Pulmonary System Notes

Upper Respiratory System Notes

Key points:
Components:
1. Nose
2. Sinuses
3. Pharynx
4. Larynx
Cause:
• Bacterial
• Viral
• Irritants
Duration:
• Acute
• Chronic

I. Nose
1. Rhinitis - Characterized by inflammation and irritation of the mucous membranes
of the nose.

Type of
Cause Key Symptoms Treatment
Rhinitis

Antihistamines,
Sneezing, runny
Allergic Allergens (pollen, corticosteroids, allergen
nose, itching, watery
Rhinitis dust, dander) avoidance, Oral decongestant
eyes
agents, saline nasal sprays

Nasal congestion, Avoidance of triggers, saline

Non-Allergic Irritants (smoke,
runny nose, no sprays, corticosteroids, Oral
Rhinitis perfumes, weather)
itching decongestant agents

Rest, hydration,
Viruses (e.g., Sneezing, decongestants, symptomatic
Viral Rhinitis
rhinovirus, congestion, sore treatment, Warm salt-water
(Infectious)
adenovirus) throat, fever gargles, Expectorant, Anti-
inflammatory drugs (NSAIDs)
 Thinning of nasal Nasal crusting, foul
Atrophic Saline rinses, antibiotics (if
mucosa, often after odor, dryness,
Rhinitis needed), surgery
surgery nosebleeds

Rhinitis
Overuse of nasal Severe rebound Discontinuation of
Medicamentos
decongestants nasal congestion decongestant, corticosteroids
a

Pregnancy, Saline rinses,

Hormonal Congestion, runny
menstrual cycle, corticosteroids, hormonal
Rhinitis nose
thyroid issues management

Medications (e.g.,
Drug-Induced Nasal congestion, Stopping the offending drug
beta-blockers, ACE
Rhinitis runny nose (under medical advice)
inhibitors)

Congestion, runny
Non-allergic
nose, similar to Nasal corticosteroids,
NARES inflammation with
allergic rhinitis but antihistamines
eosinophils
non-allergic

Combination of Symptoms of both Combination of treatments for

Mixed Rhinitis allergic and non- allergic and non- allergic and non-allergic
allergic triggers allergic rhinitis rhinitis

Nursing considerations:
• Instruct the patient to avoid or reduce exposure to allergens and irritants, such as
dust, molds, animals, fumes, odors, powders, sprays, and tobacco smoke
• Instruct the patient about the importance of controlling the environment at home
and at work
• Educate the patient about the importance of receiving an influenza vaccination
each year to achieve immunity before the beginning of the flu season
• Instruct the patient about the importance of hand hygiene technique
• Provide adequate fluid intake, rest, and prevention of chilling
• Instruct the patient about the importance of hand hygiene technique
• Educates the patient about the use of tissues when coughing and sneezing, or to
cough or sneeze into the upper arm if tissues are not available

• Instruct the patient in correct administration of nasal medications:

 a. Blow the nose before applying any medication into the nasal
cavity
b. keep the head upright and spray quickly and firmly into each
nostril away from the nasal septum
c. wait at least 1 minute before administering the second spray
Diagnosis:
Patient History: The doctor will ask about:
 Your symptoms (sneezing, runny nose, congestion, etc.).
 When and how often the symptoms occur (seasonal, constant, after exposure to
animals, dust, smoke, etc.).
 If you have other allergic conditions like asthma or eczema.
 Family history of allergies.
 Medications you take and your living or work environment.
Physical Examination: The doctor will:
 Look inside your nose for swelling, redness, or discharge.
 Check for nasal polyps (non-cancerous growths) or a deviated septum (crooked
nasal partition).
 Look in your throat for signs of post-nasal drip.
 Check your ears for fluid buildup.
Allergy Testing (for Allergic Rhinitis): If allergies are suspected:
 Skin Prick Test: Small drops of allergens are placed on your skin, and if you are
allergic, the skin will swell slightly.
 Blood Test: Measures your body's reaction to specific allergens (checking for
allergy-related antibodies in the blood).

II. NOSE-SINUSES
Rhinosinusitis
• Formerly called sinusitis
 • It is an inflammation of the paranasal sinuses and nasal cavities. The condition
affects the drainage of mucus and can lead to pressure and pain in the face.
• Classified according to duration of symptoms:
1. Acute (less than 4 weeks)
2. Subacute (4 to 12 weeks)
3. Chronic (more than 12 weeks)
Causes:
It can be caused by a bacterial or viral infection. Some are due to exposure to
environmental hazards such as paint, sawdust, and chemicals.
Signs and symptoms:
 Nasal congestion.
 Thick nasal discharge (may be yellow or green if bacterial).
 Facial pain or pressure, particularly around the forehead, eyes, or cheeks.
 Reduced or loss of sense of smell.
 Post-nasal drip (mucus draining down the back of the throat).
 Cough, sore throat, and sometimes fever.
 Fatigue and feeling generally unwell.
 Bad breath (halitosis).
 Tooth pain (particularly upper teeth, as the sinuses are near the roots).
Complications:
 Osteomyelitis
 Mucocele
 Cavernous sinus thrombosis
 Meningitis
 Brain abscess
 Ischemic brain infarction
 Severe orbital cellulitis
 Frontal epidural abscesses
 Periorbital edema

Treatment:
Viral: Symptomatic relief with nasal saline rinses, decongestants, and pain relievers
(acetaminophen or ibuprofen).
Bacterial: Antibiotics are prescribed if a bacterial infection is confirmed or suspected,
along with symptomatic treatments.
Nursing Management
• Instruct the patient about symptoms of complications
• Instructs the patient about methods to promote drainage of the sinuses
• The patient is advised to avoid swimming, diving, and air travel during the acute
infection
• Instruct the patient about the correct use of prescribed nasal sprays
• Advice patient to immediately stop smoking or using any form of tobacco
• Stresses the importance of following the recommended antibiotic regimen

Chronic Rhinosinusitis and

Recurrent Acute Rhinosinusitis
• In Chronic Rhinosinusitis, patient experienced 12 weeks or longer of two or
more of the following symptoms: mucopurulent drainage, nasal obstruction, facial
pain–pressure–fullness, or hyposmia
Cause: It may result from:
• Persistent infection (bacterial or fungal).
• Chronic inflammation from allergens, irritants, or underlying conditions like
asthma or immune system dysfunction.
• Structural abnormalities like a deviated septum or nasal polyps.
• In recurrent acute rhinosinusitis, patients experienced four or more episodes
of ABRS occur per year with no signs or symptoms of rhinosinusitis between the
episodes
Cause: Repeated viral or bacterial infections, often related to underlying issues
like allergies, a weakened immune system, or structural problems such as nasal
polyps.

Complications:
• Subperiosteal abscess
 • Cavernous sinus thrombosis
• Ischemic infarction
• Encephalitis
• Osteomyelitis
• Ptosis, proptosis, chemosis
• Intracranial infection
• Epidural abscess
• Subdural empyema
• Brain abscess
• Elevated intracranial pressure

Nursing Management
• Instruct patients to blow the nose gently and to use tissue to remove the nasal
drainage
• Increase fluid intake
• Apply local heat (hot wet packs)
• Instruct patients to sleep with the head of the bed elevated
• Caution patients to avoid caffeine and alcohol
• Encourage patients to follow up with their primary provider if symptoms persist
• Instruct patients about the importance of following the prescribed medication
regimen
• Instruct patients about signs and symptoms that require follow-up

Diagnosis:
 Physical examination: A healthcare provider will examine the nasal passages,
look for swelling, discharge, and polyps.
 Nasal endoscopy: A thin, flexible tube with a camera (endoscope) may be used
to view the inside of the nose and sinuses.
 Imaging tests: CT scans or X-rays can help visualize the sinuses and detect
structural abnormalities or blockages.
  Cultures or biopsy: In chronic cases, nasal or sinus cultures might be taken to
identify the exact cause, especially if fungal infections are suspected.
Acute Pharyngitis
• Sudden painful inflammation of the pharynx, the back portion of the throat
• Commonly referred to as a sore throat

Atelectasis
 Atelectasis is the closure or collapse of alveoli, often seen on chest x-rays.
 It can be either acute or chronic, with varying degrees of lung volume loss:

 Microatelectasis: not visible on chest x-ray.

 Macroatelectasis: noticeable loss of lung segments or lobes.

 Acute atelectasis:

 Common after thoracic or upper abdominal surgeries.

 Occurs in immobilized patients with shallow breathing.

 Chronic atelectasis:

 Caused by chronic airway obstructions, such as mucus plugs.

 May result from conditions like lung cancer compressing airways.

 Symptoms and onset vary, with chronic cases developing more slowly.

Pathophysiology
Types of Atelectasis:
 Nonobstructive atelectasis**: Results from reduced ventilation in adults.
 Obstructive atelectasis**: Caused by blockages that prevent air from reaching
alveoli, leading to the reabsorption of trapped alveolar air and collapse of the
alveoli.

Common Causes of Atelectasis

- Foreign bodies, tumors, or growths in airways.
 - Retained secretions, pain, or altered breathing patterns.
- Increased abdominal pressure or restrictive lung conditions.
- Surgical procedures, especially upper abdominal, thoracic, or heart surgeries.

Risk Factors for Postoperative Atelectasis

- Low tidal breathing due to anesthesia, analgesics, or positioning.
- Chest wall splinting, abdominal distention, or retained secretions.
- Impaired cough reflex or reluctance to cough due to pain.

Additional Causes
- Impaired cough in patients with musculoskeletal or neurological disorders.
- Compressive atelectasis from lung tissue pressure due to:
- Pleural effusion, pneumothorax, hemothorax (fluid, air, or blood in pleural space).
- Pericardial effusion, tumor growth, or elevated diaphragm.

Result: Atelectasis restricts lung expansion, reducing alveolar ventilation and leading to
airless lung segments.

Clinical Manifestations
Onset of Atelectasis: Usually develops gradually (insidiously).
General Signs and Symptoms:
 Increasing shortness of breath (dyspnea).
 Cough and sputum production.
Acute Lobar Atelectasis (involving large lung areas):
 Severe respiratory distress with symptoms like:
o Rapid heart rate (tachycardia).
o Fast breathing (tachypnea).
o Pleural pain and central cyanosis (bluish skin from low oxygen levels).
  Patients may struggle to breathe when lying flat and may experience anxiety.
Chronic Atelectasis:
 Symptoms like acute atelectasis.
 Chronic alveolar collapse can lead to infections beyond the obstruction, so
infection symptoms may also appear.
Assessment and Diagnostic Findings

Clinical Features of Significant Atelectasis:

 Increased work of breathing.

 Hypoxemia (low arterial blood oxygen levels).

Physical Findings:

 Decreased breath sounds and crackles over the affected lung area.

Diagnostic Indicators:

 Chest x-ray: May show patchy infiltrates or consolidated areas, often before
symptoms develop.
 Pulse oximetry (SpO2): May show oxygen saturation below 90%.
 Arterial blood gases (PaO2): Lower-than-normal oxygen levels.

Prevention

 Preventive Nursing Measures:

o Frequent turning and early mobilization.
o Lung expansion strategies (e.g., deep breathing, incentive spirometry).
o Secretion management techniques.
 Deep-Breathing Exercises:
o Voluntary deep-breathing every 2 hours to prevent atelectasis.
o Patient education and encouragement are crucial.
 Incentive Spirometry:
o Provides visual feedback to encourage deep, slow breaths for lung
expansion.
o Types:
 Volume Type: Sets a target volume; patient inhales, pauses, and
then exhales.
 Flow Type: Uses balls that rise and suspend with inhalation to
estimate air volume and flow.
 Secretion Management:
o Directed cough, suctioning, and aerosol nebulizer treatments followed by
chest physiotherapy (CPT).
 o Bronchoscopy and pressurized metered-dose inhalers (pMDIs) with
bronchodilators can also be used.

These interventions support lung expansion, prevent airway closure, and help clear
secretions, reducing the risk of atelectasis.

Management

 Treatment Goals:

 Improve ventilation and remove secretions.

