ADULT RESPIRATORY

CONDITIONS
BY:
JANE B. ARIEMBA
MAIN OBJECTIVE
• The student will acquire appropriate
knowledge, skills, and attitude for nursing
patients with respiratory tract illness
CONTENT
Review Anatomy and physiology of the
respiratory system
Describe respiratory tract diseases:
• Viral rhinitis/coryza/common cold
• Acute pharyngitis
• Laryngo-tracheo bronchitis
• Acute bronchitis
• Bronchiolitis
• Pneumonia
• Bronchial asthma
 Cont….
• Bronchiectasis
• COPD- Emphysema and chronic bronchitis
• Empyema
• Pleurisy
• Pleural effusion
• Lung abscess
• Haemothorax
• Pneumothorax
• Cancer of the lung
• Occupational lung diseases
 CORYZA/VIRAL RHINITIS(common cold)
• Most frequent viral infection in the general
population.
• The term “cold "refers to an afebrile, infectious,
acute inflammation and irritation of the mucous
membrane of the nasal cavity characterized by
nasal congestion, rhinorrhea, sneezing, sore
throat and general body malaise.
• Broadly, the term refers to an acute URI,
whereas terms such as “rhinitis”, “pharyngitis”,
and “laryngitis” distinguish the sites of
symptoms.
 Cont….
• “Flu”- Used when the causative virus is
influenza.
• Colds are highly contagious, coz virus is shed
for about 2 days before the symptoms appear
and during the 1st part of the symptomatic
phases . Rhinitis is classified as non allergic or
allergic, can be acute or chronic depending on
duration of infection.
 Virus implicated in the common cold
• Rhinoviruses- 40%
• Corona viruses
• Adenovirus
• Respiratory syncytical virus (RSV)
• Influenza virus
• Para influenza virus
Note!
 Each virus may have multiple strains hence the
challenge in developing a vaccine.
 Cold temp and exposure to cold rainy weather
do not increase the incidence or severity of
the common cold.
 Rhinitis can also be caused by environmental
factors such as temperature change or
humidity, odors, foods ,infections, age, drugs.
 Pathophysiology

Oedema and enlargement of the mucus

membrane and conchae develops. This
occludes the sinus openings and increases
mucus discharge.
 Clinical manifestations
• Nasal congestion
• Rhinorrhea
• Nasal discharge
• Sneezing
• Tearing watery eyes
• Scratchy or sore throat
• General malaise
• Low grade fever
• Chills
 Cont….
• Headache
• Muscle aches
• Cough
• Herpes simplex “cold sore”-In some people is
exacerbated by viral rhinitis.
• The symptoms last for 1 to 2 weeks and are
self limiting.
Cold sore
Note!
o If there is significant fever or more severe
systemic respiratory symptoms, it is no longer
considered viral rhinitis but one of the other
acute URIs.
o Allergic conditions can also affect the nose
mimicking the symptoms of the cold.
 Med mx
.No specific treament for common cold or influenza. Rx is
symptomatic

• Rest
• Prevent chilling
• Expectorants
• Warm salty water gargle for sore throat
• NSAIDs
• Antihistamines
• Topical nasal decongestants e.g. saline nose drops
 Nursing mx
 Teaching on prevention and management of
URIs.
Prevention
• Hand hygiene.
• Use disposable tissues.
• Cover mouth when coughing or sneezing.
• Avoid crowds esp. during flu season.
• Avoid people with infections.
• Annual influenza vaccination.
 Cont….
• Practice good health habits:
Adequate nutrition.
Adequate sleep, rest and exercise.
Avoid tobacco use.
Avoid smoking or second smoke.
Avoid irritants- dust, chemicals.
Use air conditioning/filters.
Prompt checkup and tx for infection.
 ACUTE PHARYNGITIS

• Is a sudden inflammation of the pharynx.

• The primary symptom is sore throat.
• Most cases are due to viral infection .
• Group A beta haemolytic streptoccoci is the
most common bacterial organism that causes
acute pharyngitis.
 Etiology
• Mostly caused by viral infection – adenovirus,
influenza, epstein-barr and herpes simplex.
• Bacterial organisms- group A beta-hemolytic
streptococci, neisseria gonorrhea, h. influenza
type B and mycoplasma.
 Pathophysiology
• Following viral or bacterial infection in the
pharynx, the body responds by triggering an
inflammatory response in the pharynx.
• This results in pain, fever, vaso dilation, 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.
 Clinical manifestations
• Fiery-red pharyngeal membrane and tonsils.
• Swollen lymphoid follicles flecked with white-
purple exudate.
• Enlarged and tender cervical lymph nodes .
• Fever, malaise, sore throat.
• Vomiting , anorexia and a scarlatina-form rash
with urticaria (Grp A Beta-hemolytic
streptococcal).
• No cough.
A, Redness and vascularity of the pillars and uvula are
mild to moderate.
B, Redness is diffuse and intense.
 Diagnostic tests
• Rapid strep test( RST) and strep culture (STCX)
• Blood culture to identify causative organism.
• Nasal swaps to identify causative organism.
 Med mx
• Pharmacology
Antibiotics- penicillins, erythromycin,
cephalosporins and macrolides (clarithromycin
and azithromycin).
Analgesics.
Nutrition
A liquid soft diet.
Warm liquids.
IV fluids.
 Nursing mx
• Drug adm
• Pt educ
• V/S
• Warm saline gargle/throat irrigations
• Mouth care
 Complications
• Uncomplicated viral infections usually subside promptly
within 2 to 3 days after onset. However pharyngitis due to
Group A Beta hemolytic streptoccal can cause severe illness.
• Untreated pharyngitis can complicate to:-
 Sinusitis
 Otitis media
 Peritonsillar abscess
 Mastoiditis
 Cervical adenitis
 Bacteremia
 Pneumonia
 Meningitis
 Rheumatic fever
 Nephritis
 CHRONIC PHARYNGITIS
• Is persistent inflammation of the pharynx.
• Is common in adults who live in dusty areas, who use their
voice much, suffer from chronic cough and habitual users of
alcohol and tobacco.
Chronic pharyngitis are of 3 types:-
 Hypertrophic:- is characterized by general thickening and
congestion of the pharyngeal mucous membrane.
 Atrophic:- is the late stage of hypertrophic pharyngitis. The
membrane is thin ,whitish, glistening, and at times wrinkled.
 Chronic granular( clergy man sore throat) :- characterized by
numerous swollen lymph follicles on the pharyngeal wall.
 Signs and Symptoms.
• Constant irritation.
• Fullness in the throat.
• Coughing.
• Difficult in swallowing.

