a
decrease in blood oxygen rather than an elevation in
carbon dioxide levels.
 Thus, administration of a high concentration of oxygen
removes the respiratory drive.
 The resulting decrease in alveolar ventilation can cause
a progressive increase in arterial carbon dioxide
pressure (PaCO2), ultimately leading to the patient’s
death from carbon dioxide narcosis and acidosis.
 Oxygen-induced hypoventilation is prevented by
administering oxygen at low flow rates (1 to 2 L/min).

OTHER COMPLICATIONS
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 Because oxygen supports combustion, there
is always a danger of fire when it is used. It is
important to post “no smoking” signs when
oxygen is in use.
 Oxygen therapy equipment is also a potential
source of bacterial cross-infection; thus, the
nurse changes the tubing according to
infection control policy and the type of oxygen
delivery equipment.

Methods of Oxygen Administration
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 Oxygen is dispensed from a cylinder or a
piped-in system.
 A reduction gauge is necessary to reduce the
pressure to a working level, and a flow meter
regulates the flow of oxygen in liters per
minute.
 When oxygen is used at high flow rates, it
should be moistened by passing it through a
humidification system to prevent it from
drying the mucous membranes of the
respiratory tract.

Methods of Oxygen Administration …
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 Oxygen delivery systems are classified as low-flow or
high-flow delivery systems.
1. Low-flow systems contribute partially to the inspired
gas the patient breathes.
The amount of inspired oxygen changes as the patient’s
breathing changes.
Examples of low-flow systems include:
1. nasal cannula,
2. oropharyngeal catheter,
3. simple mask,
4. partial-rebreather and
5. non-rebreather masks.

Methods of Oxygen Administration …
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2. High-flow systems provide the total amount of inspired
air.
 A specific percentage of oxygen is delivered independent
of the patient’s breathing.
 High-flow systems are indicated for patients who require
a constant and precise amount of oxygen.
Examples of such systems include:
1. transtracheal catheters,
2. Venturi masks,
3. aerosol masks,
4. tracheostomy collars,
5. T-piece, and
6. face tents

Chest physiotherapy
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 Includes postural drainage, chest percussion,
and vibration, and breathing retraining.
• The goals of CPT are to remove bronchial
secretions, improve ventilation, and increase
the efficiency of the respiratory muscles.

Postural drainage
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Allows the force of gravity to assist in the removal of
bronchial secretions.
The secretions drain from the affected bronchioles into
the bronchi and trachea and are removed by coughing
or suctioning.
Used to prevent or relieve bronchial obstruction caused
by accumulation of secretions.
Patient usually sits in an upright position, secretions are
likely to accumulate in the lower parts of the lungs.

Positions used for postural drainage
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Nursing Management
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• The nurse should be aware of:-
Patient’s diagnosis as well as the lung lobes or segments
involved
Cardiac status
Any structural deformities of the chest wall and spine
• Auscultating the chest before and after the procedure is
used to identify the areas that need drainage and assess
the effectiveness of treatment
• The nurse explores strategies that will enable the patient
to assume the indicated positions at home(use of objects
readily available at home, such as pillows, cushions, or
cardboard boxes

Cont…d
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• PD is usually performed two to four times
daily, before meals (to prevent nausea,
vomiting, and aspiration) and at bedtime
• The nurse makes the patient as comfortable as
possible in each position and provides an
emesis basin, sputum cup, and paper
tissues.
• If the patient cannot cough, the nurse may
need to suction the secretions mechanically.

Chest Percussion and Vibration
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Thick secretions that are difficult to cough up may be
loosened.
Help dislodge mucus adhering to the bronchioles and
bronchi.
Percussion is carried out by cupping the hands and lightly
striking the chest wall in a rhythmic fashion over the lung
segment to be drained.
The patient uses diaphragmatic breathing during this
procedure to promote relaxation
percussion over chest drainage tubes, the sternum, spine,
liver, kidneys, spleen, or breasts (in women) is avoided.
Percussion is performed cautiously in the elderly (b/c of
increase incidence of osteoporosis and risk of rib fracture)

Vibration
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• Is the technique of applying manual
compression and tremor to the chest wall during
the exhalation phase of respiration
Helps increase the velocity of the air expired
from the small airways, thus freeing the mucus.
After three or four vibrations, the patient is
encouraged to cough, contracting the abdominal
muscles to increase the effectiveness of the
cough

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Fig. showing Percussion and vibration. A. Proper hand position
for vibration. B. Proper technique for vibration. The wrists and
elbows remain stiff; the vibrating motion is produced by the
shoulder muscles. C. Proper hand position for percussion.

Nursing Management
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The nurse ensures that the patient is
comfortable, is not wearing restrictive
clothing, and has not just eaten.
Gives medication for pain, as prescribed,
before percussion and vibration and splints any
incision and
 Provides pillows for support as needed.

Cont …d
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Deep Breathing and Coughing
Effective coughing can keep the airways clear of
secretions.
An ineffective cough is exhausting and fails to bring up
secretions.
Instruct the patient to take two or three deep breaths,
using the diaphragm.
This helps get the air behind the secretions.
After the third deep inhalation, tell the patient to hold
the breath and cough forcefully.
This is repeated as necessary.
Good hydration can facilitate this process.

Incentive Spirometry
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Def:
 Incentive spirometry, also referred to as sustained
maximal inspiration (SMI).
 Incentive Spirometry is designed to mimic natural
sighing or vomiting by encouraging the patient to
take long, slow, deep breaths.
 This is accomplished by using a device that provides
patients with visual or other positive feed back when
they inhale at a predetermined flow rate or volume
& sustain the inflation for at least 5 seconds.

Purpose
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 To increase tran-pulmonary pressure &
inspiratory volumes, improve inspiratory
muscle performance, & reestablish or
simulate the normal pattern of pulmonary
hyperinflation.
 When the procedure is repeated on a
regular basis, airway patency may be
maintained & lung atelectasis prevented &
reversed.

Cont …d
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Indication:
Upper abdominal or thoracic- surgery
Lower abdominal surgery
 Prolonged bed rest
 Surgery in patients with COPD
 Lack of pain control
 Presence of thoracic or abdominal binders.

Using an Incentive Spirometer
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 The inhalation of air, in a slow and controlled manner,
helps inflate the lungs.
 The marker within the spirometer will measure the depth
of each breath.
 Assume an upright position if possible (sitting or semi-
Fowler’s).
 Breathe using your diaphragm.
 Place mouthpiece firmly in the mouth, to breathe in
deeply and slowly, holding each breath in for 3–4
seconds and exhaling slowly.
 Repeat 6–10 times per session.
 Use spirometer every hour while awake (keep it within
reach).
 Try coughing, with splinting of incision, after each use.

Incentive spirometer
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 How to use an incentive spirometer

ARTIFICIAL AIRWAYS
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 The patient with an airway disorder such as a
laryngeal obstruction or cancer may require the use
of a temporary or, in some cases, a permanent
artificial airway.
 Two types of artificial airways that may be used
include an endotracheal tube (ETT) or a
tracheostomy tube.
 General recommendations are to favor a
tracheostomy tube rather than ETT if the patient will
be intubated for 21 days or greater, and to favor the
ETT over a tracheostomy if support will be required
for 10 days or less (Morris et al., 2013).

ARTIFICIAL AIRWAYS Cont…d
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ETT and tracheostomy tubes have several
disadvantages.
 The tubes cause discomfort,
 the cough reflex is depressed because
closure of the glottis is hindered, and
 Secretions tend to become thicker because
the warming and humidifying effect of the
upper respiratory tract has been bypassed.

ARTIFICIAL AIRWAYS Cont…d
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 The swallowing reflexes are depressed
because of prolonged disuse and the
mechanical trauma produced by the
endotracheal or tracheostomy tube, thus
increasing the risk of aspiration.
 In addition, ulceration and stricture of the
larynx or trachea may develop.
 Of great concern to the patient is the inability
to talk and to communicate needs.

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Endotracheal intubation
• involves passing an endotracheal tube through
the mouth or nose into the trachea.

Cont …d
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It is a means of providing an airway for patients
who cannot maintain an adequate airway on their
own
Comatose patients,
Patients with upper airway obstruction),
For patients needing mechanical ventilation,
For suctioning secretions from the pulmonary
tree

Cont …d
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• Tracheotomy
• is a surgical procedure in which an opening is made into the
trachea.
• The indwelling tube inserted into the trachea is called a
tracheostomy tube
• It may be either temporary or permanent.
Equipment
 Sterile gloves
 Hydrogen peroxide
 Normal saline solution or sterile water
 Cotton-tipped applicators
 Dressing
 Twill tape
 Type of tube prescribed, if the tube is to be changed

Cont …d
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• A tracheotomy is used
To bypass an upper airway obstruction,
To allow removal of tracheobronchial secretions,
To permit the long-term use of mechanical
ventilation,
To prevent aspiration of oral or gastric secretions
in the unconscious or paralyzed patient (by closing
off the trachea from the esophagus)
To replace an endotracheal tube

Tracheostomy tube in place
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Tracheostomy tubes. A. Cuffed tracheostomy tube; used for
patients on mechanical ventilation. B. Cuffed fenestrated tube;
allows the patient to talk. C. Uncuffed tracheostomy tube; not
used for adult patients on mechanical ventilation; often used for
permanent tracheostomy patients who are not ventilator
dependent.
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Nursing Management
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Continuous monitoring and assessment.
Newly made opening must be kept patent by
proper suctioning of secretions.
The patient is placed in a semi-fowler’s position
to facilitate ventilation, promote drainage,
minimize edema, and prevent strain on the
suture lines After the vital signs are stable
Analgesia and sedative agents must be
administered with caution because of the risk of
suppressing the cough reflex.

Preventing Complications Associated With
Endotracheal and Tracheostomy Tubes
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• Administer adequate warmed humidity.
• Maintain cuff pressure at appropriate level.
• Suction as needed per assessment findings.
• Maintain skin integrity.
• Change tape and dressing as needed or per
protocol.
• Auscultate lung sounds.
• Monitor for signs and symptoms of infection,
including temperature and white blood cell count.

Cont …d
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• Administer prescribed oxygen and monitor
oxygen saturation.
• Monitor for cyanosis.
• Maintain adequate hydration of the patient.
• Use sterile technique when suctioning and
performing tracheostomy care.

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Lower Respiratory Tract Disorders

Pneumonia
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 Pneumonia (from the Greek pneuma, “breath”) is a
potentially fatal infection and inflammation of the lower
respiratory tract (i.e., bronchioles and alveoli) usually caused
by inhaled bacteria and viruses
 Is an inflammation of the lung parenchyma.
 Is a lung infection involving the lung alveoli (air sacs) and
can be caused by microbes, including bacteria, viruses, or
fungi.
 Pneumonitis -- immune-mediated inflammation of alveoli
Clinical Definition
Symptoms of acute LRT infection
a) Cough, sputum, chest pain
b) Fever,sweating,shiver, aches and pains
• New focal chest signs on examination OR

Classification of pneumonia
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Based on causative agent
Bacterial or typical pneumonia,
Atypical pneumonia
Viral pneumonia
Fungal pneumonia etc

Pneumonia
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 Anatomic(morphological) classification
Lobar pneumonia- homogeneous consolidation of one
or more lung lobes
Broncho- pneumonia- multiple patchy shadows in a
localized or segmental area.