 First-line measures: frequent turning, early ambulation, lung volume expansion
(deep-breathing exercises, incentive spirometry), and coughing.

 Standardized Programs:

 ICOUGHSM and similar multidisciplinary interventions can help prevent

atelectasis.

 Advanced Treatments for Unresponsive Cases:

 Positive end-expiratory pressure (PEEP), continuous positive airway breathing,

or bronchoscopy may be used if initial measures fail.
 Assess factors that could impair deep-breathing efforts (e.g., pain, sedation).

 Clearing Obstructions:

 For bronchial obstruction from secretions, use coughing, suctioning, chest

physiotherapy (CPT), postural drainage, and bronchodilators.
 Bronchoscopy may be necessary if obstructions persist, followed by airway
maintenance.

 Managing Compression:

 When caused by lung compression (e.g., pleural effusion), treatment includes

thoracentesis or chest tube insertion.
 Techniques to increase lung expansion are also applied.

 Chronic Atelectasis Management:

 Focus on removing the obstruction or compression, such as using bronchoscopy,

cryotherapy, laser therapy, or stenting.
 Surgical options may be considered if long-term collapse cannot be reversed.

Pneumonia
Pneumonia is an inflammation of the lung parenchyma caused by various
microorganisms, including bacteria, mycobacteria, fungi, and viruses. Pneumonitis is a
more general term that describes an inflammatory process in the lung tissue that may
predispose or place the patient at risk for microbial invasion. Pneumonia

Classification

Community-Acquired Pneumonia (CAP)

Overview of Community-Acquired Pneumonia (CAP):

 Common infectious disease in community settings or within 48 hours of

hospitalization.
 Hospitalization depends on pneumonia severity.
 Incidence increases with age; common in adults over 65.

Causative Pathogens:

 S. pneumoniae (pneumococcus):
o Most common bacterial cause in those <60 without comorbidities and
those ≥60 with comorbidities.
o Can cause both lobar and bronchopneumonia.
 H. influenzae:
o Common in older adults and those with chronic illnesses (e.g., COPD,
diabetes).
o Symptoms may include a persistent cough or low-grade fever.
 Mycoplasma pneumoniae:
o Spread via respiratory droplets; causes bronchopneumonia with interstitial
inflammation.
o Symptoms may include ear pain and bullous myringitis.
 Viral causes:
o Common in infants/children; previously less common in adults until
COVID-19.
o Pre-COVID, main viral pathogens were cytomegalovirus, herpes simplex
virus, adenovirus, and respiratory syncytial virus.
o Viral pneumonia involves inflammation that spreads to alveolar areas,
causing edema and exudation, with symptoms similar to bacterial
pneumonia.

Health Care–Associated Pneumonia (HCAP)

  Characterized by pathogens that are often multidrug-resistant organisms
(MDROs) due to previous exposure to healthcare environments.
 Identification of HCAP in settings like the emergency department is critical for
effective management.
 Treatment is often more challenging compared to community-acquired
pneumonia (CAP).
Initial Treatment:

 Early initiation of antibiotics is essential.

 Antibiotic regimens for HCAP may differ from those for CAP due to the likelihood
of encountering MDROs.

Hospital-Acquired Pneumonia
  Develops 48+ hours after hospitalization, not incubating at admission.
 Often linked to factors like impaired host defenses, various comorbidities, supine
positioning, aspiration, coma, malnutrition, extended hospitalization, hypotension,
and metabolic disorders.
 Increased exposure to bacteria via hospital equipment, respiratory therapy, and
hand transmission by healthcare staff.
 Interventions such as certain medications, prolonged thoracoabdominal
procedures, ET intubation, nasogastric tubes, and prolonged antibiotic use
increase HAP risk.
 High mortality rate due to virulent, antibiotic-resistant organisms and patient’s
underlying conditions.
 Most common cause of death from hospital-acquired infections, with mortality
rates up to 33%.
Ventilator-Associated Pneumonia (VAP):
 Subtype of HAP, differing by the presence of an endotracheal (ET) tube.
Common Pathogens:
 HAP pathogens include Enterobacter, E. coli, H. influenzae, Klebsiella,
Pseudomonas, Acinetobacter, MRSA, and S. pneumoniae.
 Multiple organisms often colonize patients; Pseudomonal pneumonia occurs in
debilitated or long-term intubated patients.
 Staphylococcal pneumonia can spread through inhalation or blood, with high
mortality and sepsis risk.
Antibiotic Resistance:
  Overuse and misuse of antibiotics lead to resistant pathogens, especially MRSA.
 MRSA control requires patient isolation, contact precautions, and minimized
contact.
Symptoms and Diagnosis:
 HAP typically presents as new lung infiltrates on X-ray, fever, respiratory
symptoms, purulent sputum, or leukocytosis.
 Klebsiella or other gram-negative pneumonias may cause lung tissue destructio
n and sepsis.
 Increased risk in older adults, alcoholics, those with chronic lung disease, or
diabetes.
 Symptoms include cough (or increased cough), sputum production, low-grade
fever, malaise, pleural effusion, high fever, and tachycardia.
Pneumonia in the Immunocompromised Host
Increased Incidence:
 Advances in immunosuppressive therapy, prevalence of multidrug-resistant
organisms (MDROs), and better diagnostics have led to more cases of
pneumonia in immunocompromised patients.
Common Causes:
 Organisms like Pneumocystis jiroveci (formerly Pneumocystis carinii, abbreviated
PCP), fungal pneumonias, and Mycobacterium tuberculosis are typical
pathogens.
Risk Factors:
 Immunocompromised status due to corticosteroids, immunosuppressants,
chemotherapy, malnutrition, broad-spectrum antimicrobials, AIDS, genetic
immune disorders, and prolonged advanced life support.
 The affected population is growing, making pneumonia more common in these
patients.
Higher Morbidity and Mortality:
 Immunocompromised patients face higher risks than immunocompetent ones,
even from low-virulence organisms.
 Increased susceptibility to hospital-acquired pneumonia (HAP) from gram-
negative bacteria like Klebsiella, Pseudomonas, E. coli, Proteus, Serratia, and
Enterobacteriaceae.
Clinical Presentation:
 Similar symptoms in both immunocompromised and immunocompetent patients.
 PCP in particular presents subtly, with progressive shortness of breath, fever,
and a dry cough.
Aspiration pneumonia
 Aspiration pneumonia results from inhalation of endogenous or exogenous
substances into the lower airways, most commonly bacteria from the upper
airways.
Causes:
 Bacterial infection from aspiration of upper airway bacteria.
 Common pathogens include anaerobes, S. aureus, Streptococcus species, and
gram-negative bacilli.
 Non-bacterial substances, such as gastric contents, chemicals, or gases, can
also be aspirated, impairing lung defenses, triggering inflammation, and
potentially leading to bacterial growth and pneumonia.
Pathophysiology:
 The upper airway typically blocks infectious particles from reaching the lower
respiratory tract.
 Pneumonia can arise from normal flora when host defenses are compromised or
from bloodborne pathogens trapped in the lungs.
 Inflammation in alveoli leads to exudate formation, which disrupts oxygen and
carbon dioxide diffusion.
 Neutrophils infiltrate the alveoli, filling air spaces and reducing effective
ventilation.
Ventilation-Perfusion Mismatch (V/Q Mismatch):
 Secretions, edema, and partial obstruction in bronchi or alveoli decrease oxygen
levels in affected lung areas.
 In cases of hypoventilation, a V/Q mismatch occurs, meaning blood is poorly
oxygenated as it passes through underventilated lung areas, leading to arterial
hypoxemia.
Types of Pneumonia:
 Lobar Pneumonia: Involves a substantial part of one or more lung lobes.
  Bronchopneumonia: Patchy distribution within bronchi, extending to surrounding
lung tissue; more common than lobar pneumonia.
General Presentation:
 Symptoms vary by pneumonia type, causative organism, and any underlying
diseases, but a specific diagnosis cannot be made solely based on clinical signs.
Common Symptoms in Streptococcal (Pneumococcal) Pneumonia:
 Sudden onset of chills, high fever (101°–105°F), and pleuritic chest pain
worsened by deep breathing or coughing.
 Severe illness with rapid breathing (tachypnea of 25–45 breaths/min) and
respiratory distress, including shortness of breath and use of accessory muscles.
 Relative bradycardia may indicate viral, mycoplasma, or Legionella infection.
Gradual-Onset Symptoms:
 Often starts as upper respiratory symptoms like nasal congestion and sore
throat, followed by gradual onset of headache, low-grade fever, chest pain,
muscle pain (myalgia), rash, and sore throat (pharyngitis).
 Mucoid or mucopurulent sputum develops after a few days.
Severe Pneumonia Signs:
 Flushed cheeks, central cyanosis in lips and nails (indicating hypoxemia),
orthopnea (difficulty breathing when lying down), and a need to sit upright to
breathe comfortably.
 Poor appetite, excessive sweating (diaphoresis), and fatigue.
 Sputum may be purulent, and in cases of pneumococcal, staphylococcal, or
Klebsiella pneumonia, it may be rusty or blood-tinged.
Symptoms in Immunocompromised or Chronically Ill Patients:
 Symptoms like fever, crackles, and lung consolidation signs, including increased
tactile fremitus, dullness on percussion, bronchial breath sounds, egophony, and
whispered pectoriloquy.
 Sound transmission through dense or consolidated lung tissue amplifies these
sounds.

Special Considerations for COPD Patients:

 Symptoms may present as purulent sputum or slight changes in respiratory
signs.
  It can be challenging to distinguish between a pneumonia infection and an
exacerbation of the existing COPD condition.
Diagnosis of Pneumonia:
 Based on patient history, physical exam, chest x-ray, blood culture, and sputum
examination.
 Blood culture helps detect bacteremia, common with pneumonia.
Sputum Collection:
 To avoid contamination, patients rinse their mouth with water, take deep breaths,
cough deeply, and expectorate sputum into a sterile container.
Invasive Specimen Collection:
 Used if initial sputum samples are inadequate or for patients with severe, chronic,
or refractory infections, compromised immune systems, or mechanical
ventilation.
 Techniques include:
o Nasotracheal or Orotracheal Suctioning: Uses a sputum trap.
o Fiberoptic Bronchoscopy: Employed in more severe cases, often
includes:
 Protected Brush Specimen or Bronchoalveolar Lavage to
collect lung samples.

Prevention
Pneumococcal Vaccination:
 Reduces pneumonia incidence, cardiac hospitalizations, and mortality in older
adults.
Types of Vaccines:
 PCV13 (Pneumococcal Conjugate Vaccine):
o Protects against 13 types of pneumococcal bacteria.
o Recommended for:
 All adults 65+.
 Adults 19+ with weakened immune systems (e.g., HIV, organ
transplants, leukemia, chronic kidney disease) or with specific
conditions (e.g., cerebrospinal fluid leak, cochlear implants).
  PPSV23 (Pneumococcal Polysaccharide Vaccine):
o Protects against 23 types of pneumococcal bacteria.
o Recommended for:
 All adults 65+.
 Adults 19–64 who smoke or have chronic heart, lung, liver disease,
or alcoholism.
Vaccination Schedule:
 Adults 65+ who previously received PCV13 should receive PPSV23.
 Immunocompetent adults 65+ who haven't had PCV13 should get PCV13 first,
followed by PPSV23 after at least one year.
 PCV13 and PPSV23 should not be given simultaneously.
Guideline Updates:
 Pneumococcal vaccine recommendations may change, so it’s essential to check
the CDC website regularly for the latest guidelines.
Medical Management:
 Main treatments include appropriate antibiotics (for bacterial pneumonia), rest,
hydration, and management of any complications.
 Supplemental oxygen may be prescribed if needed.
Pharmacologic Therapy:
 Antibiotics are selected based on culture and sensitivity results, although in many
cases, the specific organism is not identified at the start of treatment.
 Guidelines help determine antibiotic choice, considering resistance patterns,
common pathogens, patient risk factors, treatment setting (inpatient or
outpatient), and drug availability/cost.
Switching from IV to Oral Antibiotics:
 Inpatients can switch from IV to oral antibiotics once they are:
o Hemodynamically stable.
o Showing clinical improvement.
o Able to tolerate oral intake.
o Have a functioning gastrointestinal tract.
Criteria for Discharge:
  Patients should be discharged once they achieve clinical stability:
o Temperature ≤ 37.8°C (100°F).
o Heart rate ≤ 100 bpm.
o Respiratory rate ≤ 24 breaths/min.
o Systolic blood pressure ≥ 90 mm Hg.
o Oxygen saturation ≥ 90%.
o Ability to maintain oral intake and normal mental status.