Nursing Management.
• Symptomatic treatment since it is a viral infection.
• Avoid exposure to irritants such as smoking and alcohol.
• Early treatment of any upper respiratory, pulmonary, or cardiac
condition responsible for chronic cough.
• Nasal congestion is relieved by nasal drops or sprays containing
ephedrine( it works by narrowing the blood vessels in the nasal
area ,reducing swelling and congestion).
• Give antihistamines ( especially histamine 1 receptor
antagonist) e.g chloropheniramine 4mg or cetrizine.
• NSAIDS( Non steroidal anti-inflammatory drugs ) e,g
Aspirin and acetaminophen. These have analgesic and
anti-inflammatory action.
• Give health education to the patient to avoid alcohol,
tobacco use or second hand smoking , use protective
gears to avoid environmental or occupational pollutants.
• Take plenty of oral fluids.
• Warm saline gargles to sooth the throat.
 ACUTE SINUSITIS
• Definition:- is a sudden inflammation of the nasal sinuses.
Sinuses are 4 in number –frontal, ethmoidal, sphenoidal and
maxillary.
• Are lined with nasal mucosa and numerous goblet cells.
• Sinuses are connected with a series of ducts that drain into the
nasal cavity.
• Sinuses help in sound resonance and protect the brain in frontal
trauma. In URTI sinuses are highly involved , if their openings into
nasal passages are clear infections resolve promptly but if their
drainage is obstructed e.g by deviated septum, hypertrophied
turbinates, nasal polyps or tumors, sinus infection may persit as
secondary infection or progress to acute suppurative process.
• Sinusitis affects over 14% of the population .
Some people are more prone to sinusitis
because of their occupations e.g continuous
exposure to environmental hazards like
chemicals may result in chronic inflammation.
 Pathophysiology
• Acute sinusitis is an infection of the paranasal
sinuses. It develops as a result of upper
respiratory tract infections like unresolved
viral or bacterial infections or allergic rhinitis.
There is nasal congestion caused by
inflammation , edema and and transudation of
fluid leading to obstruction of the sinus
cavities. These provides a good media for
bacterial growth .
 Organisms that cause sinusitis.
• Bacterial organisms account for 60% of acute
cases of sinusitis.
• Streptococcus pneumonae.
• Haemophilus infuenzae.
• Moraxella catarrhalis.
• Dental infections cause acute sinusitis.
Aspergilus fumigatus:- is associated with fungal
sinusitis. Especially in immunocompromised
patients.
 Signs and symptoms.
• Facial pain or pressure over the affected sinus.
• Nasal obstruction.
• Fatigue .
• Purulent nasal discharge.
• Fever.
• Headache.
• Ear pain and fullness.
• Dental pain .
• Cough.
• Decreased sense of smell.
• Sore throat.
• Eyelid edema.
• Facial congestion or fullness.
 Note!
• Acute sinusitis is difficult to differenciate from allergic
rhinitis or URTI.
Diagnosis.
• History taking.
• Physical examination:- examine the nose, ears,
teeth ,sinuses ,pharynx.
• X-ray to detect sinus opacitis, mucosal thickness, bone
destruction and air fluid levels.
• CT scan (Computerized tomography scanning):- to rule
out tumors ,fistula and allergy.
 Complications of acute sinusitis.
• Meningitis.
• Brain abscess.
• Ischaemic infarction.
• Ostiomyelitis.
• Chronic sinusitis.
 CHRONIC SINUSITIS
• Definition:- is inflammation of the sinuses
that persists for more than 3 weeks in adults
and 2 weeks in children.
• Around 33 million people a year worldwide
develop chronic sinusitis .
 Pathophysiology.
• The narrowing or obstruction in the opening
of the sinuses i.e. frontal, ethmoidal, maxillary
prevent adequate drainage to nasal passages.
• Secretions stagnate forming an ideal media for
bacterial infection. Immunocompromised
patients are at risk of developing fungal
sinusitis with Aspergillus Fumigatus being the
most common causative organism.
 Signs and symptoms
• Impaired mucociliary clearance and ventilation.
• Cough (because the thick discharge constantly drips
backward into the nasopharynx ).
• Chronic hoarseness of voice.
• Chronic headache in the periorbital region.
• Frontal pain.
• Fatigue .
• Nasal stuffiness.
• Decrease in smell and taste.
• Fullness in the ears.
 Diagnosis
• History taking.
• Physical examination.
• CT scan and MRI:- to rule out local and
systemic infections like tumors, fistula and
allergy.
• Nasal endoscopy.
 Complications of chronic sinusitis
• Severe orbital cellulitis.
• Sub-periosteal abscess.
• Cavernus sinus thrombosis.
• Meningitis.
• Encephalitis.
• Ichaemic infarction.
 Medical management.
• Antimicrobial agents :- Augumentin,
cephalosporines, quinolonines.
• Anthistamines.
• Corticosteroids
Surgical management.
Using endoscopy surgery is performed to correct
deformities that obstruct the openings of the
sinuses. This include excising and cauterizing of nasal
polyps, correcting deviated septum, incising and
draining the sinuses and tumor removal.
 Health Education to the Patient.
• Patient to take plenty of oral fluids i.e warm
water, flesh juice .
• To take medications as prescribed and ensure
the dose is completed especially Antibiotics to
prevent drug resistance.
• Teach the patient on the condition( sinusitis) ,
how to recognize it early and its preventive
measures.
 LARYNGITIS.
• Definition:- Is inflammation of the larynx or
voice box that causes the voice to become
raspy or hoarse.
• Laryngitis can be acute or chronic depending
on the duration. In most cases it comes on
quickly and lasts for not more than 2 weeks.
Chronic symptoms lasts for 2 weeks or more.
 Causes of Laryngitis.
• Most common cause is colds or flue.
• Overuse of voice such as singing or cheering in a
sports event.
• Chemical inhalation like exposure to industrial
chemicals.
• Irritation from allergies or smoke.
• Problems with the way you talk or sing like some
preachers.
• Use of inhaled steroids( e.g those used to treat
asthma).
Acid reflux(GERD):- common cause of chronic
laryngitis. Other causes of chronic laryngitis
include nerve damage, polyps, cancer, nodules
on vocal cords.
 Clinical manifestations .
• Hoarseness of voice because of vocal cords
involvement.
• Aphonia (complete loss of voice).
• Severe coughing.
• Sore throat .
• Difficult in swallowing.
 Diagnosis.
• History taking.
• Physical examination.
Management.
Rest your voice as much as you can, talk softly
but do not whisper( whispering irritates the
larynx more than soft speaking).
Avoid smoking or smoky areas.
Drink plenty of fluids.
 Nursing Process of Upper
Respiratory Conditions.
Assessment Data:-
• Hx taking –headache, sore throat, dysphagia,
cough, fever, hoarsness of voice,
• Physical exam.- Nasal discharge,

Nursing Diagnosis.
 Ineffective airway clearance related to airway
obstruction by excessive mucus production or
inflammation as evidenced by nasal congestion.
 Nursing Diagnosis of URTI cont.
• Acute pain related to inflammation as
evidenced by patient verbalizing of nasal pain
or irritation.
• Fluid volume deficit related to nasal discharge
as evidenced by dryness of the mucus
membrane.
• Knowledge deficit related to prevention of
URTI ,treatment regimen as evidenced by
patient asking questions.
• Impaired verbal communication related to
inflammation of the vocal cords as evidenced
by hoarseness of voice.
 Planning
Goals.
Maintenance of patent airway.
Relief of pain.
Maintenance of normal hydration.
Adequate knowledge on how to prevent URTI.
Promoting verbal communication.
Absence of complications.
 Nursing Interventions.
Maintaining patent airway.
• Increase fluid intake to help thin the mucus
for easy expectoration.
• Use of steam inhalations to loosen the mucus
and reduce inflammation of mucus
membranes.
• Postural drainage.
 Relief pain and promote comfort.
• Use of analgesics.
• Warm gargles to relief pain of sore throat.
• Adequate rest to relief generalized body
malaise.
• General hygiene to prevent spread of
infection.
 Maintenance of normal hydration
• In URTI fluid loss is due to increased
respiratory rate, inflammation( increased
secretions) ,increased metabolic rate,
diaphoresis and fever.
• Encourage the patient to drink plenty of fluids
to thin secretions and promote drainage.
Knowledge on Prevention of URTI.
• Prevent spread of infections to others by
practising hand hygiene, avoid overcrowding
and adequate immunization.
• Practise good health habits through having
enough rest, take a nutrious diet, appropriate
exercise, avoid smoking or second hand
smoking and alcohol intake.
• Avoid allergens.
Managing potential complications.
• Teach the patient on signs and symptoms that
require immediate attention including
persistent high fever, increasing shortness of
breath, confusion, increasing weakness and
malaise.
• Administer antibiotics where necessary.
• Monitor vital signs.
Promoting verbal communication.
• Patient to refrain from verbal communication
as much as possible to rest the vocal cords and
enhance the return of voice.
 "It is nice to have money and the
things that money can buy, but
it's important to make sure you
haven't lost the things money
can't buy."
George Lorimer
1867-1937, Editor of "Saturday Evening Post"