Bronchopneumonia
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Infants + young children and the elderly.
Usually secondary to other conditions associated with
local and general defense mechanisms:
Viral infections (influenza, measles)
Aspiration of food or vomitus
Obstruction of a bronchus (foreign body or
neoplasm)
 Inhalation of irritant gases
Major surgery
Chronic debilitating diseases, malnutrition

Lobar pneumonia:
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 S. pneumoniae.
 Previously healthy individuals.
 Abrupt onset.
 Unilateral stabbing chest pain on inspiration
(due to fibrinous pleurisy).

Types of Pneumonia
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Community-acquired pneumonia(CAP)
 Infection of the pulmonary parenchyma acquired
from exposure in the community
Occurs either in the community setting or within
the first 48 hours after hospitalization or
institutionalization.
Infection usually spread by droplet inhalation.
Highest incidence in winter
Smoking important risk factor

“Typical” CAP:
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 History
Previously healthy with sudden onset of fever and
shortness of breath
Presents with “typical” severe, acute infection
Infectious agent (usually S. Pneumonia or H. Flu) is
culturable/ identifiable
Responsive to cell-wall active antibiotics
 Physical signs and symptoms
Tachycardia
Tachypnea
Productive cough with purulent sputum and possible
hemoptysis

Typical CAP----
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• localized:
− dullness to percussion
− decreased breath sounds
− crackles ,ronchi , egophony
Investigations
• CXR showing lobar consolidation
• CBC showing leukocytosis w/ left shift
• Sputum sample contains neutrophil, RBCs; Gram
stain may be positive depending on organism

“Atypical” CAP
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• History :
Previously healthy present with is usually sub-acute,
low grade fever, sore throat, and intractable cough
Minimal sputum production
Able to continue to work
No sick contacts, recent travel, or evidence of altered
immune system
PE reveals a mildly ill-appearing patient with diffuse
wheezes on lung exam
“Walking pneumonia” syndrome
Causative pathogens are difficult to culture/identify by
standard methods
Not responsive to penicillins

Types Of Atypical Pneumonia.
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 Mycoplasma pneumonia
 Caused by tiny bacteria mycoplasma pneumoniae.
 It is generally milder than other types
 Children and adults who are infected often show symptoms resembling
those of a cold or flu, such as coughing, sneezing, and a mild fever.
 Generally, not have to be hospitalized.
 Chlamydophila pneumonia.
 Caused by chlamydophila pneumoniae bacteria.
 School-age children at greatest risk for this type.
 Legionella pneumonia (legionnaires’ disease)
 Caused by legionella pneumophila bacteria.
 Not spread through person-to-person contact.
 Legionnaires’ disease tends to be more serious than other types of
atypical pneumonia.
 It can lead to respiratory failure and death in some cases.

Common causes Of CAP
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 The causative agents for CAP that requires hospitalization are:
 Previously healthy individual: → S. pneumoniae
 Pre-existing viral infection → Staph. aureus or S. pneumoniae
 Chronic bronchitis → Haemophilus influenzae or S. pneumoniae
 AIDS → Pneumocystis carinii, cytomegalovirus, TB
 Elderly people and those with co morbid illnesses → H. Influenzae
 Legionella, pseudomonas Aeruginosa, and other gram-negative rods.
 Viruses (infants and children)
 Atypical bacteria

The most common causes for viral
pneumonia are:
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 Influenza
 Parainfluenza
 Adenovirus
 Respiratory syncytial virus (RSV)
 appears mostly in children
 Cytomegalovirus
 In immunocompromised hosts

Features of Severe Pneumonia
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 ‘Core’ clinical adverse prognostic features
(CURB)
Confusion
Urea > 7 mM (>19.1 mg/dL)
Respiration rate >30 /min
Blood Pressure: Systolic BP < 90 mm Hg and/or
diastolic BP ≤ 60 mmHg
NOTE: Patients with 2 or more CURB are at high
risk of death

Hospital-Acquired Pneumonia
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 Also known as nosocomial pneumonia
 Is defined as the onset of pneumonia symptoms more than 48
hours after admission in patients with no evidence of infection
at the time of admission.
 Is an acute lower respiratory tract infection acquired after at
least 48 hours of admission to hospital and is not incubating at
the time of admission.
 Ventilator-associated pneumonia (VAP), is pneumonia occurring
more than 48 hours after endotracheal intubation.

Predisposing factors
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 Defense mechanisms are incompetent or overwhelmed
 Decreased cough and epiglottal reflexes (may allow
aspiration)
 Mucociliary mechanism impaired
 Pollution
 Cigarette smoking
 Upper respiratory infections
 Tracheal intubation
 Aging
 Metabolic disorder
 Mechanical ventilation (VAP)
 Supine positioning and aspiration


Pneumonia
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The common organisms responsible for HAP
Enterobacter species,
Escherichia coli,
H. influenzae,
Klebsiella species,
Proteus, Serratia marcescens,
P. aeruginosa,
methicillin-sensitive or methicillin-resistant
Staphylococcus aureus (MRSA), and
S. pneumoniae

Pneumonia
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Pneumonia in the Immunocompromised Host
Includes Pneumocystis pneumonia (PCP), fungal
pneumonias, and Mycobacterium tuberculosis.
Aspiration Pneumonia
Is the pulmonary consequences resulting from entry of
endogenous or exogenous substances into the lower
airway.

Pathophysiology of Pneumonia
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 Pneumonia results from the proliferation of microbial
pathogens at the alveolar level and the host's response
to those pathogens
 Their are three mechanisms by which pathogens reach
to the lungs
Inhalation,
Aspiration and
Hematogenous e.g. Tricuspid endocarditis

Pathophysiology pneumonia----
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Primary inhalation: when organisms bypass
normal respiratory defense mechanisms or when
the Pt inhales aerobic GN organisms that colonize
the upper respiratory tract or respiratory support
equipment
Aspiration: occurs when the Pt aspirates
colonized upper respiratory tract secretions
Stomach: reservoir of GN that can ascend,
colonizing the respiratory tract.
Hematogenous: originate from a distant source
and reach the lungs via the blood stream.

Pathology of lobar pneumonia
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 Four stage of pathiophysiological change occur due to
pneumonia
1. Congestion
Lasts < 24 hours: Out pouring of fluid from
tissue to alveoli- b/se of inflammatory process.
Alveoli filled with oedema fluid and bacteria.
Only a few neutrophil are seen at this stage.

Stage of pathiophysiological----
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2. Red hepatization
 Lungs look like the liver
 Firm, 'meaty' and airless appearance of lung.
 Alveolar capillary dilatation.
 Strands of fibrin extending from one alveolus to another
via inter-alveolar pores of Kohn.
 Also neutrophil in alveoli.
 Pleura: Fibrinous exudate.
 Characterized microscopically by the presence of many
RBC, neutrophil, micro-organisms , fibrins in the alveolar
spaces

Stage of pathiophysiological---- …
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3. Gray hepatization
 Less hyperaemia.
 Macrophages, neutrophil + fibrin
 The lung is dry, friable and gray-brown to yellow as
a consequence of a persistent fibrino-purulent
exudates
 WBC and fibrin consolidate the alveoli and lung
 Second and third stages last for 2 to 3 days each

Stage Of Pathiophysiological----
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4. Resolution
 Lyses and removal of fibrin via sputum + lymphatics.
 Begins after 8-9 days (without antibiotics).
 Sudden improvement of patient's condition.
 Characterized by enzymatic digestion of the alveolar
exudate;
 Resorption, phagocytosis or coughing up of the residual
debris and
 Restoration of the pulmonary architecture.

Clinical manifestations
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Cough producing greenish or yellow sputum
High fever that may be accompanied by
shaking chills
Shortness of breath
Tachypnea
Pleuritic chest pain
 Headache

Clinical manifestations…
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Sweaty and clammy (moist) skin,
Loss of appetite
Fatigue
Blueness of the skin
Nausea, vomiting
Mood swings
Joint pains or muscle aches

Investigations
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History
Physical exam
Chest x-ray
Gram stain of sputum
Sputum culture and sensitivity
Pulse oximeter or ABGs
CBC, differential, chemistry
Blood cultures
Invasive diagnostic techniques
 Transtracheal aspiration
 Bronchoscopy with a protected brush catheter
 Direct needle aspiration of the lung

What are the differential diagnoses?
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Alternative
diagnosis
Supporting clinical feature(s)
Exacerbation of
COPD
Known COPD, history of smoking, or industrial exposure to
inorganic dust,Bilateral polyphonic wheeze
Lack of focal chest signs
Exacerbation of
asthma
History of asthma or atopy, Bilateral polyphonic wheeze
Lack of fever and focal chest signs
Pulmonary oedema Features of left ventricular or biventricular failure (elevated
jugular venous pressure, peripheral oedema, fine bibasal
crackles in the lung)
Bronchiectasis longer history,Finger clubbing
Chronic cough productive of purulent sputum
Bilateral crackles at the lung bases
Lung cancer Haemoptysis, weight and appetite loss, smoking history
Finger clubbing
Lymphadenopathy
Cachexia

Medical management
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EMPIRIC ANTIBIOTIC THERAPY
First line (Mild):Amoxicillin 1g PO TID #5-7days and if penicillin allergy
Clarithromycin 250gm PO BID #5-7days
(Moderate): Benztylpencillin 1.2g IM QID #7days
plus
Doxycycline100mg PO BID #7days
or
Clarithromycin 500gm PO BID #7days
If penicillin allergy Cefriaxone 1gm Iv daily #7days plus
Doxycycline100mg PO BID #7days or Clarithromycin 500gm PO BID
#7days
(Severe): Benztylpencillin 1.2g IM every 4hours
plus
Gentamycin IV daily plus
Azithromycin 500mg IV/PO daily
If penicillin allergy :Cefriaxone 1gm Iv daily #7days plus Azithromycin
500mg IV/PO daily

Pneumonia cont’d…
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Medical management…
E.g. according to DACA
For community acquired ambulatory pts
(mild pneumonia):-
◦ Amoxicillin
OR
◦ Erythromycin
OR
◦ Doxycyciline

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For community acquired hospitalized pts (severe
pneumonia):-
Non-Drug treatment:
Bed rest
Frequent monitoring of temperature, blood pressure and
pulse rate.
Give attention to fluid and nutritional replacements
Administer Oxygen
Analgesia for chest pain

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Drug treatment:
Benzyl penicillin PLUS Gentamicin
OR Ceftriaxon.
Pneumonia due to staphylococcus aureus:
Cloxacillin 1-2 gm, IV or IM QID for 10-14 days.