COVID-19 Overview:
 COVID-19, caused by the SARS-CoV-2 virus, is primarily transmitted through
respiratory droplets and possibly through contact with contaminated surfaces
(fomites).
 The virus enters host cells through ACE2 receptors, which are abundant in type II
alveolar cells and vascular endothelium in the lungs.
Symptoms:
 Symptoms range from asymptomatic to severe, including fever, cough, sore
throat, fatigue, muscle aches, nasal congestion, nausea, vomiting, diarrhea, and
loss of smell and taste.
 Most cases (~81%) are mild, often with mild pneumonia or none at all.
Diagnosis:
 Diagnosed via nasal swabs for viral antigen or nucleic acid, often self-
administered to reduce transmission risk.
Management of Mild Cases:
 Patients with mild COVID-19 are typically managed at home with rest, hydration,
symptom management (e.g., acetaminophen), and monitoring.
 Criteria for ending home isolation: 72 hours fever-free without antipyretics,
improved respiratory symptoms, and at least 10 days since symptom onset.
Hospitalization for Moderate Cases:
 Moderate cases require close observation, as patients may quickly deteriorate.
  Moderate COVID-19 pneumonia is characterized by SpO2 >93% on room air,
with or without dyspnea, and diagnosed through physical exam and imaging.
 Routine lab tests include CBC with differential, metabolic panel, CK, LDH, CRP,
ferritin, and D-dimer.
 Antibiotics are generally not prescribed unless a bacterial co-infection is
suspected; anticoagulants are often given to prevent VTE.
Severe COVID-19 Management:
 Severe cases have SpO2 ≤93%, tachypnea, and require supplemental oxygen or
mechanical ventilation.
 Chest x-rays often show bilateral "ground-glass" opacities.
 Some patients deteriorate rapidly without obvious early warning signs.
Shock and Respiratory Failure

Severe complications of pneumonia include:

1. Hypotension and Septic Shock:
o These may arise when pneumonia leads to systemic infection and sepsis,
which can progress to septic shock if not managed effectively. This is
especially common in cases involving gram-negative bacterial infections
or severe SARS-CoV-2 infection, particularly among older adults.
o Risk factors for developing septic shock include delayed or inadequate
treatment, antibiotic-resistant organisms, preexisting comorbidities, or
compromised immune function.
2. Respiratory Failure:
o Respiratory failure is a significant risk, particularly in severe bacterial
pneumonias or SARS-CoV-2 infections. In severe cases, patients may
require intubation and mechanical ventilation to support breathing and
oxygenation.
These complications underscore the importance of timely and appropriate medical
management, especially for patients with higher risk factors or compromised immunity.
For a comprehensive approach to septic shock management, refer to Chapter 11.

Pleural Effusion
A parapneumonic effusion refers to any pleural effusion associated with bacterial
pneumonia, lung abscess, or bronchiectasis. It occurs when fluid accumulates in the
pleural space between the parietal and visceral pleurae of the lung due to infection.
The management of parapneumonic effusion typically begins with detection through
chest x-ray. If a pleural effusion is suspected, thoracentesis (a procedure to remove
fluid from the pleural space) is performed to collect a sample for analysis. Based on the
pathogenesis, parapneumonic pleural effusions are classified into three stages:
1. Uncomplicated: Fluid accumulation with little or no infection.
2. Complicated: Infection or inflammation of the pleural space, causing a change in
the nature of the fluid.
3. Thoracic Empyema: A severe infection in which thick, purulent (pus-filled) fluid
accumulates, often with fibrin development and the formation of loculated
(walled-off) areas of infection.
In the case of empyema, treatment typically involves:
 Chest tube insertion to establish proper drainage and remove the purulent fluid.
 Antibiotic therapy for 4 to 6 weeks to ensure sterilization of the empyema
cavity.
 In some cases, surgical intervention may be required to remove infected tissue
or provide further drainage if the infection does not resolve with antibiotics alone.
Effective management of parapneumonic effusion and empyema is crucial to prevent
further complications such as respiratory failure or sepsis.

Aspiration and Aspiration Pneumonia

Aspiration is the inhalation of foreign material (such as oropharyngeal or stomach
contents) into the lungs, which can lead to aspiration pneumonia. This is a serious
complication that can cause pneumonia, and the clinical manifestations include
tachycardia, dyspnea, central cyanosis, hypertension, hypotension, and potentially
death. Aspiration pneumonia is believed to account for 5% to 15% of community-
acquired pneumonia (CAP).
Pathophysiology of Aspiration Pneumonia
The primary factors that determine the severity and outcome of aspiration pneumonia
include the volume and character of the aspirated contents:
 Colonized oral or pharyngeal material: The bacteria in the aspirated material
lead to an acute inflammatory response in the lungs.
  Causative organisms: Common pathogens involved in aspiration pneumonia
include Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus
influenzae, and Enterobacter species.
The type of material aspirated plays a significant role in the severity of the disease:
 Solid particles: Aspiration of food can cause mechanical blockage and lead to
secondary infection.
 Acidic gastric juices: Aspiration of stomach acid can damage alveoli and
capillaries, leading to significant injury.
 Fecal contamination: More common in cases of intestinal obstruction, fecal
material introduces endotoxins into the body, which can increase mortality.
Conditions such as dysphagia, esophageal strictures, gastroesophageal reflux
disease (GERD), and tracheoesophageal fistula are also associated with an
increased risk of aspiration pneumonia.
Prevention of Aspiration
Preventing aspiration is essential, particularly in patients with impaired protective airway
reflexes. The risk of aspiration is higher in those with decreased consciousness or in a
supine position. Common risk factors for aspiration include:
 Seizure activity
 Brain injury
 Sedation or anesthesia
 Stroke
 Swallowing disorders
 Cardiac arrest

Clinical strategies to prevent aspiration include:

1. Positioning: Keeping the head of the bed elevated at a 30 to 45-degree angle to
minimize the risk of aspiration.
2. Minimize sedative use: Use sedatives sparingly to maintain protective reflexes.
3. Tube feedings: Confirm the correct placement of enteral feeding tubes, avoid
bolus feedings in high-risk patients, and assess for residuals.
 4. Swallowing evaluation: Conduct a swallowing assessment before oral feeding
in patients who have been extubated after prolonged intubation.
5. Proper airway management: For patients with an endotracheal (ET) tube,
maintain the cuff pressure between 20-30 cm H2O to prevent leakage of
secretions and perform suctioning above the cuff before deflating.
For patients at risk of aspiration, proper oral hygiene, swallowing assessments, and
head positioning are crucial in minimizing the risk.
Silent Aspiration
Silent aspiration occurs when gastric contents accumulate in the stomach due to a
malfunctioning nasogastric tube, potentially leading to pneumonia if the material is
aspirated unnoticed. This condition can often develop undetected over several hours,
emphasizing the need for vigilant monitoring in high-risk patients.
Management of Aspiration in Special Cases
For patients with impaired airway reflexes (e.g., after sedation or intubation), clinical
interventions such as using a soft diet, small bites, and positioning the head (chin
tucked and head turned) can help reduce the risk of aspiration. It is also recommended
to avoid using straws during feeding to reduce the risk of aspiration.
Conclusion
Aspiration pneumonia can be a serious, life-threatening complication, but it can often be
prevented by identifying at-risk patients and employing specific strategies such as
proper positioning, monitoring swallowing ability, and minimizing sedation. Careful
management is essential to reduce the incidence and severity of aspiration pneumonia.