01/27/2025 Dr. Wekesa . Dept of Pathology . Eger

ton University
 ACUTE BRONCHITIS
• Inflammation of the mucous membrane of the
bronchial airways.
 Etiology
1. Viruses- influenza
2. Bacteria- streptococcus, pneumococcus,
staphylococcus, and haemophilus
3. Physical and chemical agents- dusts and
fumes
 Pathophysiology
• Infection is often preceded by URTIs.
• Airways become inflamed and irritated with
increased mucous production
 Clinical Manifestations
• Dyspnea
• Fever
• Tachypnea
• Productive cough, clear to purulent sputum
• Pleuritic chest pain- occasionally
• Diffuse rhonchi and crackles heard on
auscultation
 Diagnostic Evaluation
• Chest X-ray
• Sputum culture
• PFTs
• ABGs
 Mx
• Antibiotics for 7 to 10 days
• Hydration and humidification
• Secretion clearance interventions- controlled
cough, chest physiotherapy
• Bronchodilators
• Symptomatic mx- fever, cough, chest pain
 Nursing mx
• Administer or teach self-administration of drugs
• Encourage mobilization of secretions through
hydration, physical therapy and coughing
o Educate patient that beverages with caffeine or
alcohol do not promote hydration because of
their diuretic effect
o Caution pt on the use of over-the-counter cough
suppressants, antihistamines and
decongestants- may cause drying and retention
of secretions
 Cont….
• Health educ and maintenance:
medication regimen.
worsening of condition .
dry cough may persist after bronchitis due to
irritation of airways- use humidifier and avoid
dry env.
Alternative therapies- garlic, eucalyptus.
 PNEUMONIA
• Inflammation of the alveoli, interstitial tissue
and bronchioles of the lungs (lung
parenchyma).
 Etiology
• Bacteria- streptococcus, pneumonia,
h.influenza, staphylococcus aureus; klebsiella
pneumoniae and legionella pneumophillia(in
pts with chronic disease)
• Adenovirus and influenza virus (atypical
pneumonia), resp syncytial virus (severe
pneumonia esp in children), viral upper resp
infections
• Mycoplasma pneumoniae
• Fungi- candida albicans in the
immunosuppressed
 Other predisposing factors
 Smoking
 General anaesthesia
 Chronic bronchitis
 Immobility
 Endotracheal intubation/respiratory instrumentation
 Aspiration of gastric contents
 Inhalation of smoke or toxic gases
 Physical trauma
 ISS
 Tumor
 Drugs- depress central nervous system

 Pathophysiology
• Pneumonia occurs when an organism
overcomes the body’s defenses in the resp.
tract, mucous and cilia in the upper airways that
trap pathogens, alveolar macrophages, and
neutrophils drawn to the tissues as needed.
• The predisposing factors can inhibit the
mucociliary system, enabling pathogens to
reach the alveoli and overwhelm the phagocytic
cells.
• Also some organisms release enzymes or toxins
that disable the mucociliary or macrophage
 Cont….
• Aspiration of gastric contents, inhalation of smoke
or toxic gases, physical trauma and some chronic
diseases destroy cells in the bronchial epithelium
or alveoli, creating significant inflammation that
makes it easier for the pathogens to gain entry.
• Septicemia may bring pathogens from other sites
to the pulmonary capillaries, where they cross
into interstitial tissue.
• Following all these events, inflammation and the
specific immune response cause alveolar edema
and white blood cell aggregation, producing
congestion that inhibits gas exchange and causes
 Classifications of pneumonia
A. According to causative organism
• Bacterial-typical
• Atypical- viral
• Anaerobic/cavitary
• Opportunistic
 Cont….
B. According to how it is acquired:
• Community-acquired pneumonia.
• Hospital acquired (nosocomial) pneumonia.
• Pneumonia in the immunocompromised host-
(PCP).
• Aspiration pneumonia.
 Cont….
C. According to site:
• Lobar pneumonia- affects most of the entire
lobe.
• Bronchopneumonia- involves smaller areas in
several lobes, particularly in the periphery of
the lung.
• Interstitial pneumonia- involves tissues
surrounding the alveoli and bronchi.
 Clinical Manifestations
• Sudden onset; shaking chill; rapidly rising fever
0 0
of 39.5 C to 40.5 C.
• Cough productive of purulent sputum.
• Pleuritic chest pain aggravated by respiration
or coughing.
• Dyspnea.
• Tachypnea with resp grunting.
• Nasal flaring.
• Use of accessory muscles of respiration.
• Fatigue.
 Cont….
• Rapid bounding pulse.
• Crackles, rhonchi and decreased breath
sounds on auscultation.
• Elevated WBCs.
 Diagnostic evaluation
• Chest x-ray- show white infiltrates in the
affected area.
• Gram’s stain, culture and sensitivity studies of
sputum.
• Blood culture- detect bacteremia.
• CBC.
 MX
• Antimicrobial therapy
• Oxygen therapy
• Hydration
• Antipyretics
• Analgesics
• Antitusives
• Warm, moist inhalations- relieve bronchial
irritation
• Antihistamines
• Bed rest
 Complications
• Respiratory failure
• Sustained hypotension and shock esp in gram
negative bacterial disease and elderly
• Pleural effusion
• Atelectasis – due to secretions
• Superinfection- pericariditis, bacteremia, and
meningitis
• Delirium
 Nursing interventions
• Observe for cyanosis, dyspnea, hypoxia and
confusion, indicating worsening of condition.
• Follow ABGs/Sao2 to determine oxygen need
and response to therapy.
• Administer oxygen.
• Prop up pt.
• Frequent turning and increased activity as
tolerated.
• Encourage pt to cough.
• Suction prn.
 Cont….
• Humidify air or oxygen therapy.
• Chest wall percussion and postural drainage.
• Auscultate the chest for crackles and rhonchi.
• Administer cough suppressants when
coughing is non-productive – no evidence of
retained secretions.
• Pain mx.
• Monitor for potential complications.
• Patient education and health maintenance.
 Cont….
o Fatigue, weakness and depression may be
prolonged after pneumonia.
o Rest then increase activity gradually.
o Breathing exercises.
o Chest x-ray 4 to 6 wks after recovery.
o Smoking cessation.
o Adequate nutrition, rest.
o Immunization .
o Infection prevention and control .
 Nursing process of a patient with
pneumonia.
Assessment .
• History taking:- chest pain, cough mostly with
purulent sputum, fatigue, ……….
• Physical examination:- Fever, increased
respirations(tachypnea), use of accessory
musles of respiration, bradycardia …………..
• Investigations:- chest x-ray,………
 Nursing Diagnosis
• Infective airway clearance related to bronchial
inflammation or bronchial edema or increased
sputum production as evidenced by increased
respirations, use of accessory muscles of
respirations, dyspnea, cyanosis…..
• Impaired gaseous exchange related to altered
oxygen carrying capacity of blood as
evidenced by tachycardia or cyanosis, changes
in mental status…….
 Cont.
• Risk for deficient fluid volume related to
excessive fluid loss (fever, diaphoresis,
hyperventilation , vomiting) or decreased oral
intake.
• Risk for imbalanced nutrition less than body
requirements related to increased bodly
metabolic needs (because of fever or
infection) .
 Cont.
• Acute pain related to inflammation of the lung
parenchyma or persistent coughing as
evidenced by patient verbalizing of chest pain,
headache, guarding of the affected area.
 Planning- Goals.
• Improved airway patency.
• Adequate rest to conserve energy.
• Maintenance of proper fluid volume.
• Maintain adequate nutrition.
• Adequate Knowledge on pneumonia,
treatment protocol and its prevention.
• Monitoring and managing potential
complications.
 Nursing Interventions.
Improving airway patency.
• Adequate hydration 2 to 3 litres in 24 hours to
thin and loosen pulmonary secretions.
• Humidification to liquify secretions.
• Induce coughing.
• Chest physiotherapy (percussion and postural
drainage) loosens and mobilizes secretions.
Promoting rest and conserving energy.
• Patient to assume comfortable position and
rest e,g semi fowlers and change positions
frequently to enhance secretion clearance and
ventilation perfusion in the lungs.
 Promoting fluid intake.
• Increase fluid intake as per condition 2 to 3
litres a day.

Maintaining adequate nutrition.

Due to reduced appetite ,encourage patients to
take liquid nutrious diet with electrolytes and
calories
 BRONCHIAL ASTHMA
• Is a chronic inflammatory disease of the airways that
causes airway hyperesponsiveness, mucosal edema,
mucus production.
• Asthma differs from the other obstructive lung
diseases in that it is largely reversible, either
spontaneously or with treatment.
• Patients with asthma may experience symptom-free
periods alternating with acute exacerbations, which
last from minutes to hours or days.
• Asthma occurs at any age.
 Reduced airflow is caused by
1. Acute bronchoconstriction
2. Marked hypertrophy and hyperplasia of bronchial
smooth muscles
3. Mucus gland hypertrophy leading to excessive
mucus production and airway plugging.
4. Airway oedema.
5. Impaired mucociliary clearance .