Pneumonia
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HAP (nosocomial pneumonias)
Antimicrobials effective against gram-negative & gram-positive
should be given in combination. Suitable combination is:
Cloxacillin plus Gentamicin
OR
Ceftriaxone plus Gentamicin
Ciprofloxacin
Pneumocytis pneumonia responds to Trimethoprin +
Sulfamethoxazole

Complications of Pneumonia
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 Abscess formation
 Empyema
 Failure of resolution ⇒ intra-alveolar scarring
('carnification') ⇒ permanent loss of Ventilatory function of
affected parts of lung.
 Bacteraemia:
 Infective endocarditis
 Cerebral abscess / meningitis
 Septic arthritis
 Shock and Respiratory Failure
 Pleural Effusion
 Atelectasis

Sample case scenarios
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1. A 35-year-old male patient presented to Nekemte Specialized hospital with fever
and cough. He was well 3 days back, when he suffered the onset of nasal
stuffiness, mild sore throat, and a cough productive of small amounts of clear
sputum. On Physical examination his temperature was 38.9°C , pulse 110
beats/min and regular, and his respiratory rate is 18 breaths/min. The case most
likely?
2. A 65-year-old man presented to the emergency department a few hours after the
gradual onset of left-sided weakness and expressive aphasia. On admission all
Vital signs were normal. However, On the fourth hospital day, Unfortunately, his
temperature increases to 39.3C with concomitant coughing that sounds
productive. Basilar rales are audible at the right lung base. A chest radiograph
reveals the presence of a new right lower lobe infiltrate without an associated
pleural effusion. The case most likely?

Chronic Obstructive Pulmonary Disease
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 COPD is also known as:
 Chronic obstructive lung disease (COLD),
 Chronic obstructive airway disease (COAD),
 Chronic airflow limitation (CAL) and
 Chronic obstructive respiratory disease (CORD)
 It is pulmonary disease characterized by airflow limitation
that is not fully reversible.
 Refers to chronic bronchitis and emphysema, a pair of two
commonly co-existing diseases of the lungs in which the
airways become narrowed.
 This leads to a limitation of the flow of air to and from the
lungs causing shortness of breath

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 In COPD, less air flows in and out of the airways because of one
or more of the following:
The airways and air sacs lose their elastic quality.
The walls between many of the air sacs are
destroyed.
The walls of the airways become thick and inflamed.
The airways make more mucus than usual, which tends
to clog them.

Causes
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 Smoking
 Occupational exposures
 Air pollution
 sudden airway constriction in response to
inhaled irritants,
 Bronchial hyperresponsiveness, is a
characteristic of asthma.
 Genetics-Alpha 1-antitrypsin deficiency

Pathophysiology of COPD
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Abnormal inflammatory response of the lungs
due to toxic gases
Response occurs in the airways, parenchyma &
pulmonary vasculature.
Narrowing of the airway takes place
Destruction of parenchyma leads to
emphysema.
Destruction of lung parenchyma leads to an
imbalance of proteinases / antiproteinases.
Pulmonary vascularchanges
Mucus hyper secretion dysfunction(cilia
dysfunction,airflowlimitation,corpulmonale(RVF)
Chronic cough and sputum production

Clinical features
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Chronic cough
Sputum production
Wheezing
Chest tightness
Dyspnea on exertion
Wt.loss
Respiratory insufficiency
Respiratory infections
Barrel chest- chronic hyperinflation leads to loss of
lung elasticity

DIFFERENTIAL DIAGNOSIS
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Diagnosis Suggestive feature
COPD •Onset mid-life
•Symptom slowly progressive
•History of tobacco smoking
Asthma •Onset early in life
•Symptom varies widely from day to day
•Symptom worse at night/morning
•Family history
Congestive heart failure •Chest X-ray shows dilated heart, pulmonary
edema
•Pulmonary function test shows volume restriction
not airway limitation
Bronchiectasis •Large volume of purulent sputum
•Commonly associated with bacterial infection
•Chest x-ray shows bronchial dilation
Tuberculosis •Onset all ages
•Chest x-ray shows infiltrate
•Microbiological confirmation

Assessment
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 DX: Spirometry is required to make the diagnosis; the
presence of a post-bronchodilator FEV1/FVC < 0.70
confirms the presence of persistent airflow limitation.
 According to Modified British Medical Research
Council (mMRC) :
 mMRC Grade 0:Only get breathlessness with extraneous
exercise
 mMRC Grade 1: I get short of breath when hurrying the
level
 mMRC Grade 2:I walk slower than people of the same
age the level b/se of breathlessness
 mMRC Grade 3: I stop for breath after walking 100m
 mMRC Grade 4:I am too breathlessness to leave the
house

COPD includes
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I. Bronchitis
II. Emphysema

Bronchitis
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 Bronchitis is a condition in which the bronchial tubes
become inflamed.
 Acute (short term) and chronic (ongoing).
 Infections or lung irritants cause acute bronchitis.
 Chronic bronchitis is an ongoing, serious condition.
 It occurs if the lining of the bronchial tubes is
constantly irritated and inflamed, causing a long-term
cough with mucus.

Chronic bronchitis
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Presence of recurrent or chronic productive cough for a
minimum of 3 months for 2 consecutive years.
It is defined as the presence of cough and sputum
production for at least 3 months.
Risk factors
 Bronchial irritants (e.g. cigarette smoke, exposure to
pollution)
 Genetic predisposition (alpha-1 antitrypsin deficiency)
 Respiratory infections

Chronic Bronchitis: Pathophysiology
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Chronic inflammation
Hypertrophy & hyperplasia of bronchial glands that secrete
mucus
Increase number of goblet cells
Cilia are destroyed
Bronchial smooth muscle hyper reactivity

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Narrowing of airway
 airflow resistance
 work of breathing
Hypoventilation & CO2 retention  hypoxemia &
hypercapnea

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Bronchial walls thickened, bronchial lumen narrowed,
and mucus may plug in the airway
Alveoli become damaged and fibrosed,
Altered function of the alveolar macrophages.
The patient becomes more susceptible to respiratory
infection.

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Mucus plug
Normal lumen

Signs and symptom
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Acute
 sore throat,
 fatigue (tiredness),
 fever, body aches,
 stuffy or runny nose,
 vomiting, and
 Diarrhea
 persistent cough
 cough may produce
clear mucus
 shortness of breath
Chronic
coughing,
wheezing, and
chest discomfort.
The coughing may
produce large amounts of
mucus. This type of cough
often is called a smoker's
cough.

Diagnosis
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 History - medical history
 Whether you've recently had a cold or the flu
 Whether you smoke or spend time around others
who smoke
 Whether you've been exposed to dust, fumes,
vapors, or air pollution –
 Mucus -to see whether you have a bacterial infection
 chest x ray
 lung function tests,
 CBC
 ABG analysis

MEDICAL MANAGEMENT
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 Improve ventilation
Broncho dilators like beta2agonists (albuterol)
,anticholinergics(ipratropium bromide-
atrovent).
Methylxanthines(theophylline,aminophylline)
Corticosteroids
Oxygen administration
 Remove bronchial secretion
 Promote exercises
 Control complications
 Improve general health

Surgical management
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 BULLECTOMY
Bullae are enlarged airspaces that do not contribute to
ventilation but occupy space in the
 Lung volume reduction surgery: It involves the removal
of a portion of the diseased lung parenchyma.
 Lung transplantation

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1. A 62-year-old auto mechanic who presents with progressive
shortness of breath for the past several days. His problem began four
days ago when I got a cold. Initially, the cough was dry but within 24
hours of onset, it produced abundant yellow-green sputum that he
stated , "I cough up a cup of this stuff every day." His wife states that
he "hack and spits up" every morning when he gets up from bed. The
case most likely?
2. A 38 year old female presented to wollega university referral hospital
with chief complain of mild, occasionally productive cough for the
past 3-4 months . she has been smoking about one pack per day for
the past 20 years. She has had no fever or chills. She does admit to
more shortness of breath when she exercises over the past six
months. Her case most likely?

Emphysema
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Is a pathologic term that describes an abnormal
distention of the airspaces beyond the terminal
bronchioles and destruction of the walls of the alveoli.
Is defined as enlargement of the air spaces distal to the
terminal bronchioles, with destruction of their walls of
the alveoli due to the action of the proteinases. .
As the alveoli are destroyed the alveolar surface area in
contact with the capillaries decreases causing formation
of dead spaces

Types
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 The part of the acinus affected determines the
subtype. It can be subdivided pathologically
into:
 Centrilobular (Proximal Acinar)-
The respiratory bronchiole (proximal and
central part of the acinus) is expanded.
The distal acinus or alveoli are unchanged.
Occurs more commonly in the upper lobes
is the most common type and is commonly
associated with smoking. It can also be
seen in coal workers pneumoconiosis.


Classification
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Panacinar-
 Is most commonly seen with alpha one antitrypsin deficiency.
The entire respiratory acinus from respiratory bronchiole to
alveoli, is expanded.
Occurs more commonly in the lower lobes, especially
basal segments, and anterior margins of the
lungs.
1. Paraseptal (Distal acinar) -may occur alone or in
association with above and the usual association
is spontaneous pneumothorax in a young adult.

Emphysema….
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Emphysema….
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 Clinical manifestation
 Early stages
 Barell chest
 Central cyanosis
 Finger clubbing
 Dyspnea
Wheezing
Chronic fatigue
Difficult in sleeping
Hypoxia
Polycythemia
Cough & sputum
production

Clubbing of the Fingers as a Result of
Chronic Hypoxia
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Emphysema….
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 Later stages
 Hypercapnea
 Purse-lip breathing
 Use of accessory muscles to breathe
 Underweight
No appetite & increase breathing workload

Emphysema…..
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Emphysema
Use accessory muscle Pursed lips breathing
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Assessment and Diagnostic Findings
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History (smoking, occupational exposure)
Physical exam
PFT
Spirometry -to find out airflow obstruction.
ABG analysis
CT scan of the lung.
Screening of alpha antitrypsin deficiency
X-ray radiography may aid in the diagnosis.
CBC
Sputum analysis

Medical Management
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Risk Reduction (smoking cessation)
Pharmacologic Therapy
 Bronchodilators
Beta2-Adrenergic Agonist Agents:- salbutamol, albuterol
Anticholinergic Agents:-Ipratropium bromide
Methylxanthines:- aminophylline ,theophylline
 Corticosteroids
 Other Medications(alpha1-antitrypsin augmentation therapy,
antibiotic agents, mucolytic agents, antitussive agents,
vasodilators, and narcotics.

Medical Management …….
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 Oxygen Therapy
 Surgical Management
 Lung Volume Reduction Surgery
 Pulmonary Rehabilitation
 Patient Education
 Breathing Exercises
 Activity Pacing
 Self-Care Activities
 Nutritional therapy
 Coping Measures

Nursing Management
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 Assessing the Patient
 Achieving Airway Clearance
 Improving Breathing Patterns
 Improving Activity Tolerance
 Monitoring and Managing Potential Complications
(respiratory insufficiency and failure)

Comparison of emphysema and chronic
bronchitis
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Emphysema Chronic bronchitis
Pink Puffers Blue Bloaters
Thin Appearance Airway Flow Problem
Increased CO2 retention Color is Dusky to Cyanotic
Minimal Cyanosis Recurrent Productive Cough
Purse Lip Breathing Hypoxia
Dyspnea Hypercapnia
Hyper-resonance on Chest Percussion Respiratory Acidosis
Orthopneic High Hemoglobin
Barrel Chest Increased Respiratory Rate
Exertional Dyspnea( Early) Dyspnea on Exertion(late)
Prolonged Expiratory Time Digital clubbing
Speaks in short jerky sentences Cardiac enlargement
Anxious Bilateral lower extremity edema

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E
B

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1. A 66-year-old man with a smoking history of 1 pack per day for the past
47 years presents with progressive shortness of breath and chronic
cough, productive of yellowish sputum, for the past 2 years. On
examination he appears in moderate respiratory distress, especially after
walking to the examination room, and has pursed-lip breathing. Lung
examination reveals a barrel chest and poor air entry bilaterally. Based
on the above scenarios the diagnosis is most likely?