Pulmonary Tuberculosis
Tuberculosis (TB) is an infectious disease primarily affecting the lung parenchyma,
but it can also spread to other parts of the body, including the meninges, kidneys,
bones, and lymph nodes. The disease is caused by the bacterium Mycobacterium
tuberculosis, which is an acid-fast aerobic rod that grows slowly. This bacterium is
sensitive to heat and ultraviolet (UV) light. Other less common mycobacteria, such as
Mycobacterium bovis and Mycobacterium avium, have also been linked to TB
infection but are rare.
Global Burden of Tuberculosis
TB is a significant global public health problem closely tied to poverty, malnutrition,
overcrowding, substandard housing, and inadequate healthcare. Despite advances
in treatment and prevention, mortality and morbidity rates remain high, with M.
tuberculosis infecting an estimated one-third of the world's population. It continues
to be the leading cause of death from an infectious disease worldwide.
In 2017, there were 10 million people worldwide who fell ill with TB, and there were 1.3
million TB-related deaths according to the Centers for Disease Control and
Prevention (CDC).
Tuberculosis in the United States
In the United States, 9105 cases of TB were reported in 2017, marking a 2.3%
decrease from the previous year. However, several factors continue to hinder the
complete elimination of TB in the U.S.:
1. High prevalence among foreign-born residents: Many TB cases in the U.S.
are seen in individuals born outside of the country, particularly in regions where
TB is more common.
2. Delays in detection and reporting: There are often delays in diagnosing and
reporting new cases, which can lead to further transmission.
3. Lack of protection for contacts: Not all individuals who come into contact with
people diagnosed with infectious TB are adequately protected or monitored.
4. Substantial latent TB population: Many individuals have latent TB (inactive
infection) and are unaware of their condition, which could later progress to active
TB disease.
5. Barriers to clinical and public health support: There are challenges in
providing adequate clinical care and public health resources to effectively control
TB.
Transmission and Risk Factors of Tuberculosis (TB)
Transmission:
TB spreads primarily through airborne transmission. An infected person releases
droplet nuclei (usually 1 to 5 microns in diameter) when they talk, cough, sneeze,
laugh, or sing. Larger droplets fall quickly to the ground, but smaller droplets remain
suspended in the air and can be inhaled by others, leading to infection.
Risk Factors:
Certain groups are at higher risk for developing TB due to factors that either increase
exposure or compromise the immune system. These include:
1. Close contact with someone with active TB: Prolonged exposure to an
infected person increases the risk, especially in poorly ventilated areas.
2. Immunocompromised status: Individuals with conditions such as HIV, cancer,
organ transplants, or those on high-dose corticosteroid therapy are more
susceptible.
 3. Substance use disorder: People who abuse intravenous (IV) drugs or alcohol
are at higher risk.
4. Lack of adequate healthcare: Populations experiencing homelessness,
poverty, and those from racial or ethnic minorities, particularly children under 15
and young adults (15–44 years), face a higher risk.
5. Preexisting medical conditions: Conditions like diabetes, chronic kidney
disease, malnutrition, and certain malignancies increase the risk of TB
progression.
6. Immigration or travel to high-prevalence areas: Individuals coming from
regions such as southeastern Asia, Africa, Latin America, and the Caribbean
are at higher risk.
7. Institutionalization: Those in long-term care facilities, psychiatric
institutions, or prisons are at greater risk due to crowded and unsanitary
conditions.
8. Overcrowded or substandard housing: Living conditions that don't allow for
proper ventilation increase the likelihood of transmission.
9. Health care workers: Those performing high-risk activities such as
administering aerosolized medications, sputum induction, bronchoscopy, or
caring for immunocompromised patients are at higher risk.
Pathophysiology of Tuberculosis
Initial Infection:
When a susceptible person inhales M. tuberculosis, the bacteria travel through the
airways and reach the alveoli, where they begin to multiply. The bacteria are also
transported through the lymphatic system and bloodstream to other parts of the body,
such as the kidneys, bones, brain, and to other regions of the lungs (often the upper
lobes). The body’s immune system responds by initiating an inflammatory response,
where phagocytes (such as neutrophils and macrophages) attempt to engulf and
destroy the bacteria.
Granuloma Formation:
In response to the infection, granulomas (masses of live and dead bacteria) form.
These granulomas are surrounded by macrophages, which attempt to contain the
bacteria. The central area of the granuloma becomes a Ghon tubercle, which may
undergo necrosis (tissue death), forming a cheesy mass. Over time, this mass may
become calcified, and the bacteria may become dormant, halting the progression of
active disease. At this stage, the infection is arrested, and there is no active disease
unless the bacteria reactivate.
Progression to Active Disease:
In some cases, especially when the immune system is compromised, the Ghon
tubercle may ulcerate, releasing the necrotic material into the bronchi. The bacteria
then become airborne again, spreading the disease further. If untreated, the infection
spreads to adjacent areas of the lungs, causing more inflammation,
bronchopneumonia, and further tubercle formation.
Reactivation TB:
Reactivation of dormant TB (also known as adult-type progressive TB) can occur
when the bacteria that remained dormant during the primary infection become active
again. This reactivation is a primary cause of active disease in adults.
Chronic and Progressive Nature:
TB disease often progresses slowly, with long periods of remission, followed by
reactivation. Around 10% of individuals who are initially infected with TB develop active
disease. If not arrested, the disease spreads downward to the hilum (central region) of
the lungs and may affect other lung lobes, potentially leading to severe complications
such as pneumonia.
Clinical Manifestations of Tuberculosis (TB)
The signs and symptoms of pulmonary TB are often insidious and develop
gradually. Common clinical manifestations include:
 Low-grade fever
 Cough, which may be nonproductive or produce mucopurulent sputum
 Night sweats
 Fatigue
 Weight loss
 Hemoptysis (coughing up blood)
The systemic and pulmonary symptoms are typically chronic, often present for weeks
to months. Older adults may experience less pronounced symptoms than younger
individuals. In about 20% of cases in the United States, extrapulmonary TB (involving
organs other than the lungs) occurs. This is more common in HIV-infected patients.
Assessment and Diagnostic Findings
Once a patient presents with symptoms such as fever, anorexia, weight loss, night
sweats, fatigue, cough, and sputum production, a thorough diagnostic assessment is
necessary. This typically involves:
1. Complete history and physical examination
2. Tuberculin skin test (TST)
3. Chest X-ray (often revealing lesions in the upper lobes)
 4. Sputum culture for acid-fast bacilli (AFB)
5. Drug susceptibility testing to detect resistance in M. tuberculosis
On examination, healthcare providers assess the lungs for consolidation by evaluating
breath sounds (e.g., diminished, bronchial, crackles), fremitus (vibration), and
egophony (abnormal voice sounds). If TB is present, chest X-rays typically show upper
lobe lesions. If TB is suspected, the initial M. tuberculosis isolate should undergo
drug resistance testing.
Tuberculin Skin Test (TST)
The Mantoux test is used to detect latent TB infection (LTBI). The test involves
injecting purified protein derivative (PPD) into the intradermal layer of the forearm. A
positive result indicates past exposure to the TB bacillus but does not confirm active
disease. The test is read 48 to 72 hours after injection.
 Induration (swelling) and erythema (redness) are assessed. The size of the
induration is measured in millimeters. The test result varies depending on the
individual’s immune status:
o 0 to 4 mm: Not significant.
o 5 mm or more: Significant for individuals at risk (e.g., HIV-positive, close
contacts of TB patients).
o 10 mm or more: Significant for healthy individuals with normal immunity.
o ≥15 mm: Significant in any person without risk factors.
A positive result indicates exposure but does not necessarily mean active TB.
Additional tests are needed to differentiate latent TB infection from active TB disease.
Interferon-Gamma Release Assays (IGRAs)
Two TB blood tests, QuantiFERON-TB Gold® Plus (QFT-Plus) and T-SPOT®, are
used in certain situations, such as in people who have received the BCG vaccine or
those unlikely to return for a second skin test appointment. IGRAs are rapid and provide
results within 24 to 36 hours. A positive IGRA indicates TB infection, but additional
tests are needed to determine if the infection is latent or active. A negative IGRA
suggests that the person is unlikely to have a latent or active TB infection.
Sputum Culture
A sputum sample is essential for diagnosing TB. The presence of acid-fast bacilli
(AFB) in a sputum smear may suggest TB but does not confirm the diagnosis because
some AFB may be other species of mycobacteria. A sputum culture is necessary to
confirm M. tuberculosis and assess for drug resistance. The initial isolate should be
tested for drug susceptibility, and resistance patterns should be monitored during
treatment, particularly for patients not responding to therapy.
Gerontologic Considerations in Tuberculosis (TB)
In older adults, tuberculosis (TB) may have atypical manifestations. Symptoms may
not be as obvious as in younger individuals and may include:
 Unusual behavior
 Altered mental status
 Fever
 Anorexia
 Weight loss
Additionally, older adults may have delayed reactions or no reaction at all to the
tuberculin skin test (TST) due to loss of immunologic memory or recall
phenomenon (delayed reactivity). A second test may be required 1 to 2 weeks later to
confirm results. Those in long-term care facilities are at increased risk for both
primary and reactivated TB compared to those in the community.
Medical Management of Tuberculosis
The primary treatment for pulmonary TB involves anti-TB medications for a duration
of 6 to 12 months. The long treatment course is crucial to eradicate the bacteria and
prevent relapse. However, the rise of drug-resistant TB has posed a major challenge
to therapy.
Drug-resistant TB includes:
 Multidrug-resistant TB (MDR TB): Resistant to at least isoniazid and rifampin.
High-risk groups include those who are HIV-positive, institutionalized, or
homeless.
 Extensively drug-resistant TB (XDR TB): Resistant to isoniazid, rifampin, at
least one fluoroquinolone, and one of three injectable second-line drugs (e.g.,
amikacin, kanamycin, or capreomycin). Individuals with HIV or other
immunocompromised conditions are more vulnerable to XDR TB.
Given the increasing resistance, initial treatment often involves four or more drugs to
ensure successful treatment and minimize the risk of relapse. New medications are
being developed and evaluated for use.
First-Line Antituberculosis Medications for Active Disease
The four first-line medications used in active TB treatment are:
1. Isoniazid
 2. Rifampin
3. Pyrazinamide
4. Ethambutol
Combination therapies (e.g., isoniazid + rifampin) and medications taken twice a
week (e.g., rifapentine) are used to improve adherence, though they can be more
expensive.
For MDR TB, drug sensitivity testing is essential to guide treatment, and the World
Health Organization (WHO) has issued guidelines for managing drug-resistant TB.
TB Treatment Phases
TB treatment typically follows two phases:
1. Initial Phase (Intensive Phase):
o Involves a combination of isoniazid, rifampin, pyrazinamide, and
ethambutol, along with vitamin B6 (50 mg) daily for 8 weeks.
2. Continuation Phase:
o After the initial 8 weeks, the patient continues treatment with isoniazid
and rifampin or isoniazid and rifapentine. This phase typically lasts 4 to
7 months.
o 4 months is the standard duration.
o 7 months is recommended for:
 Patients with cavitary pulmonary TB.
 Those whose sputum culture remains positive after 2 months of
treatment.
 Patients who are on once-weekly therapy with isoniazid and
rifapentine and have a positive culture at the end of the initial
phase.
Patients are generally considered noninfectious after 2 to 3 weeks of continuous
therapy, but the total number of doses is more important than the length of time to
ensure the full completion of the therapy.
Prophylactic Use of Isoniazid
Isoniazid may also be used for preventive treatment in individuals at risk for TB,
including:
 Household contacts of people with active TB
  HIV-positive individuals with a positive tuberculin skin test (TST) reaction
 Individuals with fibrotic lesions suggestive of old TB or those who show skin
test conversion (a change in TST results indicating recent exposure)
 IV drug users with a significant TST reaction (≥10 mm induration)
 Individuals with high-risk comorbid conditions (e.g., diabetes, chronic kidney
disease)
Prophylactic isoniazid treatment usually lasts 6 to 12 months, with regular monitoring
of liver enzymes, blood urea nitrogen (BUN), creatinine levels, and sputum culture
results for effectiveness and adherence.
Nursing Management for Tuberculosis
Effective nursing management in tuberculosis (TB) care includes promoting airway
clearance, supporting adherence to treatment, encouraging activity and nutrition,
and preventing transmission.
1. Promoting Airway Clearance
 Hydration: Increasing fluid intake helps thin secretions, making them easier to
clear, and acts as a natural expectorant.
 Positioning for Airway Drainage: The nurse instructs the patient on correct
positioning to use postural drainage, allowing gravity to assist in clearing
bronchial secretions (as explained in Chapter 20 of the referenced source).
2. Promoting Adherence to the Treatment Regimen
 Importance of Adherence: TB treatment requires strict adherence to prevent
transmission and control infection. Nurses educate patients on medication
schedules, possible side effects, and the consequences of nonadherence,
including the risk of drug resistance.
 Medication Instructions:
o Administration Timing: Patients are advised to take medications on an
empty stomach or at least 1 hour before meals, as food can affect
absorption, although GI upset may occur.
o Avoiding Certain Foods: Patients on isoniazid should avoid foods high
in tyramine and histamine (e.g., tuna, aged cheese, red wine) due to
potential adverse reactions.
o Rifampin: Patients are advised that this drug can discolor contact lenses
and may make some medications (like beta-blockers, oral contraceptives,
anticoagulants, and oral hypoglycemics) less effective. Regular monitoring
 of liver enzymes, BUN, and creatinine levels is necessary for patients
on rifampin to assess liver and kidney function.
 Community Support Programs:
o Directly Observed Therapy (DOT): A healthcare provider supervises
medication intake to ensure adherence, especially for high-risk patients.
o Case Management: Each TB patient is assigned a case manager who
coordinates care, offering a comprehensive approach to ensure treatment
completion.
3. Promoting Activity and Adequate Nutrition
 Activity Schedule: Patients often experience weakness and fatigue. A
progressive activity plan is essential to help rebuild muscle strength and
stamina.
 Nutrition: Patients with TB commonly suffer from anorexia, weight loss, and
malnutrition. Small, frequent meals and possibly liquid nutritional
supplements can help them meet caloric needs. For those with limited
resources, referrals to community services (e.g., soup kitchens or Meals on
Wheels) can aid in improving nutritional intake.
4. Preventing Transmission of TB Infection
 Patient Education: Patients are educated on hygiene practices to reduce the
risk of spreading TB, including mouth care, covering the mouth and nose
when coughing/sneezing, and proper disposal of tissues.
 Contact Tracing: TB is a reportable disease, and close contacts of the infected
patient are screened and treated if necessary.
 Preventing Miliary TB: TB can spread beyond the lungs to other organs in a
form known as miliary TB. This can result in widespread infection in organs like
the lungs, spleen, liver, and kidneys. Miliary TB symptoms may range from high
fever and rapid illness progression to a slow, chronic process with anemia and
mild fever. Monitoring for signs of miliary TB involves observing changes in
the patient’s temperature, renal and cognitive function, and respiratory status.
Treatment is the same as for pulmonary TB, requiring a similar rigorous
adherence to the medication regimen.
By implementing these strategies, nursing management aims to enhance treatment
outcomes, reduce TB transmission, and support patients through the complex and
prolonged recovery process.
Lung Abscess: Overview and Management
A lung abscess is a localized infection within the lung tissue, typically characterized by
a collection of pus resulting from microbial infection, often due to anaerobic bacteria
aspiration. The condition is identified on a chest x-ray as a cavity measuring at least 2
cm. Individuals with impaired cough reflexes, swallowing issues, CNS disorders, and
altered states of consciousness are at higher risk for developing lung abscesses.
Pathophysiology
 Cause: Lung abscesses primarily result from bacterial pneumonia or aspiration
of oral anaerobes. Other causes include airway obstruction, necrotizing
pneumonia, TB, pulmonary embolism, or chest trauma.
 Location: Abscesses commonly form in areas affected by aspiration and are
influenced by the patient's positioning (e.g., posterior segment of upper lobes or
superior segment of lower lobes in bedridden patients).
 Progression: The abscess becomes encapsulated by fibrous tissue over time. If
the abscess involves the bronchus, it may result in continuous sputum
production, and if it reaches the pleura, it can cause empyema. In some cases, a
bronchopleural fistula forms, creating a connection between the bronchus and
pleura.
Clinical Manifestations
 Symptoms range from mild productive cough to acute illness.
 Common Symptoms:
o Fever and productive cough with foul-smelling or bloody sputum.
o Pleuritic chest pain, dyspnea, anorexia, and weight loss.
o Physical findings may include dullness on percussion, decreased breath
sounds, pleural friction rub, and crackles.
Assessment and Diagnostic Findings
 Chest Examination: Dull percussion, decreased breath sounds, and pleural
friction rub.
 Imaging: Chest x-ray shows an air-fluid level; a CT scan may be needed for
detailed views.
 Laboratory Tests: Sputum culture identifies causative organisms; fiberoptic
bronchoscopy may aid in diagnosis.