92
 Etiology/Risk factors

1.Genetic Predisposition
This accounts for 50% of the susceptibility.

2.Environmental factors
This is illustrated by studies of occupational
asthma.

93
 Agents And Events Triggering Asthma:

1. Respiratory infection
Rhino virus, influenza, parainfluenza, mycoplasma
pneumonia.

2. Allergens
Air borne pollens (Grass, trees, weeds), house dust
mites, animal danders, cockroaches, fungal spores.

3. Environment
Cold Air, Fog, Ozone, Sulfur Dioxide, Nitrogen
Dioxide, Tobacco Smoke, Wood Smoke. 94
4. Emotions
Anxiety, stress, laughter.

5. Exercise
Particularly in cold dry climate.

6. Drugs and Preservatives

Aspirin, NSAIDS (COX inhibitors), Benzalkonium
Chloride, B – Blockers.

7. Occupational Stimuli
Bakers (flour dust), farmers (hay mold), printers (Arabic
gum), chemical workers (azo dyes).
95
 PATHOGENESIS OF ASTHMA
• Immunologic model of asthma presents it as a
disease mediated by the immunoglobulin IgE
that is produced in response to exposure to an
allergen.

• Once produced, IgE antibodies bind to mast

cells in the airway mucosa.

96
• On RE-EXPOSURE to a specific allergen, antigen-
antibody interaction on the surface of the mast
cells triggers both the release of mediators stored
in the cells' granules and the synthesis and release
of other mediators.

• The histamine, tryptase, leukotrienes C4 and D4,

and prostaglandin D2, when released, diffuse
through the airway mucosa triggering the muscle
contraction and vascular leakage responsible for
the acute bronchoconstriction of the "early
asthmatic response" 97
• Re-exposure to allergen also causes the
synthesis and release of a variety of cytokines
(interleukins 4 and 5, granulocyte-macrophage
colony stimulating factor (GM-CSF), tumor
necrosis factor (TNF), and tissue growth
factor) from T cells and mast cells.

98
• These cytokines in turn attract and activate
eosinophils and neutrophils, whose products cause
the edema, mucus hypersecretion, smooth muscle
contraction, and increase in bronchial reactivity
associated with the late asthmatic response.

• The late asthmatic response occurs 4-6 hours after

the early asthmatic response and is responsible for
the influx of inflammatory cells into the bronchial
mucosa and with an increase in bronchial
responsiveness that may last for several weeks
after a single inhalation of allergen.
99
 Signs and symptoms .
• The three most common symptoms of asthma are:-
 cough with or without mucus production.
 dyspnea .
 wheezing first on expiration and then during
inspiration as well.
• Asthma attacks often occur at night or early in the
morning, possibly due to circadian variations that
influence airway receptor thresholds.
 chest tightness.
 Cont.
 Expiration requires effort and becomes prolonged.
As the exacerbation progresses, there is:
 diaphoresis .
 Tachycardia.
 widened pulse pressure.
 Hypoxemia.
 central cyanosis (a late sign of poor oxygenation). The
hypoxemia is secondary to a ventilation–perfusion
mismatch and readily responds to supplemental o2.
 Classification of asthma.
Has 2 major ones.
A. According to severity:
• Mild intermittent Asthma:- if without treatment
any of the following occur-
• symptoms occur on less than 2 days a week.
• Symptoms do not interfere with normal activities.
• Lung function tests are normal.
• Mild persistent Asthma:- if without treatment any
of the following occur- Symptoms occur more than
2 days a week but not every day. These attacks
interfere with daily activities.
 Cont.
• Moderate persistent Asthma:- if without
treatment any of the following occur-
• symptoms occur daily.
• Inhaled short acting Asthma medication is
used every day.
• symptoms interfere with daily activities.
• Lung function tests abnormal.
 cont.
• Severe persistent Asthma:- if without
treatment any of the following are true:-
• symptoms occur throughout each day and
they severely limit daily physical activities.
• Lung function tests abnormal.
 Cont….
B. According to the cause:
Extrinsic asthma
• Hypersensitivity reaction to inhalant allergens
• Mediated by immunoglobulin E

Intrinsic Asthma
• No inciting allergen
• Infection, often viral
• Environmental stimuli e.g. air pollution
 Cont….
Mixed asthma
• Immediate type 1 reactivity seems to be
combined with intrinsic factors

Aspirin induced asthma

• Due to aspirin and related compounds
 Cont….
Exercise induced asthma
• Symptoms vary from slight chest tightness to and
cough to severe wheezing/cough and SOB that
usually occur after 5-20mins of sustained exercise.
• This is due to Exercise Induced Bronchospasm (EIB),
which is defined as a drop in FEV1 of greater than
15% to 20% of baseline.
• EIB is more easily provoked in cold, dry air.
• This however can be blocked by warm, humid air.
Occupational asthma
• Caused by inhalation of industrial fumes, dust,
allergens ad gases
 Acute Severe Asthma
• Result from uncontrolled asthma where inflammation,
airway edema, excessive accumulation of mucus and
severe bronchospasm result in a profound airway
narrowing that is POORLY responsive to usual
bronchodilator therapy.

• Patients present with severe

• dyspnoea,
• tachypnea,
• tachycardia and in severe cases
• cyanosis.

• They exhibit supraclavicular and intercostal

retractions, a hyperinflated chest and coughing. 108
 Allergic Asthma
• It’s associated with allergic encounter
and usually higher in childhood asthma.

• The allergens are air borne and evoke the

asthmatic response through the classic
allergic pathway.

109
 Nocturnal Asthma
• Worsening of asthma during sleep.

• Pathogenesis unknown, but it is

associated with diurnal patterns of
endogenous cortisol secretion and
circulating epinephrine.

110
 Factors Contributing To Asthma Severity

1.Respiratory Infections
• Viral upper respiratory tract infection is the
major cause of severe acute asthma.

• This includes; rhino virus, para influenza virus,

corona virus and influenza virus.

• Co- infections with bacteria such as Streptococcus

pneumonia, Moraxella catarrhalis have also been 111
2. Environmental and Occupational factors.
Include air pollutants e.g. sulfur dioxide and
ozone industrial inhalants.

3. Psychological Factors
Emotions and stress rarely precipitate attack
but worsen an attack in progress.

112
4. Sinusitis and Rhinitis
These are disorders of upper respiratory tract.

5. Gastro esophageal Reflux

Nocturnal asthma may be associated with night time
reflux.
Reflux of acidic gastric contents into the esophagus is
thought to initiate a vagally mediated reflex
bronchoconstriction.

6. Premenstrual Asthma This is due to altered or impaired

function of B2 – adrenergic receptors

113
7. Food, Drugs and Additives
• Allergens.
• Food additives e.g. Benzalkonium
Chloride.
• Aspirin and other NSAIDs, beta blockers

114
 Diagnostic evaluation
• A complete family, environmental and occupational
history.
• Signs and symptoms- periodic symptoms of airflow
obstruction.
• PFTs- 12% decrease in FEV1
• Peak flow >20% variability between AM and PM
measurement
• Lab test- increased serum levels of IgE in atopic asthma.
• Sputum and blood tests show eosinophilia.
• ABGs and pulse oximetry- hypoxemia.
• Skin testing- causative allergen.
• CXR- exclude other lung diseases.
 Complications
• Status asthmaticus
• Respiratory failure
• Pneumonia
• Atelectasis
• Dehydration
 Treatment.
Goals of Asthma Treatment
o Prevent chronic and troublesome symptoms (eg, coughing ,
breathlessness in the night, early morning, or after exertion).
o Maintain near-normal pulmonary function.
o Maintain normal activity levels ( exercise and other physical
activity).
o Prevent recurrent exacerbations of asthma and minimize the
need for emergency hospital visits or hospitalizations.
o Provide optimal pharmacotherapy with minimal or no adverse
effects.
o Meet patients’ and families’ expectation of and satisfaction with
asthma care.
 cont.
Non Pharmacological management
1. Patient education on basic facts about asthma e.g. what
happens to the airways in an asthmatic attack.