Asthma
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Asthma is a chronic inflammatory disorder of the airways
that is characterized:
Clinically by recurrent episodes of wheezing,
breathlessness, chest tightness, and cough,
particularly at night/early morning.
 Physiologically by widespread, reversible
narrowing of the bronchial airways and a marked
increase in bronchial responsiveness to direct or
indirect stimuli and with chronic airway
inflammation
 Is a heterogeneous disease, usually characterized by
chronic airway inflammation

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 The chronic inflammation is associated with airway
hyper‐responsiveness that leads to recurrent episodes of
wheezing , breathlessness, chest tightness and coughing
particularly at night or early morning.
 These episodes are usually associated with widespread,
but variable airflow obstruction within the lung that is
often reversible either spontaneously or with treatment
 Is a chronic inflammatory disease of the airways that causes:-
 Airway hyperresponsiveness
 Mucosal edema
 Mucus production

Asthma classification
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 Asthma is divided into two main categories, intrinsic
and
extrinsic. Intrinsic asthma is due to hypersensitivity
of the airways independent of antibodies.
 These sensitivities can include chemicals, exercise,
complement activation, cold air, infection, and
emotional stress.
 Extrinsic asthma is due to increased levels of IgE in
the plasma.

Classification----
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1. Atopic /extrinsic /allergic ( 70%)
 Due to increased levels of IgE in the plasma in responses
to environmental antigens.
 Genetically transmitted
 Childhood onset
2. Non-atopic/ intrinsic /non-allergic( 30%)
Intrinsic asthma is due to hypersensitivity of the airways
independent of antibodies
Triggered by non immune stimuli.
Patients have negative skin test to common inhalant
allergens and normal serum concentrations of ige.
Asthma may be triggered by aspirin, pulmonary infections,
cold, exercise, psychological stress or inhaled irritants..

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Pathophysiology
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Chronic inflammation
Airway Hyperresponsiveness

Pathophysiology of Asthma
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Non-modifiable Factors:
Gender
Family History
Modifiable Factors:
>Environmental Allergens
>Emotional factors/Stress
>GERD
Triggers airway
inflammation
Release of mast cells, eosinophils, histamine,
macrophages, and activated T lymphocytes
Acute Bronchoconstriction
Narrowing of the airway passages
Difficulty Of Breathing
↓ Oxygenation
chest Tightness Chest
Wheezing
Increased Goblet cells
mucus production
Cough

ETIOLOGY
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Allergy is the strongest predisposing factor for asthma.
Common allergens can be
 Seasonal (grass, tree, and weed pollens) or
 Perennial (e.g., mold, dust, roaches, animal dander).
 Common triggers for asthma symptoms and exacerbations
Airway irritants (e.g., air pollutants, cold, heat, weather changes,
strong odors or perfumes, smoke)
Exercise, stress or emotional upset
Rhino sinusitis with postnasal drip
Medications
Viral respiratory tract infections

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The three most common symptoms of asthma are
 Cough
 Dyspnea
 Wheezing
As the exacerbation progresses
 Diaphoresis
 Tachycardia
 Hypoxemia and central cyanosis (a late sign of poor
oxygenation)

Status Asthmaticus
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 The severe and prolonged asthma exacerbation with
intensive progressive respiratory failure, hypoxemia,
hypercapnia, respiratory acidosis, increased blood viscosity
and the most important sign is blockade of bronchial b2-
receptors.
Stages:
1st - refractory response to b2-agonists (relaxation of the
smooth muscles)
2nd - “silent” lung because of severe bronchial obstruction
and collapse of small and intermediate bronchi;
3rd stage – the hypercapnic coma.

Asthma….
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Hx
Physical examination
Chest X-ray
Sputum increase viscosity
CBC- eosinophills
Lung Function Tests
Arterial blood gas analysis and pulse oximetry

Pharmacological Treatment
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 A stepwise approach is recommended as follows
1. Inhaled salbutamol prn (when necessary)
2. Inhaled salbutamol prn plus low-dose inhaled
beclometasone, starting with 100ug twice daily for adults
3. Add low-dose oral theophylline to Step 3 treatment
(assuming long-acting beta agonists and leukotriene
antagonists are not available)
4. Add oral prednisolone, but in the lowest dose possible to
control symptoms (nearly always less than 10mg daily)

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REFER
The patient should be referred in the following conditions: •
 When asthma is poorly controlled
 When the diagnosis of asthma is uncertain
 When regular oral prednisolone is required to maintain
control
 5. FOLLOW UP
 Patient and family education should be provided •
 Advise the patient to carry the device always
 • Emphasize the need for adherence to drugs.
 • Advice regarding dealing with triggers


Asthma cont’d…
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Medical management
There are two general classes of asthma medications:
 Quick-relief medications for immediate treatment of
asthma symptoms and exacerbations.
 Long acting medications to achieve and maintain control
of persistent asthma.

Asthma cont’d…
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According to DACA:
Initial treatment
 Salbutamol (metered dose inhaler MDI).
Alternatives
 Aminophylline, 5mg/kg by slow I.V. push over 5 minutes.
OR
 Adrenaline, 0.5ml sc.

Asthma cont’d…
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Maintenance therapy for chronic asthma in adults:
 Requires prolonged use of anti-inflammatory drugs
mainly in the form of steroid inhalers
Intermittent asthma:
 Salbutamol, inhaler 200 microgram/puff,1-2 puffs to be
taken as needed but not more than 3-4 times a day
Alternative
 Ephedrine + Theophylline

Asthma cont’d…
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Persistent mild asthma
 Salbutamol, inhaler, 200 micro gram/puff 1-2 puffs to be
taken, as needed but not more than 3-4 times/day
PLUS
 Beclomethasone, oral inhalation 1000mcg QD for two
weeks
Alternative
 Ephedrine + Theophylline (11mg + 120mg), P.O. two to three
times a day PLUS
 Beclomethasone oral inhalation 1000mcg QD for two weeks.

Asthma cont’d…
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Persistent moderate asthma
Salbutamol, inhalation 200microgram/puff 1-2 puffs as
needed PRN not more than 3-4 times a day.
PLUS
Beclomethasone, 2000mcg, oral inhalation QD for two
weeks and reduce to 1000 mcg if symptoms improve.

ACUTE EXACERBATION OF ASTHMA
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 The following patients have a high risk of future
exacerbations and may have a poor asthma
outcome.
 Risks for exacerbation
 • Uncontrolled asthma symptoms
 • One or more severe exacerbation in previous year
 • Start of the patient’s usual ‘flare-up’ season
 • Exposures: tobacco smoke; indoor or outdoor air
pollution; indoor allergens
 • Major psychological or socio-economic problems
for child or family • Poor adherence with controller
medication, or incorrect inhaler technique

Management of Asthma exacerbation
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 Prednisolone 30–40mg for five days for adults
and 1mg per kg for three days for children, or
longer, if necessary, until they have recovered;
 Salbutamol in high doses by metered dose inhaler
and spacer (e.g. four puffs every 20 minutes for
one hour) or by nebulizer;
 Oxygen , if available, if O2 saturation levels are
below 90%)

Asthma cont’d…
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Severe persistent asthma
 Salbutamol, inhalation , 200 micro gram/puff 1-2
puffs not more than 3-4 times a day
PLUS
 Beclomethasone, 2000 mcg, oral inhalation daily

Asthma….
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Nursing management
 Assessing patients respiratory status
 The purpose and action of each medication Triggers to
avoid, and how to do so
 Proper inhalation technique

Asthma….
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Complications
Status asthmaticus
Respiratory failure
Pneumonia
Atelectasis

ACUTE RESPIRATORY DISTRESS SYNDROME
(ARDS)
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Def:
 Condition characterized by acute inflammatory lung
injury resulting in widespread pulmonary edema as a
result of increased alveolar capillary permeability and
epithelial destruction.
 “The acute onset of severe respiratory distress and
cyanosis that was refractory to oxygen therapy and
associated with diffuse CXR abnormality and
decreased lung compliance” Lancet 1967


Causes
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 Shock
 Aspiration
 Trauma
 Infections
 Inhaled fumes
 Drugs and poisons
 Miscellaneous

Pathophysiology
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 Neutrophils release inflammatory mediators --
>degrading integrity of capillary endothelial cells-
-->capillary permeability, interstitial edema.
 Influx of proteinaceous plasma fluid,
erythrocytes, and inflammatory cells into the
interstitium
 destroyed surfactant and type 1 and 2
pneumocyte
 Increases alveolar surface tension, thus
producing alveolar collapse

Stages of ARDS
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 1. Exudative (acute): 0-4 d
 2. Proliferative:4-8 d
 3. Fibrotic:>8 d
 4. Recovery

PATHOGENESIS
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Exudative Phase:
 Injury begins with activation of alveolar
macrophages by microbial or cell injury products,
locally derived in primary lung injury (pulmonary
ARDS) or systemically derived (extrapulmonary
ARDS).
 Cytokine/chemokine release by macrophages
recruits and activates circulating neutrophils,
which release myriad inflammatory molecules.
 they also injure the normally tight alveolar
endothelial–epithelial barrier consisting of
adherent cell-cell contacts and glycocalyx linings.

PATHOGENESIS Cont …d
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 Alveolar type II pneumocytes secrete surfactant and
along with type I pneumocytes reabsorb alveolar
fluid by active ion transport back into the interstitium
for lymphatic clearance.
 As a result of loss of the normal low permeability
characteristics, the alveolar space fills with an
inflammatory cell-rich proteinaceous edema fluid
(exudative phase of ARDS), a prime determinant of
lung injury severity, alveolar collapse, and
derecruitment

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The proliferative phase of ARDS:
 Clearance of pathogens and damaged host cells from
the alveolar space,
 the immune response is recalibrated to prioritize repair
and restoration of normal function.
 Clearance involves neutrophil apoptosis and removal,
expansion of resident fibroblasts and interstitial matrix
reformation, and
 Regrowth of alveolar epithelium by differentiation of type
II alveolar cells into type I cells.
 If the proliferative phase is impaired or prolonged,
ongoing inflammation and fibroblast proliferation impair
alveolar clearance and functional recovery

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Fibrotic phase:
 It is likely that uncleared, insoluble proteins in the
alveolar space (forming hyaline membranes
observed histologically) seed the formation of fibrotic
tissue by mesenchymal cells,
 Ultimately leading to the long-term consequence of
fibrosing alveolitis (fibrotic phase of ARDS) in some
but not all patients.