Prevention
  Dental Hygiene: Good oral hygiene and antibiotics before dental procedures for
those at risk (e.g., patients with infected gums) reduce risk.
 Timely Treatment of Pneumonia: Ensures early management of infections to
prevent abscess formation.
Medical Management
 Antibiotics:
o IV Therapy: Clindamycin, ampicillin-sulbactam, or carbapenem are
typically used for anaerobic infections and administered for extended
periods to penetrate necrotic tissue.
o Treatment Duration: IV antibiotics for approximately 3 weeks, followed by
oral antibiotics for an additional 4-12 weeks based on clinical progress to
prevent relapse.
 Drainage:
o Postural Drainage and Chest Physiotherapy facilitate abscess
drainage.
o Percutaneous Chest Catheter: May be used for long-term drainage if
necessary.
 Nutritional Support: A high-protein, high-calorie diet supports healing during
chronic infection.
 Surgical Intervention: Rare but may be required if there is significant
hemoptysis or failure to respond to treatment, involving procedures like
lobectomy.
Nursing Management of Lung Abscess
Effective nursing management for lung abscess involves diligent monitoring, support,
and patient education to promote recovery and prevent complications.
In-Hospital Nursing Management
1. Administration of Medications:
o Antibiotics and IV Therapy: Administer as prescribed, monitoring closely
for potential adverse effects. Antibiotic treatment is often prolonged, so
vigilance in observing patient responses is essential.
2. Chest Physiotherapy (CPT):
o Initiate CPT as prescribed to assist in draining the abscess. Techniques
such as chest percussion and postural drainage help mobilize secretions,
making it easier for the patient to expectorate sputum.
 3. Breathing Exercises:
o Educate the patient on deep-breathing and coughing exercises to
enhance lung expansion, oxygenation, and secretion clearance. These
exercises are typically performed every two hours.
4. Nutritional Support:
o Encourage a diet high in protein and calories, which is critical for healing,
especially in the context of chronic infection. Ensure adequate intake to
support immune function and tissue repair.
5. Emotional Support:
o Lung abscesses may take a considerable time to heal, and patients may
experience fatigue or frustration. Providing emotional support can help in
managing these feelings and improve adherence to the therapeutic
regimen.
Promoting Home, Community-Based, and Transitional Care
1. Patient Education for Self-Care:
o Wound and Drain Care: If discharged with an open wound or drain,
educate the patient and caregivers on dressing changes to prevent skin
irritation, odor, and infection.
o Monitoring for Infection: Teach the signs and symptoms of infection,
such as fever, increased pain, or drainage changes.
o Breathing Exercises and CPT: Reinforce the need for deep-breathing,
coughing exercises, and, if needed, show caregivers how to perform chest
percussion and postural drainage.
2. Continuing and Transitional Care:
o Arrange referrals for home health or transitional care if ongoing therapy is
required at home. Home visits allow the nurse to:
 Assess the patient’s physical health, nutritional status, and home
environment.
 Ensure that the patient and family are managing the therapeutic
regimen.
 Reinforce education and provide nutritional counseling to support
optimal health.
o Emphasize completing the antibiotic course fully to prevent relapse and
stress the importance of balancing rest with activity for recovery.
 3. Support for Home-Based IV Therapy:
o For patients needing extended IV antibiotics, coordinate home health
services to set up and oversee the administration, providing training to the
patient or family if necessary. Some patients may receive IV therapy at a
nearby clinic or provider’s office.
4. Health Promotion:
o Use the opportunity to address broader health promotion strategies,
especially for patients who may have previously neglected their health.
Topics may include routine health screenings, smoking cessation if
applicable, and follow-up care to monitor recovery.

Sarcoidosis
Sarcoidosis is a type of interstitial lung disease that is also an inflammatory,
multisystem, granulomatous disease of unknown etiology (King, 2019a). Although 90%
of patients demonstrate thoracic involvement, any organ may be affected. Sarcoidosis
usually presents between 20 and 40 years of age and is slightly more common in
women than in men (Weinberger et al., 2019). In the United States, the disease is more
common in African Americans, and the estimated prevalence is 10 to 20 per 100,000
people (King, 2019a).
Nursing Management of Sarcoidosis
Nursing care for patients with sarcoidosis focuses on managing symptoms, supporting
the medical treatment plan, and providing education on long-term care and lifestyle
adjustments to optimize quality of life.
Nursing Interventions
1. Supporting Medical Regimen:
o Corticosteroid Therapy: Educate patients on the importance of adhering
to corticosteroid therapy as prescribed. Emphasize tapering doses, as
instructed by their healthcare provider, and discuss potential side effects
like weight gain, mood changes, and risk of infection.
o Monitoring for Adverse Effects: Observe patients for adverse effects
associated with corticosteroid use, including hyperglycemia, hypertension,
and gastrointestinal discomfort.
2. Patient Education:
o Medication Education: Instruct on proper corticosteroid usage, including
timing, dose adjustment, and management of side effects. Educate on the
necessity of reporting persistent symptoms, such as cough, dyspnea, or
chest pain, as these may indicate disease progression.
o Lifestyle Modifications: Encourage patients to maintain a balanced diet,
adequate hydration, and avoid smoking or exposure to lung irritants to
support respiratory health.
o Follow-up Care: Reinforce the importance of regular follow-up visits every
3–6 months to monitor disease progression, lung function, and overall
 health. Explain that periodic testing, including imaging and pulmonary
function tests, may be required.
3. Psychosocial Support:
o Sarcoidosis is a chronic condition that can impact multiple organ systems,
causing anxiety or feelings of uncertainty. Providing emotional support and
validating the patient's concerns can help in managing the psychological
impact.
o Encourage connection with support groups, such as the Foundation for
Sarcoidosis Research, to provide a sense of community and additional
resources.
4. Home and Community-Based Care:
o Self-Care Empowerment: Educate patients to self-monitor for symptoms
of disease exacerbation and encourage communication with healthcare
providers for any new or worsening symptoms.
o Community Resources: Direct patients to local or online sarcoidosis
support networks, which can offer assistance, coping strategies, and
further education about the disease.

Pleurisy
Pleurisy (or pleuritis) is the inflammation of both the parietal and visceral layers of the
pleura—the membranes surrounding the lungs and lining the chest cavity. This
condition often causes intense chest pain and can develop alongside respiratory
infections, diseases like tuberculosis (TB), or after chest trauma. Pleurisy may also
accompany other conditions such as pulmonary embolism, cancer, or after thoracic
surgery.
Clinical Manifestations of Pleurisy
The hallmark of pleurisy is sharp, stabbing pain that worsens with respiratory
movements. Key characteristics include:
 Pain with Respiratory Movements: The pain intensifies with actions like deep
breathing, coughing, or sneezing, due to the inflamed pleural layers rubbing
against each other. Holding the breath can temporarily reduce the pain.
 Pain Location: Typically, pleuritic pain is unilateral (affecting only one side of the
chest), though it may radiate to areas such as the shoulder or abdomen.
 Pain Variation with Fluid Accumulation: If pleural fluid builds up over time, the
intensity of pain may lessen as the inflamed surfaces are separated.
Pathophysiology of Pleurisy Pain
The parietal pleura contains nerve endings, while the visceral pleura does not. When
these inflamed layers move against each other during respiration, the resulting friction
and irritation lead to the characteristic "knife-like" pain.
Assessment and Diagnostic Findings for Pleurisy
During the early stages of pleurisy, when fluid accumulation is minimal, a distinctive
pleural friction rub—a grating sound—can often be heard via stethoscope as the
inflamed pleural layers rub together. As more fluid builds up and separates these layers,
the sound may disappear. Diagnostic steps include:
 Chest X-rays: Used to detect inflammation and identify underlying conditions.
  Sputum Analysis: Examines sputum for infectious agents if respiratory infection
is suspected.
 Thoracentesis: Involves the extraction of pleural fluid for laboratory analysis,
helping to identify infection, malignancy, or other underlying causes.
 Pleural Biopsy: Less commonly, a biopsy of the pleura may be taken if needed
to confirm a diagnosis.
Medical Management of Pleurisy
Treatment focuses on addressing the underlying cause and managing pain. As the root
condition (e.g., infection, pneumonia) is treated, pleuritic inflammation often subsides.
Management includes:
 Pain Relief: Analgesics and NSAIDs are typically prescribed to manage pain and
allow deep breathing. Heat or cold applications may also alleviate symptoms.
 Monitoring for Pleural Effusion: Patients are observed for signs of fluid
buildup, such as shortness of breath or pain that eases when in certain positions.
 Severe Pain Management: For persistent, intense pain, an intercostal nerve
block may be used to provide additional relief.
Nursing Management of Pleurisy
Pleurisy (or pleuritis) is an inflammation of the pleural layers, often presenting with
severe pain that worsens during breathing. Effective nursing care can help alleviate
symptoms, support medical treatment, and improve patient comfort.
Key Nursing Interventions
1. Pain Management:
o Positioning: Encourage the patient to turn frequently onto the affected
side. This splints the chest wall and reduces stretching of the inflamed
pleura, helping alleviate pain.
o Splinting: Teach the patient to use their hands or a pillow to splint the rib
cage when coughing, which can lessen the pain experienced during deep
breaths or coughing.
2. Monitoring and Assessment:
o Regularly monitor respiratory status, including rate, rhythm, and breath
sounds.
o Assess for the development of pleural effusion by observing symptoms
such as worsening dyspnea, reduced chest wall expansion, or changes in
respiratory sounds (e.g., pleural friction rub).
3. Administering Medications:
o Administer prescribed analgesics, including NSAIDs, to control pain and
promote effective breathing.
o If prescribed, apply topical heat or cold to the chest area to provide
additional pain relief.
4. Patient Education:
o Educate the patient on the nature of pleurisy, its association with
respiratory movement, and the importance of pain management.
o Emphasize the need to take deep breaths despite the discomfort to
prevent atelectasis, a common complication due to shallow breathing.
5. Emotional Support:
 o Reassure the patient that, with treatment of the underlying cause (e.g.,
pneumonia or infection), pleuritic pain typically resolves.
Goal of Nursing Care
To reduce pain and discomfort associated with pleurisy, support medical treatment,
prevent complications like pleural effusion, and help the patient engage in essential
breathing exercises and movement without excessive discomfort.

Pleural Effusion
Pleural effusion is the abnormal accumulation of fluid in the pleural space, typically
secondary to an underlying condition rather than a primary disease. The pleural space
normally holds a small amount of lubricating fluid (5 to 15 mL) to allow smooth
movement between the pleural layers. However, in certain conditions—such as heart
failure, tuberculosis (TB), pneumonia, pulmonary infections, nephrotic syndrome,
connective tissue diseases, pulmonary embolism (PE), or cancers (especially
bronchogenic carcinoma)—excess fluid may accumulate.