 Patient education on roles of medication and skills

– How medicine works.
– What drugs to use for long term control.
– What drugs to use for quick relief
– Inhaler use/ inhaler technique
– Symptom monitoring,
– peak flow monitoring and recognizing early signs of
deterioration.
118
• Patient education on environment.
– control measures, how to identify and avoid environment
precipitates of an asthmatic attack.
• Educate patient on daily self – management plan and
action plan.

2. Oxygen therapy in patients requiring emergency

therapy for acute severe asthma.

3. Mechanical ventilation may be required in severe

respiratory distress.

119
 PHARMACOLOGICAL THERAPY
• Several classes of drugs with different
mechanisms of action are used:
1. Beta- 2 adrenoceptor agonists
2. Methylxanthines
3. Antimuscarinic agents
4. Corticosteroids
5. Inhibitors of mast cell degranulation
6. Leukotriene pathway inhibitors
7. Monoclonal anti- IgE antibodies
120
 Pharmacological management
• Management depends upon frequency and
severity of patient symptoms.

• Infrequent attacks: treat each attack when it

occurs (PRN therapy) with reliever therapy.

• Frequent attacks: Preventive therapy needs to

be instituted IN ADDITION TO reliever therapy.

121
• Preferred route of administration of
therapeutic agents is by inhalation.

• This allows direct drug delivery to airways in;

1.smaller doses,

2.faster onset of action and

3.fewer side effects than use of systemic

routes.
122
 Terms used:-

• ‘Reliever’*: is used for agents that give

immediate relief of symptoms (these drugs are
given PRN, ONLY during an active attack).

• ‘Controllers*’/protectors’/ ‘preventers’ are

agents that act to reduce inflammation or give
long term bronchodilation. (these drugs are
given on a daily basis).

123
 Pharmacologic agents
1. RELIEVER medications
– Used in all classes of asthma
– Used to treat acute asthma symptoms
– Are generally rapid acting.
E.G.
• B2-Agonists reliever meds
– Short acting beta agonists (SABAs) such as albuterol
(salbutamol) Metered-dose inhaler 2 puffs every 4-6 hours.
Tablets 4mgs tds or qid.
– Terbutaline inhalers- 2 inhalations separated by 60 seconds
every 4-6hours. Tablets 5mgs 3 times a day.
– Note:-Do not exceed 15mgs in 24 hours.
– AND other oral B2 agonists. 124
 Cont.
• Anti-Cholinergics
– ipratropium bromide- 8 inhalations every 20
minutes up to 3 hours. Onset of action is within 15
-30min. And lasts for 3-5 hrs.
– tiotropium.
• Methylxanthines
– Aminophyline
 Pharmacologic agents cont….
2. CONTROLLER medications

Used for persistent forms of asthma

Used to PREVENT asthma symptoms

Eg.
Inhaled corticosteroids: betamethasone, budesonide,
fluticasone
Systemic corticosteroids: prednisolone
Antileukotrienes: montelukast and zafirlukast
Long acting beta agonists (LABA): salmeterol,
formoterol 126
 Controller medications cont…..
Cromones: Cromolyn sodium and nedocromil
sodium
Immunomodulatory drugs.
Steroid sparing drugs
 E.G. Methotrexate, cyclosporine, azathioprine,
gold, and intravenous gamma globulin
 Have a relatively high risk of side effects.
Anti-IgE antibodies: omalizumab
Methylxanthines: theophyline
127
Mx of exacerbations
• Early treatment and education (a written
action plan) of the patient.
• Quick acting beta2-adrenergic agonists-
inhalers.
• Systemic corticosteroids to decrease airway
inflammation in patients who fail to respond
to inhaled beta-adrenergic medications.
• Oxygen supplementation to relief hypoxaemia.
• Serial measurement of lung function.
Peak flow monitoring
• Peak flow meters measure the highest airflow
during a forced expiration
• Daily peak flow monitoring is recommended for all
asthma patients as it helps measure asthma
severity and progress adding to symptoms
monitoring indicating the current degree of asthma
control. The patient is instructed in the proper
technique, particularly to give maximal effort.
• This should be monitored for 2-3wks after
receiving optimal asthma therapy.
 Cont….
• Volume is measured in color coded zones:
• Green zone- 80%-100% of personal best
• Yellow zone- 60% -80%
• Red zone- < 60%