Gas Exchange impairment in ARDS
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 Abnormalities from areas with reduced
ventilation-to-perfusion (VA/Q) ratios and
intrapulmonary shunting to high VA/Q ratios and
dead space.
 Low VA/Q and shunt are responsible for
increased venous admixture and arterial
hypoxemia. Given little or no ventilation to these
areas, arterial hypoxemia is insensitive to global
increases in ventilation.

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Signs and symptoms
In the first 24 to 48 hours, signs and symptoms
include dyspnea, tachypnea, dry cough,
fatigue, and tachycardia.
Even with supplemental oxygen, a patient’s
skin may look cyanotic and mottled.
Auscultation reveals adventitious breath
sounds (crackles, rhonchi, and wheezes) or
increasingly diminished breath sounds.

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Signs and symptoms
As oxygenation and perfusion diminish, the
patient may become agitated, anxious,
confused, and restless.
 A chest X-ray shows diffuse infiltrates, and
ABG results indicate respiratory alkalosis with
very low PaO2 levels. In the later stages,
hypercapnia may develop. Further metabolic
imbalances can lead to mixed acidosis,
signaling a low ventilation-to-perfusion (V./Q.)
ratio and a deteriorating P/F ratio.

Medical Management
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 The primary focus in the management of ARDS
includes identification and treatment of the
underlying condition.
 Aggressive, supportive care must be provided to
compensate for the severe respiratory
dysfunction.
 This supportive therapy almost always includes
intubation and mechanical ventilation.
 In addition, circulatory support, adequate fluid
volume, and nutritional support are important.

Medical Management Cont…d
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 Positive end-expiratory pressure (PEEP) is a critical part of the
treatment of ARDS.
 PEEP usually improves oxygenation, but it does not influence
the natural history of the syndrome.
 Use of PEEP helps to increase functional residual capacity
and reverse alveolar collapse by keeping the alveoli open,
resulting in improved arterial oxygenation and a reduction in
the severity of the ventilation–perfusion imbalance.
 By using PEEP, a lower FiO2 may be required. The goal is a
PaO2 greater than 60 mm Hg or an oxygen saturation level of
greater than 90% at the lowest possible FiO2.

Medical Management Cont…d
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PHARMACOLOGIC THERAPY
Numerous pharmacologic treatments are under
investigation to stop the cascade of events leading to
ARDS.
These include:
 Human recombinant interleukin-1 receptor antagonist,
 Neutrophil inhibitors, pulmonary-specific vasodilators,
 Surfactant replacement therapy, antisepsis agents,
 Antioxidant therapy, and corticosteroids late in the
course of ARDS

Cont….d
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NUTRITIONAL THERAPY
Adequate nutritional support is vital in the
treatment of ARDS.
Patients with ARDS require 35 to 45 kcal/kg
per day to meet caloric requirements. Enteral
feeding is the first consideration; however,
parenteral nutrition also may be required.

Nursing Management
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GENERAL MEASURES
 The patient with ARDS is critically ill and requires close
monitoring because the condition could quickly change
to a life threatening situation.
Most of the respiratory modalities used in this situation:
 Oxygen administration,
 Nebulizer therapy,
 chest physiotherapy,
 Endotracheal intubation or tracheostomy,
 Mechanical ventilation,
 Suctioning,
 Bronchoscopy).

Nursing Management of ARDS
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5 P’s of ARDS therapy
 Managing patients with ARDS requires maintaining
the airway, providing adequate oxygenation, and
supporting hemodynamic function.
 The five P’s of supportive therapy include perfusion,
positioning, protective lung ventilation, protocol
weaning, and preventing complications.

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Perfusion
 The goal of care for ARDS patients is to
maximize perfusion in the pulmonary capillary
system by increasing oxygen transport between
the alveoli and pulmonary capillaries.
 To achieve the goal, you need to increase fluid
volume without overloading the patient.
 Give either crystalloids or colloids to replace the
fluids that have leaked from the capillaries into
the alveolar spaces.

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Positioning
 Patient positioning also affects perfusion.
 If a patient is standing, blood flow moves to the base
of the lung and away from the apex.
 If a patient is supine, the posterior area of the lung
will be more perfused than the anterior area.
 Because the better aerated surfaces of the lungs are
the nondependent areas, the result is a
ventilation/perfusion mismatch.

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Positioning
 Three positioning therapies can decrease these
complications and improve perfusion in ARDS
patients:
1. Kinetic Therapy (bilateral turning of a patient 40
degrees or more per side)
2. Continuous lateral rotational therapy (bilateral
turning of a patient no more than 40 degrees per side)
3. prone positioning.
 These therapies improve oxygenation by mobilizing
secretions, resolving atelectasis, improving V./Q.
ratio

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Protective Lung Ventilation
During the early stages of ARDS, use mechanical
ventilation to open collapsed alveoli.
The primary goal of ventilation is to support organ
function by providing adequate ventilation and
oxygenation while decreasing the patient’s work of
breathing.
But mechanical ventilation itself can damage the
alveoli, making protective lung ventilation necessary.

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Indication for mechanical ventilation
PaO2 < 50 mm Hg with FiO2 > 0.60
PaO2 > 50 mm Hg with pH < 7.25
Vital capacity < 2 times tidal volume
Negative inspiratory force < 25 cm H2O
Respiratory rate > 35/min

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Protective Lung Ventilation
Current recommendations for protective lung
ventilation include:
 limiting plateau pressures to less than 30 cm H2O,
maintaining positive end-expiratory pressure
(PEEP) of at least 5 cmH2O is required reducing
FiO2 to 50% to 60%,
 Intermittent positive pressure breathing (IPPB) is a
technique used to provide short term or intermittent
mechanical ventilation via mouthpiece or mask.

Nursing Management of ARDS 634
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 There are three types of positive-pressure
ventilators, which are classified by the method of
ending the inspiratory phase of respiration:
pressure-cycled, time-cycled, and volume-cycled.
 Another type of positive-pressure ventilator used
for selected patients is noninvasive positive-
pressure ventilation.

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Preventing complications
The most common complications are VILI,
deep vein thrombosis (DVT), pressure ulcers,
decreased nutritional status, and ventilator-
associated pneumonia (VAP).

Respiratory Failure
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Def:
 Respiratory failure is a condition where there’s
not enough oxygen or too much carbon dioxide
in the body.
 Respiratory failure is a condition where there is
no enough oxygen in the tissues (hypoxia) or
when you have too much carbon dioxide in your
blood (hypercapnia).
 It can happen all at once (acute) or come on
over time (chronic).
 Many underlying conditions can cause it.
 Acute respiratory failure is life-threatening.

Types of Respiratory Failure
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 It is important to distinguish between acute
respiratory failure (ARF) and chronic respiratory
failure.
1. Chronic Respiratory Failure
 Chronic respiratory failure is defined as a
deterioration in the gas exchange function of the
lung that has developed insidiously or has
persisted for a long period after an
episode of ARF.
 The absence of acute symptoms and the
presence of a chronic respiratory acidosis
suggest the chronicity of the respiratory failure.

1. Chronic Respiratory Failure …
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Two causes of chronic respiratory failure are:
 COPD and
 neuromuscular diseases.
 Patients with these disorders develop a tolerance to
the gradually worsening hypoxemia and hypercapnia.
However, a patient with chronic respiratory failure
may develop ARF.
 This is seen in the COPD patient who develops an
exacerbation or infection that causes additional
deterioration of the gas exchange mechanism.

Acute Respiratory Failure
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 Def: Respiratory failure is a sudden and life-threatening
deterioration of the gas exchange function of the lung.
 It exists when the exchange of oxygen for carbon
dioxide in the lungs cannot keep up with the rate of
oxygen consumption and carbon dioxide production by
the cells of the body.
 Acute respiratory failure (ARF) is defined as a fall in
arterial oxygen tension (PaO2) to less than 50 mm Hg
(hypoxemia) and a rise in arterial carbon dioxide
tension (PaCO2) to greater than 50 mm Hg
(hypercapnia), with an arterial pH of less than 7.35.

ARF Cont ..d
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 Respiratory system mechanisms leading to
ARF include:
• Alveolar hypoventilation
• Diffusion abnormalities
• Ventilation–perfusion mismatching
• Shunting

Etiology
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Common causes of ARF can be classified into
four categories:
1. Decreased respiratory drive
2. Dysfunction of the chest wall
3. Dysfunction of the lung parenchyma
4. Other causes.

Pathogenesis related to the cause
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1. Decreased respiratory drive:
Decreased respiratory drive may occur with
severe brain injury, large lesions of the brain
stem (multiple sclerosis), use of sedative
medications, and metabolic disorders such
as hypothyroidism.
These disorders impair the normal response
of chemoreceptors in the brain to normal
respiratory stimulation.

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2. Dysfunction of the chest wall:
The impulses arising in the respiratory
center travel through nerves that extend
from the brain stem down the spinal cord
to receptors in the muscles of respiration.
Thus, any disease or disorder of the
nerves, spinal cord, muscles, or
neuromuscular junction involved in respiration
seriously affects ventilation and may ultimately
lead to ARF.

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2. Dysfunction of the chest wall:
These include:
 musculoskeletal disorders (muscular dystrophy,
 polymyositis), neuromuscular junction disorders
(myasthenia gravis, poliomyelitis),
 some peripheral nerve disorders, and spinal cord
disorders (amyotrophic lateral sclerosis, Guillain-
Barré syndrome, and cervical spinal cord injuries).
dysfunction of the lung parenchyma, and other causes.

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3. Dysfunction of the lung parenchyma
These are conditions that interfere with ventilation
by preventing expansion of the lung. They
include:
 Pleural effusion,
 hemothorax,
 pneumothorax, and
 upper airway obstruction.
These conditions, which may cause respiratory
failure, usually are produced by an underlying lung
disease, pleural disease, or trauma and injury.

3. Dysfunction of the lung parenchyma ….
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Other diseases and conditions of the lung
that lead to ARF include:
 pneumonia,
status asthmaticus,
lobar atelectasis,
pulmonary embolism, and
pulmonary edema.

3. Other causes. 561
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In the postoperative period, especially after major
thoracic or abdominal surgery, inadequate ventilation
and respiratory failure may occur because of several
factors.
For example, ARF may be caused by the effects of:
 anesthetic agents,
 analgesics, and sedatives,
 These may depress respiration as described earlier or
enhance the effects of opioids and lead to
hypoventilation.
 Pain may interfere with deep breathing and coughing.
 A mismatch of ventilation to perfusion is the usual
cause of respiratory failure after major abdominal,
cardiac, or thoracic surgery.

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 Early signs are those associated with
impaired oxygenation; and may include:
 restlessness,
 fatigue,
 headache,
 dyspnea,
 air hunger,
 tachycardia, and
 increased blood pressure.

Clinical Manifestations Cont …d
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As the hypoxemia progresses, more obvious
signs may be present; may including:
confusion,
lethargy,
tachycardia,
tachypnea,
central cyanosis,
diaphoresis, and finally respiratory arrest.

Clinical Manifestations Cont …d
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Physical findings are those of acute respiratory
distress, including :
use of accessory muscles,
decreased breath sounds if the patient cannot
adequately ventilate, and
other findings related specifically to the
underlying disease process and cause of
ARF.