Pathophysiology
The fluid in pleural effusion can vary in nature and is classified as either a transudate
or an exudate:
 Transudate: A clear, filtrate-type fluid resulting from imbalances in hydrostatic or
oncotic pressures across intact capillary walls. Transudative effusion generally
indicates that the pleural membranes are not directly diseased and often results
from conditions like heart failure.
 Exudate: Fluid resulting from inflammation or damage to the pleural surfaces,
often due to infection (e.g., bacterial), malignancy, or inflammatory diseases.
Exudative effusion often presents with more complex fluid content, such as
proteins or inflammatory cells, indicating pleural involvement.
Pleural effusion is associated with symptoms like pain and dyspnea, and its pathologic
accumulation typically warrants further investigation and management depending on the
cause and fluid type.

Clinical Manifestations
Symptoms of pleural effusion often stem from the underlying disease. For example:
 Pneumonia-related effusions may cause fever, chills, and pleuritic chest pain.
 Malignant effusions may result in symptoms like dyspnea, difficulty lying flat,
and cough.
The severity of symptoms correlates with the size of the effusion and the rate of fluid
accumulation. Large effusions typically cause noticeable dyspnea, while small-to-
moderate effusions may lead to minimal or no symptoms.

Assessment and Diagnostic Findings

Physical examination of pleural effusion may reveal:
 Decreased or absent breath sounds over the affected area
 Reduced fremitus (vibration felt on the chest wall)
 Dullness or flatness on percussion
In cases of significant pleural effusion, there may be acute respiratory distress with
tracheal deviation away from the affected side. Diagnostic tools include:
 Chest x-ray and CT scan to visualize the fluid accumulation
 Thoracentesis for fluid sampling and analysis, aiding in identifying the cause
 Lateral decubitus x-ray to allow fluid to "layer out," highlighting an air-fluid line
Fluid analysis may include bacterial culture, Gram stain, AFB stain for TB, cell counts,
and chemistry studies. Cytology can also be performed to check for malignant cells, and
a pleural biopsy may be indicated for further diagnosis.

Medical Management
Treatment aims to:
1. Identify and address the underlying cause (e.g., managing heart failure or
infection).
2. Prevent fluid reaccumulation.
3. Alleviate discomfort and respiratory compromise.

For symptomatic relief, thoracentesis is performed to remove fluid, obtain samples,

and relieve dyspnea. For larger effusions, a chest tube with a water-seal drainage or
suction system may be used to re-expand the lung.
In cases of malignant pleural effusion, fluid often recurs, making repeated
thoracentesis less ideal. Chemical pleurodesis—using an irritant like talc—is
performed after draining the pleural space to fuse the pleural layers and prevent fluid
reaccumulation. The procedure may use a chest tube or thoracoscopic approach, with
the tube clamped for 60–90 minutes to ensure agent distribution.
Alternative treatments for malignant effusions include surgical pleurectomy, PleurX®
catheter placement for outpatient drainage, or pleuroperitoneal shunt implantation.
The latter allows patients to manually pump pleural fluid into the peritoneal space,
providing relief from effusion symptoms.

Nursing Management
In managing a patient with pleural effusion, the nurse plays a critical role in supporting
the medical regimen and ensuring patient comfort throughout the diagnostic and
treatment process. The nurse’s responsibilities include:
1. Preparation and Support for Thoracentesis:
o Positioning and Comfort: The nurse ensures the patient is positioned
appropriately for thoracentesis (typically sitting upright with the arms
resting on a table), and provides emotional support during the procedure.
o Monitoring and Documentation: After the procedure, the nurse records
the volume of fluid removed and ensures it is sent for appropriate
laboratory analysis.
2. Chest Tube Management:
o If a chest tube with a water-seal system is used to drain the pleural
space, the nurse monitors the system’s functionality. This includes
checking for proper suction and ensuring the drainage is collected and
recorded at prescribed intervals.
 o The nurse must also ensure the integrity of the chest tube system and
monitor for complications such as air leaks or displacement.
3. Pain Management:
o Pain relief is a priority, and the nurse assesses the patient’s pain level
regularly. Analgesics are administered as prescribed.
o If the patient is undergoing pleurodesis (e.g., talc instillation) for a
malignancy-related pleural effusion, the nurse assists the patient in
assuming positions that minimize pain while facilitating the spread of the
talc over the pleural surface.
4. Patient Education:
o Outpatient Management: For patients discharged with a pleural
catheter for drainage, the nurse educates both the patient and their family
on the proper care and management of the catheter and drainage system.
o This includes how to maintain hygiene, recognize signs of infection or
complications, and manage fluid drainage at home.
In all aspects of care, the nurse's role includes continuous monitoring for complications
and providing holistic support to ensure comfort and effective treatment outcomes.

Empyema
An empyema is an accumulation of thick, purulent fluid within the pleural space,
which often forms loculated areas (walled-off pockets) where infection is contained.
This condition typically results from a bacterial infection but can have other causes as
well.

Pathophysiology
 Causes: Empyema usually develops as a complication of bacterial pneumonia
or lung abscesses. Other causes include:
o Penetrating chest trauma.
o Hematogenous infection (spread from other parts of the body).
o Nonbacterial infections.
o Iatrogenic causes, such as after thoracic surgery or thoracentesis.
 Progression: Initially, the pleural fluid is thin with a low leukocyte count. Over
time, the infection progresses into a fibropurulent stage where the fluid
becomes thicker and contains more cells. Eventually, this can result in a
loculated empyema, where the infection becomes walled-off within the pleural
space, enclosing the lung in a thick exudative membrane.

Clinical Manifestations
The symptoms of empyema are often similar to those of a severe respiratory
infection or pneumonia, including:
 Fever and night sweats.
 Pleural pain (sharp chest pain, often worsened by breathing or coughing).
 Cough.
 Dyspnea (shortness of breath).
 Anorexia (loss of appetite).
 Weight loss.
In patients who are immunocompromised or have been treated with antimicrobial
therapy, the symptoms may be more subtle or vague, making diagnosis more
challenging.

Assessment and Diagnostic Findings

 Physical examination: On chest auscultation, breath sounds will often be
decreased or absent over the affected area. Percussion will show dullness,
and there may be decreased fremitus (vibrations felt on palpation).
 Imaging: A chest CT is essential for confirming the diagnosis. In some cases, a
diagnostic thoracentesis (needle aspiration of pleural fluid) is performed, often
with the guidance of ultrasound to aid in accurate fluid removal.

Medical Management
The main goals of treatment are to drain the pleural cavity and achieve complete lung
expansion. Management typically involves:
1. Drainage of pleural fluid, based on the severity of the condition and the stage of
the disease:
o Thoracentesis (needle aspiration): This is used when the fluid volume is
small, and the fluid is not excessively purulent or thick.
o Tube thoracostomy: A chest tube is inserted for drainage, often with the
instillation of thrombolytic agents (drugs that help dissolve the loculated
or thick pleural fluid). This is often used for loculated pleural effusions.
o Open chest drainage: In severe cases, a thoracotomy may be
necessary to remove the thickened pleura, pus, and debris. This might
involve rib resection to access and drain the pleural space.
2. Antibiotic therapy: Once the causative organism is identified, appropriate
antibiotics (often starting intravenously) are prescribed. The treatment typically
lasts 4 to 6 weeks to sterilize the pleural cavity and resolve the infection.
3. Surgical interventions:
o Decortication: In cases of long-standing inflammation, an exudate may
form over the lung, which can trap it and interfere with normal lung
expansion. This exudate needs to be removed surgically through
decortication.
o The patient may need to remain in the hospital for a prolonged period, with
serial chest x-rays to monitor progress and confirm the obliteration of the
pleural space.
4. Home care: Patients may be discharged with a chest tube in place and must
continue to monitor and drain pleural fluid at home.

Nursing Management
 Support and education: The nurse’s role is crucial in helping the patient cope
with the prolonged nature of the condition and recovery process.
o Teach lung-expanding breathing exercises to help restore normal
respiratory function.
 o Provide care specific to the method of drainage being used (e.g., needle
aspiration, chest tube, rib resection, etc.).
o If a patient is discharged with a drainage tube or system, the nurse should
educate the patient and family on:
 Care of the drainage system and site.
 Measuring and observing drainage.
 Recognizing signs and symptoms of infection.
 When to contact the primary healthcare provider.

Acute Respiratory Failure

Definition and Diagnosis
Acute respiratory failure is a life-threatening condition where the lungs fail to provide
adequate oxygenation or ventilation. It is characterized by:
 Hypoxemia: A decrease in arterial oxygen tension (PaO2) to less than 60 mm
Hg.
 Hypercapnia: An increase in arterial carbon dioxide tension (PaCO2) to greater
than 50 mm Hg.
 Acidosis: An arterial pH of less than 7.35.
Acute respiratory failure is distinct from chronic respiratory failure, which occurs
gradually and may be a long-term issue due to conditions like COPD or neuromuscular
diseases. Chronic respiratory failure can evolve into acute failure, especially in
situations like COPD exacerbations or infections.

Pathophysiology
Acute respiratory failure occurs when there is either an impairment in ventilation or
oxygenation mechanisms:
1. Ventilatory failure: This is when the ability to move air in and out of the lungs is
compromised. Causes include:
o Central nervous system dysfunction (e.g., drug overdose, head trauma,
infections, sleep apnea).
o Neuromuscular dysfunction (e.g., conditions like myasthenia gravis,
Guillain-Barré syndrome, amyotrophic lateral sclerosis, or spinal
cord trauma).
o Musculoskeletal dysfunction (e.g., chest trauma, kyphoscoliosis,
malnutrition).
o Pulmonary dysfunction (e.g., COPD, asthma, cystic fibrosis).
2. Oxygenation failure: This occurs when there is insufficient oxygen being
transferred to the bloodstream. Causes include:
o Pneumonia.
o Acute Respiratory Distress Syndrome (ARDS).
o Heart failure.
 o COPD.
o Pulmonary embolism (PE).
o Restrictive lung diseases, which limit lung volumes (e.g., fibrosis,
interstitial lung disease).

Postoperative Respiratory Failure

Acute respiratory failure can also occur after major thoracic or abdominal surgery due to
several factors:
 Anesthetic, analgesic, and sedative agents: These can depress respiration or
enhance the effects of opioids, leading to hypoventilation.
 Pain: Pain from surgery can interfere with deep breathing and effective coughing.
 V/Q mismatch: This is a common cause of respiratory failure after major
surgeries like abdominal, cardiac, or thoracic procedures. It refers to a
ventilation/perfusion mismatch, where the air and blood flow to the lungs are
not well-matched, leading to poor oxygen exchange.

Clinical Manifestations
The signs and symptoms of acute respiratory failure are progressive and correlate
with the severity of hypoxemia (low oxygen) and hypercapnia (high carbon dioxide
levels):
 Early signs (due to impaired oxygenation):
o Restlessness
o Fatigue
o Headache
o Dyspnea (difficulty breathing)
o Air hunger (a sensation of not getting enough air)
o Tachycardia (increased heart rate)
o Increased blood pressure
 As hypoxemia worsens:
o Confusion and lethargy
o Tachycardia and tachypnea (increased heart rate and rapid breathing)
o Central cyanosis (bluish color in the lips, face, or extremities)
o Diaphoresis (excessive sweating)
o Respiratory arrest (if untreated)
 Physical findings:
o Use of accessory muscles to breathe (indicating difficulty in breathing)
o Decreased breath sounds (if the patient cannot adequately ventilate)
o Signs related to the underlying disease process contributing to acute
respiratory failure (e.g., pneumonia, COPD, or trauma).

Medical Management
The primary goals of treatment for acute respiratory failure are:
1. Correct the underlying cause (such as pneumonia, COPD exacerbation, or
heart failure).
2. Restore adequate gas exchange in the lungs to normalize oxygen and carbon
dioxide levels.
In some cases, endotracheal (ET) intubation and mechanical ventilation may be
required to support the patient's breathing while the underlying condition is treated.