N.B: If peak falls below the red zone, the pt should

take the appropriate actions prescribed by his or
her health care provider. This reinforces
compliance, independence, and self-efficacy.
 Nursing interventions
• Monitor V/S, skin color, retraction and degree of
restlessness which may indicate hypoxia, severity of
symptoms.
• Provide nebulization and oxygen therapy.
• Monitor airway functioning through peak flow meter
or PFTs and pulse oximetry.
• The nurse administers medications as prescribed and
monitors the patient’s responses to those
medications.
• Encourage fluid intake
• Position- sitting upright (leaning forward on a table)
• Encourage adaptive breathing techniques e.g. pursed-
 Cont….
• Chest physiotherapy and postural drainage
• Reassure pt
• Pt educ and health maintenance:
o D’se, triggers, tx
o Peak flow monitoring
o Use of MDIs and nebulisation equipment
o Adaptive breathing techniques and exercises
o Environmental control
o Optimal health practices- nutrition, exercises,
rest, follow-up
 ASSIGNMENT.
• Stepwise management of Asthma. 10 mks.
 STATUS ASTHMATICUS
• Definition- Status asthmaticus is severe and
persistent asthma that does not respond to
conventional therapy.
• The attacks can last longer than 24 hours.
Infection, anxiety, nebulizer abuse,
dehydration, increased adrenergic blockage,
and nonspecific irritants may contribute to
these episodes. An acute episode may be
precipitated by hypersensitivity to aspirin.
 Pathophysiology
• The basic characteristics of asthma (constriction of the
bronchiolar smooth muscle, swelling of the bronchial
mucosa, and thickened secretions) decrease the diameter
of the bronchi and are apparent in status asthmaticus.
• A ventilation–perfusion abnormality results in hypoxemia
and respiratory alkalosis initially, followed by respiratory
acidosis. There is a reduced PaO2 and an initial respiratory
alkalosis, with a decreased PaCO2 and an increased pH.
• As status asthmaticus worsens, the PaCO2 increases and
the pH falls, reflecting respiratory acidosis.
 Signs and symptoms.
• labored breathing,
• prolonged exhalation,
• engorged neck
• veins, and
• wheezing. However, the extent of wheezing
does not indicate the severity of the attack. As
the obstruction worsens, the wheezing may
disappear, and this is frequently a sign of
impending respiratory failure.
 Diagnosis.
• Same as earlier.
Medical mx.
 SABA and Corticorcosteroids.
 supplemental oxygen therapy is initiated to treat
dyspnea, central cyanosis, and hypoxemia.
Humidified oxygen by either mask or nasal
catheter.
 intravenous fluids for hydration.
 Sedative medications are contraindicated, why?
 Cont.
• Mechanical ventilation -it is used for patients in
respiratory failure, for those who tire and are too
fatigued by the attempt to breathe, or for those whose
conditions do not respond to initial treatment.
Death from asthma is associated with several risk
factors.:-
• Past history of sudden and severe exacerbations.
• Prior endotracheal intubation for asthma.
• Prior admission to the intensive care unit for an
asthma exercerbation.
 Cont.
• Two or more hospitalizations for asthma within the past
year.
• Three or more emergency care visits for asthma in the past
year.
• Excessive use of short-acting beta-adrenergic inhalers (more
than two canisters per month).
• Recent withdrawal from systemic corticosteroids.
• Comorbidity of cardiovascular disease or COPD.
• Psychiatric disease.
• Low socioeconomic status.
• Urban residence.
 Nursing mx.
• Vital signs monitored frequently till the status
asthmaticus is under control.
• The nurse also assesses the patient’s skin turgor
to identify signs of dehydration.
• Fluid intake is essential to combat dehydration, to
loosen secretions, and to facilitate expectoration.
• intravenous fluids are administered as prescribed,
up to 3 to 4 L/day, unless contraindicated.
• Adequate rest.
 Cont.
• The room should be quiet and free of
respiratory irritants, including flowers, tobacco
smoke, perfumes, or odors of cleaning agents.
• A non allergenic pillow should be used to
elevate the pts head.
 BRONCHIECTASIS
• Is a chronic, irreversible dilatation of the
bronchi and bronchioles due to inflammation
and destruction of their walls
 Etiology
• Pulmonary infections
• Obstruction of bronchi
• Aspiration of foreign bodies, vomitus or
material from URT
• Diffuse airway injury
• Abnormal host defense e.g. ciliary dyskinesia,
Immunodeficiency
• Genetic disorders e.g. cystic fibrosis
• Idiopathic causes
 Pathophysiology
• There is damage to bronchial wall, which leads
to the buildup of the thick sputum, causing
obstruction
• Severe coughing results in the permanent
dilation of the bronchial walls
• Usually involves the lower lobes
• As the process progresses, there is atelectasis
and fibrosis, which lead to respiratory
insufficiency
 Clinical manifestations
• Persistent cough with production of copius
amounts of purulent sputum
• Intermittent hemoptysis
• Breathlessness
• Recurrent fever and bouts of pulmonary
infection
• Crackles and rhonchi over involved lobes
• Finger clubbing
 Diagnostic evaluation
• CXR
• Sputum exam
• CT scan
 Mx
• Antibiotic
• Smoking cessation
• Secretion clearance techniques
• Bronchodilators
• Surgical resection (segmental resection)
 Complications
• Progressive suppuration
• Hemoptysis, major pulmonary hemorrhage
• COPD
• Chronic respiratory insufficiency
 Nursing interventions
• Secretion clearance techniques
• Increased intake of fluids
• Pt. educ and health maintenance:
o Avoiding noxious fumes, dusts, smoke and
other pulmonary irritants
o Monitoring of sputum
o Secretion clearance techniques
o Regular dental care- copius sputum prd may
affect dentition
o Prompt tx of resp infections
o
 CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
• COPD is a term that refers to a group of
conditions characterized by airflow limitation
that is not fully reversible
• Includes :
1. Chronic bronchitis
2. Pulmonary emphysema
 Chronic bronchitis
• Is a chronic inflammation of the mucous
membrane of the bronchial airways,
characterized by cough and sputum
production for at least 3 months in each of
two consecutive years.
 Pulmonary emphysema
• Is a complex lung disease characterized by
destruction of the alveoli, enlargement of
distal airspaces, and a breakdown of the
alveoli walls
 Pathophysiology
 The person with COPD may have:
• Excessive secretion of mucus and chronic
infection within the airways (bronchitis)---local
hyperemia---hypertrophy of mucous glands---
increase in size and number of mucus-
producing elements in bronchi (mucus glands
and goblet cells)---inflammation and edema---
narrowing and obstruction of the airflow
 Cont….
• Increase in size of airspaces distal to the
terminal bronchioles, with loss of alveolar
walls and elastic recoil of the lungs
(emphysema)
N.B: There may be an overlap in these
conditions
• As a result, there is subsequent derangement
of airway dynamics e.g. obstruction to airflow
 Etiology
• Tobacco smoking
• Passive smoking
• Air pollution
• Occupation exposure-dust, chemicals
• Allergy
• Autoimmunity
• Infection
• Aging
• Genetic predisposition- alpha1-antitrypsin
deficiency, an enzyme inhibitor that protects
the lung parenchyma from injury
 Clinical manifestations
Chronic bronchitis
• Productive cough lasting at least 3 months a yr
for 2 successive yrs
• Production of thick gelatinous sputum; greater
amts produced during superimposed
infections
• Wheezing and dyspnea as disease progresses
 Cont….
Emphysema
• Dyspnea
• Decreased exercise tolerance
• Lean forward posture and use of accessory
muscles of respiration
• Cough may be minimal especially with resp
infection
• Sputum expectoration-mild
• Increased anteroposterior diameter of the
chest (barrel chest) due to air trapping with
diaphragmatic flattening
A. Normal chest B. Barrel chest
 Diagnostic evaluation
• PFTs demonstrate airflow obstruction-
reduced FEV1
• ABGs- decreased paO2, PH, and increased CO2
• CXR
• Alpha1-antitrypsin assay
 Mx
• Smoking cessation
• Bronchodilators
• Antibiotics
• Corticosteroids
• Secretion clearance techniques
• Breathing retraining
• Supplemental oxygen
• Pulmonary rehabilitation
 Cont….
• Regular IV infusions (every 1 to 2 wks) of
human alpha1-antitrypsin (Prolastin)
replacement therapy
• Lung transplantation
 Complications
• Respiratory failure
• Pneumonia
• Right heart failure
• Dysrhythmias
• Depression
• Skeletal muscle dysfunction
 Nursing interventions
• Cessation of smoking
• Keep pt’s room as dust free as possible
• Add moisture (humidifier, vaporizer) to indoor
environment if appropriate
• Administer bronchodilators
• Secretion clearance techniques
• Controlled coughing
• High fluid intake
• Breathing exercises
• Positioning to decrease dyspnea
 Cont….
• Recognize early symptoms of respiratory
infection
• Obtain sputum for smear and culture
• Administer antibiotics
• Assess for signs of respiratory failure
• Review ABGs
• Monitor oxygen saturation
• Give supplemental oxygen
• Monitor and minimize CO2 retention by giving
lower oxygen rates
 Cont….
• Assess the nutritional status
• Encourage frequent small meals-high calorie,
high protein
• Encourage regular exercises- increases
physical endurance
• Maintain a balanced schedule of activity and
rest
• Enhance coping-good listener, sensitive,
reassuring, pulmonary rehabilitation program,
sexual educ.
 Cont….
• Patient education and health maintenance:
o General education-d’se, cause, tx, prevention
o Avoid exposure to respiratory irritants
o Prevent and treat respiratory infection