Medical Management
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 The objectives of treatment are to correct
the underlying cause, and
 To restore adequate gas exchange in the
lung.
Intubation and mechanical ventilation may
be required to maintain adequate ventilation
and oxygenation while the underlying cause
is corrected.

Nursing Management
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Nursing management of the patient with ARF
includes:
 Assisting with intubation and,
 maintaining mechanical ventilation.
The nurse assesses the patient’s respiratory
status by:
monitoring the patient’s level of response,
arterial blood gases,
pulse oximetry, and vital signs and,
assessing the respiratory system.

Nursing Management
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The nurse implements strategies such
as:
 turning schedule,
mouth care,
skin care,
range of motion of extremities to prevent
complications.

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The nurse also assesses the patient’s
understanding of:
 the management strategies that are used and,
 initiates some form of communication to enable the
patient to express his or her needs to the health care
team.
 Nursing care also addresses the problems that led to
ARF.
 As the patient’s status improves, the nurse assesses
the patient’s knowledge of the underlying disorder,
 provides teaching as appropriate to address the
underlying disorder.

Bronchiectasis
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Is a chronic, irreversible dilation of the bronchi
and bronchioles.
Bronchiectasis is a chronic respiratory disease
characterized by a syndrome of productive cough
and recurrent respiratory infections due to
permanent dilatation of the bronchi.
Bronchiectasis represents the final common
pathway of different disorders, some of which may
require specific treatment.

Cont …d
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Bronchiectasis may be caused :-
Airway obstruction
Diffuse airway injury
Pulmonary infections and obstruction of the
bronchus or complications of long-term
pulmonary infections
Genetic disorders such as cystic fibrosis
Abnormal host defense (eg, ciliary dyskinesia
or humoral immunodeficiency)
Idiopathic causes

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Etiology
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 Congenital causes (e.g. Mounier-Kuhn syndrome)
 COPD, and smoking
 Cystic fibrosis
 Mucociliary dysfunction (e.g. primary ciliary
dyskinesia)
 Primary or secondary immune deficiency
 Pulmonary fibrosis and pneumoconiosis
 Post obstruction (e.g. with a foreign body)
 Post infection (e.g. TB, recurrent pneumonia)
 Recurrent small volume aspiration
 Allergic bronchopulmonary aspergillosis
 Systemic inflammatory diseases (eg. rheumatoid
arthritis, sarcoidosis)

Features suggest Bronchiectasis
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 Diagnosis of asthma that is unresponsive to usual
management
 Digital clubbing (this is rare in COPD and asthma)
 Lack of a significant smoking history (less than an average
of 20 cigarettes per day for 10 years) in a person with
suspected COPD
 History of recurrent and/or severe pneumonia including
tuberculosis
 Presence of ‘unusual organisms’ in sputum (e.g.
Aspergillus, atypical/nontuberculous mycobacterium,
Pseudomonas aeruginosa, Escherichia coli, Klebsiella
pneumoniae)
 Childhood associated with significant environmental and
social disadvantage

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Chief complaints are:
Chronic cough,
Purulent sputum(Copious and purulent and pools in
the dilated airways).
Dyspnea and
Sometimes haemoptysis
Clubbing of the fingers also is common because of
respiratory insufficiency.
Wheezes and crackles
Repeated episodes of pulmonary infection

Diagnostic tests
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History
Sputum culture
The chest CT is the golden standard diagnostic
tool for Bronchiectasis with the typical
presentation of bronchial diameter larger than
nearby pulmonary artery without normal bronchial
tapering.

Medical management
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Antibiotics may be used intermittently or for prolonged
periods.
Bronchodilators improve airway obstruction.
Mucolytic agents help thin secretions
Chest physiotherapy helps mobilize secretions
Oxygen is used if hypoxemia is present

Nursing management
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Encourage to stop smoking & other factors that increase
the production of mucus
Teaching the patient and family
How to perform postural drainage
Assess patients’ nutritional status/appetite
Teach the patient about early signs of respiratory
infection and the progression of the disorder.

Chest trauma
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Chest trauma is classified as either blunt or
penetrating. Blunt chest trauma results from
sudden compression or positive pressure
inflicted to the chest wall.
Common Causes of Bunt Chest Trauma are:
 Motor vehicle crashes (trauma due to steering
wheel, seat belt),
 falls, and,
 bicycle crashes (trauma due to handlebars).

Chest trauma Cont …d
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Penetrating trauma occurs when a foreign
object penetrates the chest wall.
The most common causes of penetrating
chest trauma include:
Gunshot wounds and stabbings.
1. BLUNT TRAUMA
 is more common,
 it is often difficult to identify the extent of the damage
because the symptoms may be generalized and vague.
 In addition, patients may not seek immediate medical
attention,

Pathophysiology
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Injuries to the chest are often life-threatening and result in
one or more of the following pathologic mechanisms:
 Hypoxemia from disruption of the airway; injury to the
lung parenchyma, rib cage, and respiratory musculature;
massive hemorrhage; collapsed lung; and pneumothorax
 Hypovolemia from massive fluid loss from the great
vessels, cardiac rupture, or hemothorax
 Cardiac failure from cardiac tamponade, cardiac
contusion, or increased intrathoracic pressure

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Time is critical in treating chest trauma.
Therefore, it is essential to assess the patient
immediately to determine the following:
• When the injury occurred
• Mechanism of injury
• Level of responsiveness
• Specific injuries
• Estimated blood loss
• Recent drug or alcohol use
• Pre hospital treatment

Assessment and Diagnostic Cont…d
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The initial assessment of thoracic injuries
includes:
 Assessment of the patient for airway
obstruction,
Tension pneumothorax,
Open pneumothorax,
Massive hemothorax,
Flail chest, and cardiac tamponade.
These injuries are life-threatening and need
immediate treatment.

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Secondary assessment would include:
 Simple pneumothorax,
 Hemothorax,
 Pulmonary contusion,
 Traumatic aortic rupture,
 Tracheobronchial disruption,
 Esophageal perforation,
 Traumatic diaphragmatic injury, and
 Penetrating wounds to the mediastinum (Owens,
Chaudry, Eggerstedt & Smith, 2000).
Although listed as secondary, these injuries may be life-
threatening as well depending upon the circumstances.

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 The vital signs and skin color are assessed for signs of
shock.
 The thorax is palpated for tenderness and crepitus; the
position of the trachea is also assessed.
The initial diagnostic workup includes:
 a chest x-ray,
 CT scan,
 complete blood count,
 clotting studies, type and cross-match,
 electrolytes,
 oxygen saturation, arterial blood gas analysis, and
 ECG.
The patient is completely undressed to avoid missing
additional injuries that can complicate care.

Medical Management
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The goals of treatment are to evaluate the
patient’s condition and to initiate aggressive
resuscitation.
 An airway is immediately established with
oxygen support
 in some cases, intubation and ventilatory
support.
 Re-establishing fluid volume and negative
intrapleural pressure and draining intrapleural
fluid and blood are essential.

Flail Chest
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 Flail chest is frequently a complication of blunt chest
trauma from a steering wheel injury.
 It usually occurs when three or more adjacent ribs
(multiple contiguous ribs) are fractured at two or more
sites, resulting in free-floating rib segments.
PATHOPHYSIOLOGY
 During inspiration, as the chest expands, the detached
part of the rib segment (flail segment) moves in a
paradoxical manner (pendelluft movement) in that it is
pulled inward during inspiration, reducing the amount of
air that can be drawn into the lungs.

Flail Chest
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Flail chest is caused by a free
floating segment of rib cage
resulting from multiple rib
fractures.
 (A) Paradoxical movement
on inspiration occurs when
the flail rib segment is
sucked inward and the
mediastinal
structures shift to the
unaffected side. The
amount of air drawn into the
affected lung is reduced.
 (B) On expiration, the flail
segment bulges outward
and the mediastinal
structures
shift back to the affected

MEDICAL MANAGEMENT
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 As with rib fracture, treatment of flail chest is usually
supportive.
 Management includes providing ventilatory support,
clearing secretions from the lungs, and controlling pain.
 The specific management depends on the degree of
respiratory dysfunction.
 When a severe flail chest injury is encountered,
endotracheal intubation and mechanical ventilation are
required to provide internal pneumatic stabilization of the
flail chest and to correct abnormalities in gas exchange.
 This helps to treat the underlying pulmonary contusion,
serves to stabilize the thoracic cage to allow the
fractures to heal.

2. PENETRATING TRAUMA
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GUNSHOT AND STAB WOUNDS
 Gunshot and stab wounds are the most common types
of penetrating chest trauma.
They are classified according to their velocity:
 Stab wounds are generally considered of low velocity
because
the weapon destroys a small area around the wound.
 Knives and switchblades cause most stab wounds.
 The appearance of the external wound may be very
deceptive;
 Because pneumothorax, hemothorax, lung contusion,
and cardiac tamponade, along with severe and
continuing hemorrhage, can occur from any small
wound, even one caused by a small-diameter
instrument such as

Gunshot & Stab wound Cont…d
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 Open pneumothorax is one form of traumatic
pneumothorax.
It occurs when a wound in the chest wall is large
enough to allow air to pass freely in and out of the
thoracic cavity with each attempted respiration.
Because the rush of air through the hole in the chest
wall produces a sucking sound, such injuries are
termed sucking chest wounds.
In such patients, not only does the lung collapse, but
the structures of the mediastinum (heart and great
vessels) also shift toward the uninjured side with
each inspiration and in the opposite direction with
expiration.

Medical Management
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Nursing Allert! Traumatic open pneumothorax calls for
emergency interventions. Stopping the flow of air through
the opening in the chest wall is a life threatening measure.
 Medical management of pneumothorax depends on its
cause and severity.
 The goal of treatment is to evacuate the air or blood from
the pleural space.
 A small chest tube (28 French) is inserted near the
second intercostal space; this space is used because it
is the thinnest part of the chest wall, minimizes the
danger of contacting the thoracic nerve, and leaves a
less visible scar.

Medical Management Cont …d
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If the patient also has a hemothorax, a large-diameter chest
tube (32 French or greater) is inserted, usually in the fourth or
fifth intercostal space at the midaxillary line.
 The tube is directed posteriorly to drain the fluid and air.
 Once the chest tube or tubes are inserted and suction is
applied (usually to 20 mm Hg suction), effective
decompression of the pleural cavity (drainage of blood or air)
occurs.
 If an excessive amount of blood enters the chest tube in a
relatively short period, an autotransfusion may be needed.
 This technique involves taking the patient’s own blood that
has been drained from the chest, filtering it, and then
transfusing it back into the patient’s vascular system.

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In such an emergency, anything may be used
that is large enough to fill the chest wound;
a towel, a handkerchief, or the heel of the
hand.
If conscious, the patient is instructed to inhale
and strain against a closed glottis.
This action assists in reexpanding the lung
and ejecting the air from the thorax.

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In the hospital, the opening is plugged by
sealing it with gauze impregnated with
petrolatum.
A pressure dressing is applied.
Usually, a chest tube connected to water-seal
drainage is inserted to permit air and fluid to
drain.
Antibiotics usually are prescribed to combat
infection from contamination.