Nursing Management
Nurses play a crucial role in managing patients with acute respiratory failure, especially
in the intensive care unit (ICU). Key responsibilities include:
1. Assisting with intubation and mechanical ventilation:
o Provide support and help maintain the patient's airway.
o Monitor the settings and function of the mechanical ventilator.
2. Continuous assessment of the patient's respiratory status:
o Monitor the level of responsiveness: Check for signs of confusion or
lethargy.
o Arterial blood gases (ABGs): Regularly assess to evaluate oxygenation
and ventilation levels.
o Pulse oximetry: Continuously monitor oxygen saturation.
o Vital signs: Monitor heart rate, blood pressure, and respiratory rate.
3. Prevention of complications:
o Implement a turning schedule to prevent pressure ulcers and improve
lung expansion.
o Perform mouth care and skin care to maintain hygiene and prevent
infections.
o Provide range of motion exercises for the extremities to promote
circulation and prevent stiffness.
4. Communication:
o Since patients on mechanical ventilation may not be able to speak, the
nurse helps the patient communicate by using alternative methods (e.g.,
writing, signaling).
o Assess the patient's understanding of their treatment plan and involve
them in decision-making as possible.
5. Addressing underlying problems:
o Treat the root cause of respiratory failure, such as infection, trauma, or
disease exacerbation (e.g., COPD or pulmonary embolism).
6. Patient education:
o As the patient's condition stabilizes, the nurse provides education about
the underlying disorder (e.g., pneumonia, asthma) and self-care strategies
to prevent future episodes.

Acute Respiratory Distress Syndrome (ARDS)

ARDS is a severe clinical syndrome characterized by widespread inflammation in the
lungs, which leads to acute, progressive pulmonary edema, and impaired gas
exchange. It is a serious condition that often follows various insults to the lungs, both
direct and indirect.

Pathophysiology
The pathophysiology of ARDS begins with inflammatory triggers that release cellular
and chemical mediators, which damage the alveolar-capillary membrane. This damage
leads to a cascade of events:
1. Inflammatory Response: The release of mediators causes injury to lung tissue,
resulting in edema and inflammation.
2. Alveolar Collapse: Due to the influx of inflammatory cells, fluid, and dysfunction
of surfactant, the alveoli collapse, reducing their ability to exchange gases.
3. V/Q Mismatch: Severe ventilation/perfusion (V/Q) mismatching occurs, where
blood is pumped through nonventilated areas of the lung, causing a shunt (blood
passing through nonfunctioning alveoli).
4. Impaired Gas Exchange: Blood that does not come into contact with functioning
alveoli leads to severe hypoxemia (low oxygen levels in the blood), which is
refractory to oxygen supplementation.
5. Decreased Lung Compliance: The inflammation leads to decreased lung
compliance, reducing the lung's ability to expand and impairing normal
respiratory function.
These pathophysiologic changes lead to acute, severe respiratory failure that
requires immediate medical intervention.

Risk Factors for ARDS

ARDS can develop due to a variety of direct or indirect insults to the lungs. Common
risk factors include:
 Aspiration (e.g., gastric contents, drowning, hydrocarbons)
 Infections (e.g., COVID-19 pneumonia, pneumonia of any etiology)
 Sepsis
 Trauma (e.g., pulmonary contusion, head injury)
 Shock (due to any cause)
 Fat or air embolism
 Drug overdose and ingestion
 Pancreatitis
 Major surgeries
 Inhalation injuries (e.g., smoke, toxic chemicals)
 Hematologic disorders (e.g., DIC, massive transfusion, cardiopulmonary
bypass)
 Metabolic disorders (e.g., uremia)
Patients who are immunocompromised, have pre-existing lung disease, or have
experienced a trauma are at higher risk for developing ARDS.

Clinical Manifestations
The clinical presentation of ARDS can range from mild to severe, progressing over time:
 Mild ARDS: Patients may experience moderate hypoxemia, tachypnea, and
dyspnea.
 Severe ARDS: Marked hypoxemia unresponsive to supplemental oxygen, use of
accessory muscles to breathe, and cyanosis.
As ARDS progresses, the following signs may appear:
 Increased work of breathing (use of accessory muscles)
  Hypoxemia that does not improve with oxygen supplementation
 Tachypnea (rapid breathing) and tachycardia (fast heart rate)
 Cyanosis (bluish color of lips or extremities)
 Decreased breath sounds and bilateral infiltrates on chest x-ray

Mortality and Prognosis

ARDS has a mortality rate ranging from 27% to 50%, depending on the severity and
the presence of other complications. Patients who survive the acute phase may suffer
from long-term complications, often related to secondary infections such as hospital-
acquired pneumonia (HCAP) or sepsis.
Nursing Alert: E-cigarette and Vaping-Associated Lung Injury (EVALI)
EVALI is a newly recognized condition linked to vaping, particularly with substances
containing THC and other additives. The Centers for Disease Control and Prevention
(CDC) has reported cases of acute lung injury associated with e-cigarette use, with
symptoms similar to ARDS. Nurses should be vigilant for ARDS in patients with a
history of vaping.

Medical Management
The primary goals of ARDS treatment are:
1. Oxygenation Support: Mechanical ventilation (often with high PEEP [positive
end-expiratory pressure]) to improve oxygenation.
2. Management of underlying cause: Treat infections, trauma, or other underlying
conditions contributing to ARDS.
3. Fluid management: Careful management of fluids to avoid exacerbating
pulmonary edema.
4. Medications: Antibiotics for infections, steroids or other agents for inflammation,
and neuromuscular blockade in severe cases to improve ventilation.

Nursing Management
Nurses play a vital role in the care of patients with ARDS, particularly in the intensive
care unit (ICU). Key aspects of nursing care include:
 Monitor oxygenation and ventilation: Use pulse oximetry, ABGs, and ventilator
settings to assess oxygenation and ventilation.
 Positioning: Prone positioning may be used to optimize lung function.
 Ventilator Management: Assist with mechanical ventilation, ensuring
appropriate settings for ARDS, including high PEEP and low tidal volumes to
minimize ventilator-associated lung injury.
 Fluid Management: Maintain fluid balance to avoid fluid overload, which can
worsen pulmonary edema.
 Prevent complications: Prevent ventilator-associated pneumonia (VAP) by
providing oral care, suctioning, and other infection control measures.
 Patient and family education: Educate patients and families about the
condition, its treatment, and recovery expectations.
ARDS remains a serious condition with complex pathophysiology that requires careful,
multidisciplinary management. Nurses play a crucial role in stabilizing the patient,
preventing complications, and supporting the family through the critical care process.
Pulmonary Edema (Noncardiogenic)

Pulmonary edema is a condition characterized by the abnormal accumulation of fluid in

the lung tissue or alveolar spaces. This condition can be life-threatening and is often
classified into two main types:
1. Cardiogenic Pulmonary Edema: Caused by heart-related issues, such as left
heart failure.
2. Noncardiogenic Pulmonary Edema: Caused by factors unrelated to heart
failure, often due to damage to the pulmonary capillary lining or other systemic
conditions.
This discussion focuses on noncardiogenic pulmonary edema, which occurs due to
damage to the pulmonary capillaries, leading to fluid leakage into the lungs. The
primary causes are as follows:

Causes of Noncardiogenic Pulmonary Edema

1. Direct Lung Injury:
o Chest Trauma: Injury to the chest wall can lead to damage of the
pulmonary capillaries.
o Aspiration: Inhalation of foreign substances like food or gastric contents
can cause inflammation and fluid buildup in the lungs.
o Smoke Inhalation: Toxic substances from smoke can damage lung tissue
and capillaries, leading to edema.
2. Hematogenous Injury:
o Sepsis: Severe infection can cause systemic inflammation, damaging the
capillaries in the lungs.
o Pancreatitis: Inflammation of the pancreas can lead to systemic
inflammatory responses affecting the lungs.
o Multiple Blood Transfusions: A high volume of transfusions can cause
capillary damage, leading to edema.
o Cardiopulmonary Bypass: The process of connecting a patient to a
heart-lung machine during surgery can result in damage to lung
capillaries.
3. Elevated Hydrostatic Pressures:
o Though noncardiogenic pulmonary edema is not primarily due to cardiac
causes, elevated pressures in the circulatory system (as seen in some
forms of shock or severe inflammation) can contribute to the development
of fluid accumulation in the lungs.

Pathophysiology
The pathophysiologic mechanism behind noncardiogenic pulmonary edema involves
the damage to the pulmonary capillary lining, which increases its permeability. This
allows fluid to leak out into the interstitial space and alveolar spaces.
 Intrapulmonary Shunting: This is a key issue in noncardiogenic pulmonary
edema. Blood passes through nonfunctioning areas of the lung (where gas
 exchange is impaired), leading to refractory hypoxemia (low oxygen levels that
do not improve despite high levels of supplemental oxygen).
 Impaired Oxygen Exchange: With the alveoli flooded with fluid, the exchange of
oxygen and carbon dioxide is significantly impaired, which leads to severe
hypoxemia (low oxygen levels in the blood).
This fluid accumulation and shunting impair the lungs’ ability to oxygenate the blood,
even when supplemental oxygen is provided at high concentrations.
Clinical Manifestations
The symptoms of noncardiogenic pulmonary edema are similar to those of cardiogenic
pulmonary edema but may be more difficult to correct due to the underlying causes:
 Severe Shortness of Breath (Dyspnea)
 Tachypnea (rapid breathing)
 Cyanosis (bluish color of the lips, extremities)
 Orthopnea (difficulty breathing when lying flat)
 Crackles on Auscultation: Due to fluid in the alveoli, crackles or rales may be
heard when listening to the lungs.
 Tachycardia (increased heart rate) as a compensatory response to low oxygen
levels.
Patients may show signs of hypoxemia, including confusion, restlessness, and
increased work of breathing. As the condition worsens, respiratory failure and cardiac
arrest can occur without prompt intervention.
Management
The management of noncardiogenic pulmonary edema involves addressing both the
underlying cause and supporting respiratory function. It shares some similarities with
the treatment of cardiogenic pulmonary edema, but the approach differs slightly due
to the unique pathophysiology.
1. Oxygen Therapy: High concentrations of supplemental oxygen are used, but
hypoxemia may persist despite oxygen administration because of the
intrapulmonary shunting.
2. Mechanical Ventilation: In severe cases, intubation and mechanical
ventilation may be necessary. Positive end-expiratory pressure (PEEP) is
used to help open collapsed alveoli and improve oxygenation.
3. Treating the Underlying Cause:
o For conditions like sepsis, appropriate antibiotic therapy is essential.
o In cases of pancreatitis, managing the inflammatory response may be
critical.
o Bronchodilators and steroids may be used in certain cases, especially if
inflammation plays a significant role.
4. Fluid Management: Careful fluid management is necessary. Unlike cardiogenic
pulmonary edema, where fluid restriction may be required, noncardiogenic
pulmonary edema may require aggressive fluid management to avoid further
worsening of pulmonary edema.
5. Supportive Care: Additional therapies may include diuretics (though they are
less effective in noncardiogenic cases), sedation, and analgesia to manage
discomfort and improve breathing.
 6. Ventilator Support and Monitoring: In severe cases, patients may need
continuous monitoring with blood gas analysis and ventilator adjustments.

Nursing Management
Nurses play a critical role in managing patients with noncardiogenic pulmonary edema:
 Assess Respiratory Status: Constant monitoring of oxygen saturation,
respiratory rate, and breath sounds is crucial.
 Oxygen Therapy and Ventilator Management: Administering high
concentrations of oxygen and managing mechanical ventilation if necessary.
 Fluid Balance: Monitoring intake and output, as well as potential signs of fluid
overload or dehydration.
 Positioning: Placing the patient in a position that optimizes lung expansion, such
as upright or semi-Fowler's position, can help improve oxygenation.
 Patient Education: Educating the patient and family about the condition, causes,
and expected outcomes.
In summary, noncardiogenic pulmonary edema is a life-threatening condition caused
by damage to the pulmonary capillaries, and its management requires prompt
intervention to support oxygenation and treat the underlying cause. Despite high
concentrations of oxygen, hypoxemia may be challenging to correct due to the nature of
the disease. Nurses play an essential role in monitoring and supporting patients during
their treatment.