o Reduce bronchial secretions
o Improve airflow-use of MDIs
o Breathing exercises
o General health
 EMPYEMA
• Is an accumulation of thick purulent fluid
within the pleural space, often with a
fibrin(mesh) development and a loculated
area where infection is located
 Etiology
• Bacterial pneumonia
• Lung abscess
• Penetrating chest trauma
• Infection of the pleural space
• Iatrogenic causes- after thoracic surgery or
thoracentesis
 Pathophysiology
• At first, the pleural fluid is thin with a low
leukocyte count but it frequently progresses
to a fibropurulent stage, and finally to a stage
where it encloses the lung within a thick
exudate membrane (loculated empyema)
 Clinical manifestations
• Fever
• Night sweats
• Pleural pain
• Cough
• Dyspnea
• Anorexia
• Weight loss
 Diagnostic evaluation
• Chest auscultation- decreased or absent
breath sounds over the affected area
• Chest percussion- dullness and decreased
fremitus (vibratory tremors)
• CXR
• Chest CT
• Thoracentesis under U/S guidance
 Mx
• Drainage of the pleural fluid:
a. Needle aspiration (thoracentesis)- for small
volume, not too purulent or too thick fluid
b. Tube thoracostomy- chest drainage using a
large diameter intercostal tube attached to a
water seal drainage with fibrinolytics agents
instilled through the chest tube in patients
with loculated or complicated pleural
effusion
 Cont….
c. Open chest drainage via thoracostomy,
including potential rib resection to remove the
thickened pleura, pus and debris and to
remove the underlying diseased pulmonary
tissue
• 4 to 6 weeks of antibiotics to sterilize
empyema cavity
• Decortication- surgical removal of an exudate
over the lung with long-standing inflammation
 Nursing interventions
• Psychological support
• Lung expansion breathing exercises
• V/S
• Small frequent high calorie, high protein meals
• Administer drugs
• Oxygen as need be
• Assist with drainage of pleural fluid
• Health educ on discharge- care of drainage
system, s/s of infection, follow CXR
 PLEURISY
• Is a clinical term to describe pleuritis
(inflammation of the pleura, both parietal and
visceral)
 Etiology
• Pneumonia (bacterial, viral)
• TB
• Pulmonary infarction
• Embolism
• Pulmonary abscess
• URTIs
• Pulmonary neoplasm
 Pathophysiology
• Inflammation of the pleura stimulates nerve
endings, causing pain
 Clinical manifestations
• Chest pain- becomes severe, sharp, and
knifelike on inspiration (pleuritic pain)
• Intercostal tenderness
• Pleural friction rub- grating or leathery sounds
• Fever
• Malaise
• Increased WBCs
 Diagnostic evaluation
• CXR- pleural thickening
• Sputum exam
• Examination of pleural fluid for smear and
culture
• Pleural biopsy
• CBC
 Mx
• Treat the underlying disease
• Pain relief
• Intercostal nerve block when pain causes
hypoventilation
 Complications
• Severe pleural effusion
 Nursing interventions
• Relieving pain
• Psychological support
• Administering meds
• V/S
• Patient education and health maintenance:
o Early intervention for pulmonary disease
o Report SOB- indicate pleural effusion
 PLEURAL EFFUSION
• Refers to a collection of fluid in the pleural
space
 Etiology
 A complication of:
• Disseminated cancer- lung, breast, lymphoma
• Pleuropulmonary infections- pneumonia
• Pulmonary embolus
• CHF
• Cirrhosis
• Nephrosis
• Sarcoidosis
• SLE
• Peritoneal dialysis
 Pathophysiology
 May be either transudative or exudative
Transudative effusions
• Is an accumulation of low-protein, low cell count
fluid- filtrate of plasma move across intact
capillary walls
• Occur primarily in noninflammatory conditions
when factors influencing the formation and
reabsorption of pleural fluid are altered, usually
by imbalances in hydrostatic or oncotic pressures
• Most commonly results from heart failure
 Cont….
Exudative effusions
• Is an accumulation of high-protein fluid
• Occur in an area of inflammation or tumors
involving the pleural surfaces
 Clinical manifestations
• Dyspnea
• Pleuritic chest pain
• Cough
• Dullness or flatness on percussion (over areas
of fluid)
• Decreased or absent breath sounds
 Diagnostic evaluation
• CXR or ultrasound to detect presence of fluid
• Thoracentesis - Analysis of pleural fluid
 Mx
• Treat underlying cause
• Thoracentesis- to remove fluid, to collect a
specimen and to relieve dyspnea
• For malignant effusions- chest tube drainage,
radiation, chemotherapy, surgical
pleurodectomy, pleuroperitoneal shunt, or
pleurodesis- production of adhesions between
the parietal and visceral pleura accomplished
by tube thoracostomy, pleural space drainage
and intrapleural instillation of a sclerosing
agent (tetracycline)
 Complications
• Respiratory failure
 Nursing interventions
• Administer tx
• Assist with thoracentesis
• Maintain chest drainage as needed
• Provide care after pleurodesis:
• Assess for level of pain- excessive pain may cause
hypoventilation
• Administer analgesics
• Administer oxygen if indicated
• Observe pt’s breathing pattern, oxygen saturation
and V/S
• Instruct pt to seek early intervention for unusual
 LUNG ABSCESS
• Is a localized, pus-containing, necrotic lesion in
the lung characterized by cavity formation
 Etiology
• Aspiration of vomitus, foreign body or infected
material from URT into the lung
• Pulmonary embolus
• Trauma
• TB
• Necrotizing pneumonia- tumor- infection
distal to the growth
• The organisms most often seen are Klebsiella
pneumoniae and staphylococcus aureus
 Pathophysiology
• The right lung is involved more frequently
than the left because of dependent position of
the right bronchus, the less acute angle that
the right main bronchus forms within the
trachea, and its larger size
• In the initial stages, the cavity in the lung may
or may not communicate with the bronchus
 Cont….
• Eventually, the cavity becomes surrounded or
encapsulated by a wall of fibrous tissue,
except at one or two points where the
necrotic process extends until it reaches the
lumen of some bronchus or pleural space and
establishes a communication with the
respiratory tract, the pleural
cavity(bronchopleural fistula) or both
 Clinical manifestations
• Cough
• Fever
• Malaise
• Headache
• Anaemia
• Weight loss
• Dyspnea
• Weakness
• Pleuritic chest pain
 Cont….
• Production of mucopurulent sputum, often
foul smelling; blood streaking common; may
become profuse after abscess ruptures into
bronchial tree
• Chest may be dull to percussion
• Decreased or absent breath sounds
• Intermittent pleural friction rub
 Diagnostic evaluation
• CXR
• Direct bronchoscopic visualization
• Sputum culture and sensitivity
• CBC
 Mx
• Antibiotics- IV- clindamycin, then oral; 4 to 8
wks
• Drainage through postural drainage and chest
physiotherapy
• Secretion clearance techniques
• High calorie, high protein diet
• Insertion of chest tube for drainage
• Lobectomy- in massive hemoptysis
 Complications
• Hemoptysis – from erosion of a vessel
• Empyema
• Bronchopleural fistula
• Brain abscess
 Nursing interventions
• Administer antibiotics and monitor pt’s
response
• Take V/S esp. temp
• Carry out drainage procedures
• Encourage adequate fluids
• Promote comfort- positions, massage, oral
hygiene
• Encourage rest and limitation of physical
activity during febrile periods
• Monitor chest tube functioning
 Cont….
• Provide high protein, high calorie diet
• Pt education and health maintenance:
o Antimicrobial therapy- 4 to 8 wks
o Periodontal care
o Follow up CXR
o Optimal state of health
 PNEUMOTHORAX
• Air in the pleural space.
 Pathophysiology
• Occurs when the parietal or visceral pleura is
breached and the pleura space is exposed to
positive atmospheric pressure .
• Normally, the pressure in the pleural space is
negative or subatmospheric; this is required to
maintain lung inflation
• When either pleura is breached, air enters the
pleura space, and the lung or a portion of it
collapses
 Classification
a. Spontaneous/simple pneumothorax- sudden
onset of air in the pleural space with deflation
of the affected lung in the absence of trauma
b. Open/traumatic pneumothorax (sucking
wound of chest)- implies an opening in the
chest wall large enough to allow air to pass
freely in and out of thoracic cavity with each
attempted respiration
• Mainly results from chest trauma
• Often accompanied by hemothorax-
hemopneumothorax
 Cont….
c. Tension pneumothorax- a build up of air under
pressure in the pleural space resulting in
interference with filling of both the heart and
the lungs
 Etiology
• Rupture of air filled subpleural bleb/blister or
bronchopleural fistula- spontaneous
pneumothorax
• Secondary to chronic respiratory diseases
• Trauma
• Idiopathically
• Family hx of pneumothorax
 Clinical manifestations
• Hyperresonance
• Diminished breath sounds
• Reduced mobility of the affected half of thorax
• Tracheal deviation away from the affected side
in tension pneumothorax
• Air hunger, agitation, hypotension and
cyanosis- in open or tension
• Mild to moderate dyspnea and chest
discomfort- in spontaneous
 Diagnostic evaluation
• CXR
 MX
Spontaneous pneumothorax
• Observe and allow for spontaneous resolution
for less than 50% pneumothorax
• Needle aspiration or chest tube drainage to
achieve reexpansion of collapsed lung if
greater than 50% pneumothorax
• Pleurodesis or thoracotomy with resection of
apical blebs in pts with recurrent spontaneous
pneumothorax
Tension pneumothorax
• Immediate decompression to prevent
cardiovascular collapse by thoracentesis or
chest tube insertion to let air escape
• Chest tube drainage- to allow for full lung
expansion and healing
Open pneumothorax