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 The pleural cavity can be decompressed by needle aspiration
(thoracentesis) or chest tube drainage of the blood or air.
 The lung is then able to re-expand and resume the function of
gas exchange.
 As a rule of thumb, the chest wall is opened surgically
(thoracotomy) when more than 1,500 mL of blood is aspirated
initially by thoracentesis (or is the initial chest tube output) or
when chest tube output continues at greater than 200
mL/hour.
 The urgency with which the blood must be removed is
determined by the respiratory compromise.
 An emergency thoracotomy may also be performed in the
emergency department if there is suggested cardiovascular
injury secondary to chest or penetrating trauma.

CARDIAC TAMPONADE
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 Cardiac tamponade is the compression of the heart
as a result of fluid within the pericardial sac.
 It usually is caused by blunt or penetrating trauma to
the chest.
 A penetrating wound of the heart is associated with a
high mortality rate.
 Cardiac tamponade also may follow diagnostic
cardiac catheterization, angiographic procedures,
and pacemaker insertion, which can produce
perforations of the heart and great vessels.

CARDIAC TAMPONADE Cont …d
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 Pericardial effusion with fluid compressing the
heart also may develop from metastases to
the pericardium from malignant tumors; such
as:
 Breast,
 lung, and mediastinum
 and may occur with lymphomas and
leukemias,
 Renal failure,
 TB, and high-dose radiation to the chest.

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Pneumothorax 579
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 Literally means “air in the chest”
 Is used to describe conditions in which air has entered the
pleural space outside the lungs.
TYPES
1.Simple Pneumothorax or spontaneous pneumothorax
occurs when air enters the pleural space through a breach of
either the parietal or visceral pleura.
It may be associated with diffuse interstitial lung disease and
severe emphysema.

Pneumothorax……
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2. Traumatic pneumothorax
Occurs when air escapes from a laceration in the lung itself
and enters the pleural space or from a wound in the chest
wall.
It may result from blunt trauma (eg, rib fractures),
penetrating chest or abdominal trauma (eg, stab wounds or
gunshot wounds), or diaphragmatic tears.
Occur during invasive thoracic procedures (ie,
thoracentesis, transbronchial lung biopsy, insertion of a
subclavian line)
Chest surgery

Pneumothorax……
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3. Tension pneumothorax
 If a pneumothorax is closed, air, and therefore tension,
builds up in the pleural space.
 In tension pneumothorax, air enters but cannot leave the
chest.
 As the pressure increases, the heart and great vessels are
compressed and the mediastinal structures are shifted
toward the opposite side of the chest.
 The trachea is pushed from its normal midline position
toward the opposite side of the chest, and the unaffected
lung is compressed.

Open Pneumothorax Vs Tension
Pneumothorax
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In open pneumothorax, air enters the chest during
inspiration and exits during expiration. A slight shift of
the affected lung may occur because of a decrease in
pressure as air moves out of the chest.
In tension pneumothorax, air enters but cannot leave
the chest. As the pressure increases, the heart and
great vessels are compressed and the mediastinal
structures are shifted toward the opposite side of the
chest.

Pneumothorax……
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 Clinical Manifestations
 Signs and symptoms associated with pneumothorax depend
on its size and cause
Pain(sudden & plueritic)
Dyspnea
Respiratory distress
Increased use of accessory muscles
Centeral cynosis
Expansion of chest decreased
Breath sound may diminished
Normal sounds or hyperresonance on percussion.


Pneumothorax……
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 In a tension pneumothorax,
The trachea is shifted away from the affected side
Chest expansion may be decreased or fixed in a
hyperexpansion state.
Breath sounds are diminished or absent
Percussion to the affected side is hyperresonant.

HEMOTHORAX.
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 It is the presence of blood in the pleural space.
 Can occur with or without accompanying pneumothorax.
 Cause:-
Traumatic injury (often).
Lung cancer,
Pulmonary embolism
Anticoagulant use.

HEMOTHORAX. ……
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Diagnostic Tests
History
Physical examination
Chest x-ray examination
Arterial blood gases and oxygen saturation

HEMOTHORAX. ……
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Medical Management
Depends on its cause and severity.
The goal of treatment is to evacuate the air or blood from
the pleural space.
A small pneumothorax :_
- May absorb with no treatment other than rest
-Trapped air may be removed with a small bore needle
inserted into the pleural space
Chest tubes connected to a water seal drainage system are
used to remove larger amounts of air or blood from the
pleural space.

HEMOTHORAX. ……
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If the pneumothorax is recurrent
Other treatments can be used to prevent additional episodes.
Sterile talc or certain antibiotics (such as tetracycline) can
be injected into the pleural space via thoracentesis, irritating
the pleural membranes and making them stick together,
-this is called pleurodesis or sclerosis.

CHEST TUBES AND PLEURAL DRAINAGE
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 Whenever fluid or air accumulates in the pleural space,
the pressure becomes positive instead of negative and
the lungs collapse.
 Chest tubes are inserted to drain the pleural space and
reestablish negative pressure, allowing for proper lung
expansion.
 Tubes may also be inserted in the mediastinal space to
drain air and fluid postoperatively.
 Chest tubes are approximately 20 inches (51 cm) long
and vary in size from 12F to 40F.
 The size inserted is determined by the patient’s
condition. Large (36F to 40F) tubes are used to drain
blood, medium (24F to 36F) tubes are used to drain
fluid, and small (12F to 24F) tubes are used to drain air.

Chest Tube Insertion
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 Insertion of a chest tube can take place in the
emergency department, at the patient’s bedside, or in
the operating room.
 The patient is positioned with the arm raised above the
head on the affected side to expose the midaxillary
area, the standard site for insertion.
 Elevate the patient’s head 30 to 60 degrees, when
possible, to lower the diaphragm and reduce the risk of
injury.
 A chest x-ray is used to confirm the affected side.
 The area is cleansed with an antiseptic solution.

Chest Tube Insertion
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 The chest wall is prepared with a local anesthetic, and a small
incision is made over a rib.
 The chest tube is advanced up and over the top of the rib to
avoid the intercostal nerves and blood vessels that are behind
the rib inferiorly.
 Once inserted, the tube is connected to a pleural drainage
system
 Two tubes may be connected to the same drainage unit with a
Y-connector.
 The incision is closed with sutures, and the chest tube is
secured.
 The wound is covered with an occlusive dressing.
 Some clinicians prefer to seal the wound around the chest
tube with petroleum gauze.
 Proper tube placement is confirmed by chest x-ray.

Chest Tube Insertion Cont …d
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 Pleural Drainage
The second type of chest drainage is larger and less
portable, and it contains three basic compartments,
each with a separate function (see Fig. 28-8).
 The first compartment, or collection chamber, receives
fluid and air from the pleural or mediastinal space.
 The drained fluid stays in this chamber while the air
vents to the second compartment.
 The second compartment, called the water-seal
chamber, contains 2 cm of water, which acts as a one-
way valve.
 The incoming air enters from the collection chamber and
bubbles up through the water.

Pleural Drainage Cont …d
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 The water prevents backflow of air into the patient from
the system.
 Initially, brisk bubbling of air occurs in this chamber when
a pneumothorax is evacuated.
 Intermittent bubbling during exhalation, coughing, or
sneezing (when the patient’s intrathoracic pressure is
increased) will continue as long as there is air in the
pleural space.
 As the source of the air in the pleural space gets smaller,
it will take more and more positive intrapleural pressure
to force air out.
 Eventually, the air leak seals and the lung is fully
expanded

Pleural Drainage Cont…d
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 The incoming air enters from the collection chamber and
bubbles up through the water.
 The water prevents backflow of air into the patient from the
system.
 Initially, brisk bubbling of air occurs in this chamber when a
pneumothorax is evacuated.
 Intermittent bubbling during exhalation, coughing, or sneezing
(when the patient’s intrathoracic pressure is increased) will
continue as long as there is air in the pleural space.
 As the source of the air in the pleural space gets smaller, it will
take more and more positive intrapleural pressure to force air
out.
 Eventually, the air leak seals and the lung is fully expanded

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 Normal fluctuation of the water within the water-seal
chamber is called tidaling.
 This up and down movement of water in concert with
respiration reflects the intrapleural pressure changes
during inspiration and expiration.
 Investigate any sudden cessation of tidaling, since this
may signify an occluded chest tube.
 Gradual reduction and eventual cessation of tidaling are
expected as the lung reexpands.
 The parietal and visceral pleura will form a tight seal
around the chest tube openings, obliterating the
response to changes in intrapleural pressures with
respiration.

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 The third compartment, the suction control chamber, applies
suction to the chest drainage system.
 There are two types of suction control: water and dry.
 The water suction control chamber uses a column of water
with the top end vented to the atmosphere to control the
amount of suction from the wall regulator.
 The chamber is typically filled with 20 cm of water.
When the negative pressure generated by the suction source
exceeds the set 20 cm, air from the atmosphere enters the
chamber through the vent on top and the air bubbles up
through the water, causing a suction-breaker effect.
 As a result, excess pressure is relieved.

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HEMOTHORAX. ……
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Nursing management
Close monitoring & frequent assessment of:-
 Level of consciousness,
 Skin and mucous membrane color,
 Vital signs,
 Respiratory rate & depth
 Presence of dyspnea,
 Chest pain,
 Restlessness, or anxiety
 Lung sounds

EMPYEMA
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An accumulation of thick, purulent fluid within the pleural space,
often with fibrin development and a loculated (walled-off) area
where infection is located.
Pathophysiology
Most empyemas occur as complications of bacterial pneumonia or
lung abscess.
Penetrating chest trauma, hematogenous infection of the pleural
space, nonbacterial infections, and iatrogenic causes (after thoracic
surgery or thoracentesis).
At first the pleural fluid is thin, with a low leukocyte count, but it
frequently progresses to a fibropurulent stage
Finally, to a stage where it encloses the lung within a thick
exudative membrane (loculated empyema).

Cont… d
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Fever
Night sweats
Pleural pain
Cough
Dyspnea
Anorexia
Weight loss

Cont …d
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 Assessment and Diagnostic Findings
 Chest auscultation(decreased or absent breath
sounds over the affected area.
 Chest percussion there is dullness on as well as decreased
fremitus.
 The diagnosis is established by chest CT.
 Usually a diagnostic thoracentesis is performed, often
under ultra sound guidance

Medical Management
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The objectives of treatment are
 To drain the pleural cavity
 To achieve complete expansion of the lung.
Fluid is drained, and appropriate antibiotics (Sterilization
of the empyema cavity requires 4 to 6 weeks of
antibiotics) are used.

Cont …d
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373
Drainage of the pleural fluid depends on the stage of the
disease and is accomplished by one of the following methods:
Needle aspiration (thoracentesis) with a thin percutaneous
catheter, if the volume is small and the fluid is not too
purulent or too thick.
Tube thoracostomy (chest drainage using a large diameter
intercostal tube attached to water-seal drainage.
Open chest drainage via thoracotomy, including potential
rib resection, to remove the thickened pleura, pus, and debris
and to remove the underlying diseased pulmonary tissue.