Pulmonary Hypertension (PH)

Pulmonary hypertension (PH) is a serious condition characterized by elevated blood
pressure in the arteries of the lungs, specifically in the pulmonary arteries. It is defined
as a mean pulmonary arterial pressure greater than 25 mm Hg at rest and greater
than 30 mm Hg with exercise. This condition can lead to right heart failure due to the
increased workload on the right side of the heart.
Clinical Presentation
PH may not present with obvious symptoms until it has progressed significantly. The
early signs of PH can be subtle, and the disease often remains undiagnosed until later
stages. One of the earliest and most common symptoms is dyspnea (shortness of
breath), especially during exertion. However, patients may not have other apparent
clinical manifestations until the condition is more advanced.
Clinical Recognition of PH is often based on the following:
 Dyspnea on exertion (shortness of breath with physical activity)
 Fatigue and exercise intolerance
 Chest pain, particularly on exertion
 Dizziness or syncope (fainting) during activity, due to reduced oxygen delivery
to tissues
 Edema (swelling) in the legs and abdomen, reflecting right heart failure
 Ascites (fluid accumulation in the abdomen) in later stages
Since pulmonary pressures cannot be measured indirectly, PH is confirmed through
specialized testing. The gold standard for diagnosing PH is right heart
catheterization, which directly measures the pressures in the pulmonary arteries.
Classification of Pulmonary Hypertension
PH is classified into five groups based on its cause and underlying mechanisms, as
defined by the World Health Organization (WHO):
1. Group 1: Pulmonary Arterial Hypertension (PAH)
o Includes conditions such as idiopathic pulmonary arterial hypertension,
hereditary PAH, and PAH due to other causes (e.g., connective tissue
diseases, congenital heart disease, HIV infection, liver disease, and drug
use).
2. Group 2: Pulmonary Hypertension Due to Left Heart Disease
o This is the most common cause of PH and includes left-sided heart failure,
mitral valve disease, and other conditions affecting the left heart, which
leads to increased pressure in the pulmonary veins and arteries.
3. Group 3: Pulmonary Hypertension Due to Lung Disease or Hypoxia
o Conditions such as chronic obstructive pulmonary disease (COPD),
interstitial lung disease, sleep apnea, and other causes of hypoxia can
lead to PH.
4. Group 4: Chronic Thromboembolic Pulmonary Hypertension (CTEPH)
o This type of PH results from chronic blood clots in the lungs, leading to
obstruction of the pulmonary arteries.
5. Group 5: Pulmonary Hypertension Due to Miscellaneous Causes
o Includes a wide range of conditions, such as hematologic disorders,
sarcoidosis, and metabolic disorders, that can contribute to PH.
Pathophysiology
In PH, the small pulmonary arteries become narrowed, blocked, or damaged, leading to
increased resistance to blood flow in the lungs. As a result, the right ventricle of the
heart must work harder to pump blood through the lungs. Over time, this leads to right
heart failure. The increase in pulmonary pressure can also lead to vascular
remodeling, which further exacerbates the problem.
As the right ventricle struggles to overcome the high pressure in the pulmonary arteries,
it can become enlarged and weakened, eventually resulting in right-sided heart
failure. This is characterized by symptoms such as peripheral edema, jugular venous
distention, and ascites.
Diagnosis
Diagnosis of PH involves a combination of clinical suspicion, imaging, and invasive
testing:
 Echocardiogram: This is a non-invasive test commonly used to evaluate the
heart's function and estimate pulmonary artery pressure.
 Right Heart Catheterization: This is the definitive diagnostic test, where a
catheter is inserted into the pulmonary artery to directly measure the pressures.
 Chest X-ray and CT Scan: These imaging tests may reveal signs of right heart
enlargement or lung pathology contributing to PH.
 Pulmonary Function Tests (PFTs): Used to assess lung function and potential
underlying lung diseases.

Medical Management
The management of PH focuses on improving symptoms, reducing right heart strain,
and slowing the progression of the disease. The specific approach depends on the
underlying cause (as classified by WHO groups):
1. Group 1 (PAH):
o Vasodilators (e.g., prostacyclins, endothelin receptor antagonists,
phosphodiesterase inhibitors) to reduce pulmonary vascular resistance.
o Oxygen therapy may be used for patients with hypoxemia.
o In some cases, lung transplantation may be considered for severe
cases.
2. Group 2 (PH due to left heart disease):
o Treating the underlying heart condition (e.g., improving left ventricular
function, managing heart failure).
3. Group 3 (PH due to lung disease):
o Treatment of the underlying lung disease (e.g., inhalers for COPD,
corticosteroids for interstitial lung diseases).
o Oxygen therapy to reduce hypoxia.
4. Group 4 (CTEPH):
o Surgical intervention (e.g., pulmonary thromboendarterectomy) to
remove chronic blood clots.
o Anticoagulants to prevent further clotting.
o Pulmonary vasodilators may be used for symptom management.
5. Group 5 (Miscellaneous causes):
o Management is based on the underlying condition (e.g., treating
sarcoidosis, managing hematologic disorders).

Nursing Management
Nursing care focuses on supporting the patient through both the management of PH
and the underlying conditions:
 Assessment: Nurses regularly monitor vital signs, oxygen saturation, and
symptoms of right heart failure (e.g., edema, ascites).
 Oxygen Therapy: Administer oxygen as prescribed to maintain adequate
oxygenation and relieve symptoms.
 Medication Management: Administer prescribed medications (e.g., vasodilators,
diuretics) and monitor for side effects.
 Patient Education: Teach the patient about lifestyle modifications, such as the
importance of weight management to reduce fluid retention, and smoking
cessation if applicable.
 Monitoring for Complications: Monitor for signs of right heart failure,
arrhythmias, and thromboembolic events.

Prognosis
The prognosis for pulmonary hypertension depends on its underlying cause, the degree
of right heart failure, and the response to treatment. Early diagnosis and appropriate
management can improve quality of life and survival rates, but PH remains a
progressive condition that can be life-threatening, particularly in severe cases.
In summary, pulmonary hypertension is a serious condition that can result in right heart
failure. Its management involves treating the underlying cause, reducing symptoms, and
improving heart and lung function. Nurses play a vital role in monitoring the patient’s
condition, managing symptoms, and providing education to improve quality of life.

Pulmonary Embolism (PE)

Pulmonary embolism (PE) is a condition where a thrombus (blood clot) or multiple

thrombi obstruct the pulmonary artery or one of its branches, blocking blood flow to the
lungs. This can lead to significant complications, such as impaired gas exchange, right
heart failure, and even death.

Pathophysiology
PE most commonly results from a deep vein thrombosis (DVT), which occurs when a
blood clot forms in the deep veins of the legs or pelvis. These clots can travel to the
lungs, where they obstruct blood flow in the pulmonary arteries, causing pulmonary
vascular obstruction. This blockage reduces the amount of blood reaching the lungs
for oxygenation and can lead to impaired gas exchange.
In some cases, a PE can also arise from thrombi that originate from the right side of
the heart, or from fat, air emboli, or tumor cells. These may enter the pulmonary
circulation, leading to similar issues.
Types of Pulmonary Embolism
 Massive PE: A large clot or multiple clots that obstruct a significant portion of the
pulmonary circulation, leading to severe hemodynamic compromise and right
heart failure.
 Submassive PE: A smaller clot that still causes moderate pulmonary obstruction
and can affect the heart but with less immediate hemodynamic instability.
 Small PE: Clots that are small enough to not immediately cause hemodynamic
collapse but can still lead to hypoxemia and chronic pulmonary hypertension
over time.
Risk Factors
 Deep vein thrombosis (DVT): The majority of PEs arise from DVT in the lower
extremities.
 Immobilization: Prolonged bed rest, especially after surgery, injury, or during
prolonged travel (e.g., long-haul flights).
 Heart disease: Particularly atrial fibrillation and right-sided heart failure.
 Cancer: Certain cancers, especially those of the pelvis and abdomen, increase
the risk of venous thromboembolism.
 Surgical procedures: Especially orthopedic surgeries (e.g., hip and knee
replacement).
 Pregnancy and the postpartum period increase the risk of clot formation.
 Oral contraceptive use and hormone replacement therapy.
 Obesity, smoking, and genetic clotting disorders.

Clinical Manifestations
The clinical presentation of PE can vary widely depending on the size of the clot, the
location of the obstruction, and the individual’s health status. The following symptoms
may be seen:
 Dyspnea (shortness of breath) is the most common symptom.
 Pleuritic chest pain: Sharp, stabbing pain that worsens with breathing.
 Cough, sometimes with hemoptysis (coughing up blood).
 Tachypnea (increased respiratory rate).
 Tachycardia (increased heart rate).
 Hypoxemia: Low oxygen levels, which may be detected through pulse oximetry
or arterial blood gases (ABGs).
 Syncope (fainting), particularly in the case of massive PE, when significant
hemodynamic compromise occurs.
 Leg swelling or pain in the case of DVT in the lower extremities.

Diagnostic Evaluation
 Clinical assessment: The clinical history and physical examination, in
combination with risk stratification tools such as the Wells score, are used to
assess the likelihood of PE.
 D-dimer test: A blood test that detects the presence of fibrin degradation
products. Elevated D-dimer levels suggest the possibility of PE but are not
definitive.
 CT pulmonary angiography (CTPA): This is the gold standard for diagnosing
PE, providing clear imaging of the pulmonary arteries and any blockages.
 Ventilation-perfusion (V/Q) scan: This can be used in cases where a CT scan
is not available or suitable. It evaluates the ventilation (airflow) and perfusion
(blood flow) in the lungs to identify areas with mismatched ventilation and
perfusion, which may suggest PE.
 Ultrasound of the legs: If DVT is suspected as the source of the embolism,
ultrasound of the lower extremities may be performed.

Medical Management
The primary goal of treatment for PE is to reduce the size of the clot, prevent further clot
formation, and restore normal blood flow to the lungs. The approach to treatment
depends on the severity of the PE and the patient's overall health.
 Anticoagulation therapy:
o Heparin (IV or subcutaneous) or low-molecular-weight heparin
(LMWH) is used initially to prevent further clot formation.
o Warfarin or direct oral anticoagulants (DOACs), such as rivaroxaban
or apixaban, are used for long-term anticoagulation.
 Thrombolytic therapy (fibrinolytics): In cases of massive PE or hemodynamic
instability, thrombolytic agents such as tPA (tissue plasminogen activator) may
be used to break down the clot rapidly.
 Inferior vena cava (IVC) filter: In patients who are contraindicated for
anticoagulation therapy or who have recurrent PE despite anticoagulation, an
IVC filter may be placed to prevent clots from traveling to the lungs.
  Surgical intervention: In severe cases, surgical thrombectomy (removal of the
clot) may be necessary, particularly if thrombolytic therapy is not effective.

Nursing Management
Nursing care of a patient with PE includes the following key aspects:
 Assessment: Continuous monitoring of vital signs, oxygen saturation, and
respiratory status. Observe for signs of worsening hypoxemia, cardiac arrest, or
complications.
 Oxygen therapy: Administer oxygen to maintain adequate oxygen saturation
and relieve hypoxemia.
 Anticoagulation monitoring: For patients on heparin, monitor aPTT (activated
partial thromboplastin time) to ensure therapeutic levels. For patients on warfarin,
monitor INR (international normalized ratio).
 Pain management: Provide analgesia for pleuritic chest pain using appropriate
medications (e.g., opioids, NSAIDs).
 Prevention of further embolism: Ensure the patient is appropriately
anticoagulated and monitor for signs of bleeding or adverse effects.
 Patient education: Teach the patient about the importance of medication
adherence, prevention of future DVTs, and strategies to minimize venous
stasis, such as early mobilization after surgery, and compression stockings.

Prognosis
The prognosis for PE depends on the size of the embolism, the degree of hemodynamic
compromise, and the promptness of treatment. Massive PE can be fatal, while small
PEs may resolve with anticoagulation and supportive care. Early diagnosis and
treatment significantly improve outcomes, and many patients recover fully, particularly
when PE is detected early and managed aggressively. However, PE can lead to
chronic pulmonary hypertension or post-PE syndrome, in which patients may
experience persistent symptoms such as shortness of breath and reduced exercise
tolerance.