• Close the chest wound immediately

• Insertion of chest tube- to evacuate fluid/air
• Surgical intervention to repair trauma
• Antibiotics
 Complications
• Acute respiratory failure
• Cardiovascular collapse with tension
pneumothorax
 Nursing interventions
• Provide emergency care as indicated:
o Petrolatum gauze to sucking chest wound
o Assist with emergency thoracentesis or
thoracostomy
o CPR
o Meds
• Suction as needed
• Upright position
• Maintain patency of chest tubes
 Cont….
• Assist pt splint chest and administer pain meds
• Encourage use of inspiratory spirometer
• Monitor ABGs and oximetry
• Provide oxygen as needed
• Pt educ:
o ct use of spirometer,
o report sudden dyspnea immediately- indicates
a recurrence of spontaneous pneumothorax
 HAEMOTHORAX
• Blood in pleural space
 Etiology
• Penetrating or blunt chest trauma
 Clinical manifestations
• May be asymptomatic
• Dyspneic
• Apprehensive or in shock
• Can result in hidden blood loss
 Mx and nursing interventions
• Assist with thoracentesis to aspirate blood
from pleural space if being done before a
chest tube insertion
• Assist with chest tube insertion and set up
drainage system to accomplish complete and
continuous removal of blood and air
• Auscultate lungs and monitor for relief of
dyspnea
• Monitor amount of loss in drainage
• Replace volume with IV fluids or blood
 CANCER OF THE LUNG
(Bronchogenic Cancer)
• Refers to a malignant tumor of the lung arising
within the wall or the epithelial lining of the
bronchus
• The lung is also a common site of metastasis
from cancer elsewhere in the body by way of
venous circulation or lymphatic spread
 Pathophysiology
• Arise from a single transformed epithelial cell
in the tracheobronchial airways, in which the
carcinogens binds to and damage the cell’s
DNA.
• This damage results in cellular changes ,
abnormal cell growth, and eventually a
malignant cell
• As the damaged DNA is passed to daughter
cells, the DNA undergoes further changes and
become unstable
 Cont….
• With the accumulation of genetic changes, the
pulmonary epithelium undergoes malignant
transformation from normal epithelium
eventually to invasive carcinoma
o It has been found that carcinoma tends to
arise at sites of previous scarring (TB, Fibrosis)
in the lung
 Classification (according to cell type)
1. Epidermoid (squamous cell)- best prognosis;
usually more centrally located and arises more
commonly in the segmental and subsegmental
bronchi
2. Adenocarcinoma- most prevalent; occurs
peripherally as peripheral masses and nodules
and often metastasizes
3. Small cell (oat cell) carcinoma- arise in the major
bronchi and spread by infiltration through the
bronchial wall
4. Large cell (undifferentiated) carcinoma- fast-
 Predisposing factors
• Cigarette smoking
• Occupational exposure to asbestos, arsenic,
chromium, nickel, iron, radioactive
substances, isopropyl oil, coal tar products,
petroleum oil mists; alone or in combination
with tobacco smoke
• Diet low in fruits and vegetables
• Genetic
 Staging
• Anatomical extent of tumor, lymph node
involvement, and metastatic spread
• Its done by:
Tissue diagnosis
Lymph node biopsy
Mediastinoscopy
 Clinical manifestations
• Cough, especially a new type or changing
cough, results from bronchial irritation
• Dyspnea, wheezing (suggests partial bronchial
obstruction)
• Chest pain (poorly localized and aching)
• Excessive sputum production,
• Repeated URTIs
• Hemoptysis
• Malaise
• Fever
• Fatigue
 Cont….
• Paraneoplastic syndrome- metabolic or
neurologic disturbances related to the secretion
of substances by the neoplasm
• Symptoms of metastases:
o bone pain, abdominal discomfort, nausea and
vomiting from liver involvement
o pancytopenia from bone marrow involvement
o Headache from CNS metastasis

 Usual sites of metastases- lymph nodes, bones,

 Diagnostic evaluation
• CXR including fluoroscopy and tomography
(lung cancers may be partly or completely
hidden by other structures)
• Cytologic exam of sputum/chest fluids
• Fiberoptic bronchoscopy
• CT
• Lymph node biopsy
• Mediastinoscopy
• PFTs
 Mx
• Surgical resection- lobectomy,
pneumonectomy
• Radiotherapy
• Chemotherapy
• Immunotherapy
 Complications
• Superior vena cava syndrome-caused by
obstruction of major blood vessels draining the
head, neck, and upper torso
• Hypercalcemia-from bone metastases
• Syndrome of inappropriate ADH (SIADH) secretion
with hyponatremia and abnormal water
retention(Oat-cell tumors produce ADH-like
substances)
• Pleural effusion
• Infectious complications esp. URTIs
• Brain metastasis
 Nursing interventions
• Elevate head of the bed to promote gravity
drainage and prevent fluid collection in upper
body (from superior vena cava syndrome)
• Breathing retraining exercises
• Administer expectorant, antibiotics
• Augment pt’s ability to cough fully:
o Splint chest
o Inspire fully and cough 2 to 3 times in one
breath
o Provide humidifier/vaporizer
 Cont….
• Psychological support
• Administer oxygen as need be
• Energy conservation by decreasing activity
• Allow pt to sleep in a reclining chair if severely
dyspneic
• Small frequent amounts of high calorie and
high protein food and vitamin supplement
• Controlling pain
• Pt educ. and health maintenance
 OCCUPATIONAL LUNG DISEASES
Types
1. Asbestosis
2. Silicosis
3. Coal Worker’s Pneumoconiosis (CWP)
 Asbestosis
• Is a diffuse interstitial fibrosis of the lung
caused by inhalation of asbestos dust and
particles
• Asbestos- a fibrous, incombustible form of
magnesium and calcium silicate used to make
insulating materials
 Etiology
• Found in workers involved in asbestos mining
and manufacturing, construction, roofing,
demolition work, brake linings, floor tiles,
paints, plastics, shipyards, and insulation
 Pathophysiology
• Asbestos fibers are inhaled and enter alveoli,
which in time, are obliterated by fibrous tissue
that surrounds the asbestos particles
• Fibrous pleural thickening and pleural plague
formation produce restrictive lung disease,
decrease in lung volume, diminished gas
transfer, and hypoxemia with subsequent
development of Cor Pulmonale

N.B: There is high incidence of lung carcinoma

 Clinical Manifestations
• Progressive dyspnea
• Persistent dry cough
• Mild to moderate chest pain
• Anorexia
• Malaise
• Weight loss
• Bibasilar crackles
• Clubbing of fingers
• Cor pulmonale
• Respiratory failure
 Mx
• Controlling infection and treating the lung
disease
• Oxygen therapy
• Avoiding additional exposure to asbestos
• Stop smoking
 Silicosis
• Is a chronic pulmonary fibrosis caused by
inhalation of silica dust
 Etiology
• Mining- gold, coal, tin, copper ; the earth’s
crust is composed of silica and silicates
• Stone cutting
• Quarrying
• Manufacture of abrasives
• Ceramics, pottery and foundry work
 Pathophysiology
• When silica particles which have fibrinogenic
properties are inhaled, nodular lesions are
produced throughout the lungs
• These nodules undergo fibrosis, enlarge and
fuse
• Dense masses form in the upper portion of
the lungs; restrictive and obstructive lung
disease forms
 Clinical manifestations
• Dyspnea
• Fever
• Weight loss
• Cough
• Slow progressive symptoms indicative of
hypoxemia, severe airflow obstruction and
right sided heart failure
• Edema due to cardiac failure
 Mx
• Supportive therapy in managing complications
and preventing infection
• Test to check other lung disease e.g. TB, lung
cancer and sarcoidosis
• Tx TB if present
• Oxygen therapy
• Diuretics
• Inhaled beta-adrenergic agonists
• Anticholinergics
• Bronchodilator therapy
 CWP (“Black lung disease”)
• A respiratory disease found in coal workers in
which there is an accumulation of coal dust in
the lungs, causing a tissue reaction in its
presence
 Pathophysiology
• Coal dust are inhaled and deposited in the
alveoli and respiratory bronchioles
• There is an increase in macrophages that
engulf the particles and transport them to
terminal bronchioles
• When normal clearance mechanisms no
longer can handle the excessive dust load, the
respiratory bronchioles and alveoli become
clogged with coal dust, dying macrophages,
and fibroblasts, which lead to the formation of
the coal macule , the primary lesion of CWP
 Cont….
• As macules enlarge, there is dilatation of the
weakening bronchiole, with subsequent
development of focal or centrilobular
emphysema
 Clinical manifestations
• Chronic cough with sputum production
• Dyspnea on exertion ; progressive and
irreversible
• Susceptibility to lower respiratory tract
infections
• Expectoration of varying amounts of black
fluid (melanoptysis) esp. smokers
• Cor pulmonale and respiratory failure
 Mx
 No effective tx
• Early dx and mx of complications
 Diagnostic evaluation
• CXR
• PFTs- restrictive pattern
• Bronchoscopy with lavage
• CT
• Sputum exam
• Lung biopsy
 Nursing interventions
• A history of occupational, family or
neighborhood exposure
• Ascultate for breath sounds
• Monitor and document changes in sputum
• Administer bronchodilators, mucolytics
• Administer oxygen
• Monitor ABGs
• Secretion clearance techniques
• Adequate fluids
• Positioning upright
 Cont….
• Monitor for complications
• Frequent small meals, high calorie and protein
• Balance activity with rest
• Psychological support
• Pt educ. and health maintenance