Nursing management
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 Instructs the patient in lung-expanding breathing
exercises to restore normal respiratory function.
 Provides care specific to the method of drainage of the
pleural fluid (eg, needle aspiration, closed chest
drainage, rib resection and drainage

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SUBCUTANEOUS EMPHYSEMA
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 When the lung or the air passages are injured, air may
enter the tissue planes and pass for some distance under
the skin (eg, neck, chest).
 The tissues give a crackling sensation when palpated,
 Fortunately, subcutaneous emphysema is of itself usually
not a serious complication.
 The subcutaneous air is spontaneously absorbed if the
underlying air leak is treated or stops spontaneously.
 In severe cases in which there is widespread
subcutaneous emphysema, a tracheostomy is indicated if
airway patency is threatened.

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379

PULMONARY TUBERCULOSIS
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In 46o B.C. The Greek physician Hippocrates
described tuberculosis as an "almost always fatal disease
of the lungs.
Called phthisis from Greek term phthinein which
means wasting or decay.
In English, pulmonary TB was long known by the term
“consumption.” disease would have felt hopeless,
much like how people feel about many cancers
today.
TB was treated with gold, arsenic, cod liver oil,
herbs, bed rest, sunshine and fresh air, etc.

Tuberculosis (TB)-Definition
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 Neo-Latin word :
Tubercle”-Round nodule/Swelling
“Osis” – Condition
 Tuberculosis (TB) :
Is an infectious disease that primarily affects the lung
parenchyma.
Is a potentially fatal contagious disease that can affect almost
any part of the body but is mainly an infection of the lungs.
Is a chronic bacterial infectious disease that primarily affects
the lungs, but can also infect other organs in the body.
 It also may be transmitted to other parts of the body, including the
meninges, kidneys, bones, and lymph nodes.

Cont …d
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 The primary infectious agent, M. tuberculosis, is an acid-fast
aerobic rod that grows slowly and is sensitive to heat and
ultraviolet light.
 Mycobacterium bovis and Mycobacterium avium have rarely
been associated with the development of a TB infection
 Common causative bacilli:
Mycobacterium tuberculosis (most cases)
M. bovis – bovine tubercle bacillus
M. Africana – West Africa
M. Microti
M. Canetti

MODE OF TRANSMISSION
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Airway droplets: the main mode of transmission from person infected with
pulmonary TB to others by respiratory droplets.
Ingestion: Less frequently transmitted by ingestion of mycobacterium bovis
found in unpasteurized milk products
Direct inoculation
TB spreads from person to person by airborne transmission.
An infected person releases droplet nuclei (usually particles 1 to 5 um in
diameter) through talking, coughing, sneezing, laughing, or singing.
Larger droplets settle; smaller droplets remain suspended in the air and are
inhaled by a susceptible person.

Factors influence transmission
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 The number of bacilli in the droplets,
 The virulence of the bacilli,
 Exposure of the bacilli to UV light,
 Degree of ventilation, and
 Occasions for aerosolization all influence
transmission

HIGH RISK FOR PROGRESSION
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 Persons more likely to progress from LTBI to TB disease
includes:
 HIV infected persons
 Persons with a history of prior, untreated TB or fibrotic
lesions on CXR
 Recent TB infection (within the past 2 years)
 Injection drug users
 Age ( very young or very old)
 Patients with certain medical conditions ( DM, chronic
renal failure, hemodialysis, solid organ transplantation,
cancer, malnourished patient, silicosis)

SPREAD OF TB TO OTHER PARTS OF
THE BODY
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Spread if infection will take place by:
A. Local spread: to the surrounding lung tissue and pleura
B. Lymphatic spread: along bronchi, leading to
tuberculous bronchopneumonia
C. Hematogenous spread: leading to:
 Lungs (85% of all cases)
 Pleura
 CNS
 Lymph nodes
 Genitourinary system
 Bones and joints
 Disseminated ( eg miliary)

Classification
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 Tuberculosis
Pulmonary TB
oPrimary Disease
oSecondary Disease
Extra pulmonary
i. Lymph node TB
ii. Pleural TB
iii. TB of upper airways
iv. Skeletal TB
v. Genitourinary TB
vi. Miliary TB
vii. Pericardial TB
viii. Gastrointestinal TB
ix. Tuberculous Meningitis

Pathogenesis
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Exposure to the
source
Aerosolizatio
n of droplet
nuclei
Inhalation
of the
bacteria
Bacteria reach
the lung ,enter
the
macrophages
Bacteria
multiply in the
macrophages
Granulomatous
lesion begin to
form caseous
necrosis
Bacteria
cease to
grow, lesion
calcify
Reactivatio
n
Lesion liquefies
Bacteria
coughed up
in the sputum
Spread blood
, organs
Death

Primary pulmonary TB
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Also called ghon’s complex or childhood tuberculosis.
Is an infection of persons who have not had prior contact with the tubercle
bacillus
The infection of an individual who has not been previously
infected or immunized
Lesions forming after infection is peripheral and accompanied by
hilar which may not be detectable on chest radiography.
Inhaled bacilli are commonly deposited in alveoli immediately beneath the
pleura, usually in the lower part of the upper lobes or the upper part of the
lower lobes
Macrophages ingest the bacilli and transport them to
regional lymph nodes

Primary infection----
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 The primary infection characteristically produces a " Ghon
complex" formed of:
 Ghon focus: small area of pneumonic consolidation about 1-3 cm
in diameter, sub pleural in location present in the base of the upper
lobe or apex of the lower lobe
 Tuberculous lymphangitis: of the draining
lymphatic channels
 Tuberculous lymphadenitis: of the tracheobronchial nodes which
are enlarged, matted together and their cut surface show areas of
caseous necrosis

MICROSCOPIC PICTURE
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 The Ghon focus consists of a central area of pink caseous
necrosis surrounded by inflammatory infiltrate and walled of by
an area of granulation tissue containing multinucleated
Langhans giant cells
FATE OF PRIMARY TB
 This depends on:
 Virulence of the organism
 Dose of infection
 Degree of resistance of the host
 A. If the patient resistance is good and the organism is of low
virulence, Ghon complex undergo healing and over time usually
evolve to fibrocalcific nodules
 B.If the patient resistance is poor and/or the organism of high virulence,
progressive pulmonary tuberculosis will develop, the primary Ghon focus in
the lung enlarges rapidly, erodes the bronchial tree, and spread

Secondary Tuberculosis
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 The infection that individual who has been previously
infected or sensitized is called secondary or post primary or
reinfection or chronic tuberculosis.

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 As the cellular processes tuberculosis develop differently,
according to the status of the patient’s immune system.
 Stages include latency, primary disease, primary
progressive disease, and extra pulmonary disease
Early infection
 Immune system fights infection
 Infection generally proceeds without signs or symptoms
 Patients may have fever, paratracheal lymphadenopathy,
or dyspnea
 Infection may be only subclinical and may not advance to
active

Early primary progressive (active)
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Immune system does not control initial infection
Inflammation of tissues ensues Patients often have
nonspecific signs or symptoms (eg, fatigue, weight loss,
fever)
Nonproductive cough develops
Diagnosis can be difficult: findings on chest radiographs
may be normal and sputum smears may be negative for
mycobacteria
Late primary progressive (active)
 Cough becomes productive
 More signs and symptoms as disease progresses
 Patients experience progressive weight loss, rales,
anemia
 Findings on chest radio - graph are normal

Latent
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 Mycobacteria persist in the body
 No signs or symptoms occur
 Patients do not feel sick
 Patients are susceptible to reactivation of disease
 Granulomatous lesions calcify and become fibrotic,
become apparent on chest radiographs
 Infection can reappear when immunosuppression
occurs

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Symptom of pulmonary TB
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 Productive cough lasting for more than 2 weeks(the most
common) .
 Shortness of breath,
 Chest pains and hemoptysis (coughing up blood)
 Lose appetite,
 Lose weight, fever or night sweats, or feel tired.
 Symptoms may vary depending on a person’s age, hiv status and
the site of the infection (pulmonary or extra pulmonary).

Diagnostic Tests For Tuberculosis
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 Sputum smear: Detect acid fast bacilli within 24hours
 Sputum culture: Identify Mycobacterium tuberculosis for
3-6 weeks with solid media, 4-14 days with high-pressure
liquid chromatography
 Polymerase chain reaction: Identify M tuberculosis
within hours
 Tuberculin skin test : Detect exposure to mycobacteria
within 48-72 hours
 Quanti FERON TB test: Measure immune reactivity to M
tuberculosis within 12 -24 hours
 Chest radiography : Visualize lobar infiltrates with
cavitations within minutes

Approaches for TB diagnosis
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 Medical history
2. Physical examination
3. Bacteriologic
◦ AFB Smear FM/ ZN
microscopy
◦ Culture & Drug
Susceptibility testing
◦ Molecular tests
4. Antibody detection
◦Tuberculin Skin Test
◦IGRA
5. Radiology
◦ Chest radiography
◦ CT scan
◦ Ultrasound
6. Histo-pathologic exam
◦ FNAC, Biopsy
7. Other Nonspecific Tests like
o ESR,CRP

Currently recommended diagnostic
methods
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 Conventional Phenotypic Methods
• AFB Microscopy /ZN and FM Methods
• Culture Identification
• Culture-based drug susceptibility testing (DST)
2. Molecular Genotypic Methods
• Line Probe Assay
• GeneXpert MTB/RIF

Cont …d
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401
 History
 Physical examination
 Tuberculin skin test
 Chest x-ray(reveals lesions in the upper lobes)
 Acid-fast bacillus smear
 Sputum culture

MEDICAL MANAGEMENT
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 The two aims of TB treatment are :-
To interrupt transmission by rendering patients
noninfectious and
To prevent morbidity and death by curing patients with
TB while preventing the emergence of drug resistance.
Four major drugs are considered the first-line agents for
the treatment of TB: isoniazid, rifampin, pyrazinamide,
and ethambutol.

Cont …d
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403
Standard short-course regimens are divided into an initial, or
bactericidal, phase and a continuation, or sterilizing, phase.
During the initial phase, the majority of the tubercle bacilli are
killed, symptoms resolve, and usually the patient becomes
noninfectious.
The continuation phase is required to eliminate persisting
mycobacteria and prevent relapse.
The treatment regimen of choice for virtually all forms of TB in
adults consists of a 2-month initial phase of isoniazid, rifampin,
pyrazinamide, and ethambutol followed by a 4-month
continuation phase of isoniazid and rifampin
Streptomycin is the only anti-TB drug documented to
have harmful effects on the human fetus (congenital
deafness) and should not be used.

Recommended Antituberculosis Treatment Regimens
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Initial Phase Continuation
Phase
Indication Duration,
months
drugs Duration,
months
drugs
New smear- or culture-positive
cases
2 HRZE 4 HR
New culture-negative cases
2 HRZE 4 HR
Pregnancy 2
HRE 7 HR
Relapses and treatment default
(pending susceptibility testing)
3
HRZES 5 HRE
Abbreviation:- E, ethambutol; H, isoniazid; R, rifampin; S, streptomycin Z, pyrazinamide.

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