Module 3: Lower Respiratory Problems Flashcards
Acute Bronchitis
Self-limiting inflammation of bronchi; most caused
by viruses
Other triggers: pollution, chemical inhalation,
smoking, chronic sinusitis, and asthma
Symptoms: cough, clear/purulent sputum,
headache, fever, malaise, dyspnea, chest pain
Cough is most common symptom
May last as long as 3 weeks
Main reason for seeking medical care
More frequent at night
Diagnosis—based on assessment
Breath sounds: crackles or wheezes
Treatment goal—symptom relief and prevent
pneumonia; supportive
Cough suppressants, oral fluids, humidifier
Beta2-agonist inhaler—wheezing or underlying lung
problems
Avoid irritants; wash hands often
Influenza—antivirals within 48 hours
See HCP (health care provider) if: fever, dyspnea, or duration >4 week
Pertussis (whooping cough)
Bordetella pertussis
Gram-negative bacteria attach to cilia, release toxins
results in inflammation
Highly contagious; increased incidence in United
States
Immunity from DPT decreases over time
CDC recommends a 1-time vaccine for adolescents
(greater than 11+ years) and adults who did not have
Tdap
Manifestations/Symptoms:
Stage 1 (1 to 2 weeks): low-grade fever, runny nose,
watery eyes, general malaise, and mild,
nonproductive cough
Stage 2 (2 to 10 weeks): paroxysms of cough
Stage 3 (2 to 3 weeks): less severe cough, weak
-Hallmark characteristic: uncontrollable, violent,
cough with “whooping” sound lasting 6-10 weeks
“Whoop” sound from air against obstructed glottis
Often not present in teens and adult
Diagnosis
Community: history and physical
Clinical setting: nasopharyngeal cultures, PCR of
nasopharyngeal secretions, or serology testing
Treatment: macrolides (antibiotics)
Cough suppressants, antihistamines cause coughing
Infectious immediately through 3rd week after onset
of symptoms or until 5 days after antibiotic therapy
Routine and droplet precautions
Prophylactic antibiotics for close contact
Pneumonia
Acute infection of lung parenchyma (functional tissue of the lung that is involved in gas exchange. This includes the alveoli, alveolar ducts, and respiratory bronchioles.
Unlike the structural framework (which includes the bronchi, bronchioles, blood vessels, and connective tissues), the parenchyma is specifically where oxygen is absorbed into the blood and carbon dioxide is expelled from the bloodstream.)
Associated with significant morbidity and
mortality rates
Pneumonia and lower respiratory tract infections
4th leading cause of death worldwide in 201
Pneumonia Etiology: Normal Lung Defenses
The etiology of pneumonia involves understanding how various factors can lead to the condition by compromising the lung’s normal defense mechanisms or overwhelming them. Pneumonia is an infection of the lungs that can be caused by bacteria, viruses, fungi, or other organisms. The body has multiple defense mechanisms to protect the lungs from infection, including:
Air Filtration: The nasal passages filter out large particles from the air we breathe, reducing the number of pathogens that reach the lungs.
Epiglottis Closure over the Trachea: The epiglottis closes during swallowing to prevent food and liquids from entering the trachea (windpipe) and reaching the lungs, which can cause aspiration pneumonia.
Cough Reflex: This reflex helps to clear the airways of mucus, fluids, and foreign particles, preventing them from reaching the lower respiratory tract.
Mucociliary Escalator: The cilia (tiny hair-like structures) in the respiratory tract move mucus and trapped particles upward toward the throat, where they can be swallowed or expelled.
Reflex Bronchoconstriction: This reflex narrows the airways in response to irritants or allergens, helping to prevent harmful substances from reaching the deeper parts of the lungs.
Immunoglobulins (IgA and IgG): These antibodies in the respiratory tract help neutralize pathogens.
Alveolar Macrophages: These immune cells in the alveoli engulf and digest microorganisms and foreign particles that reach the alveoli.
Pneumonia Etiology: Risk Factors
When these defense mechanisms become incompetent or overwhelmed, the risk of developing pneumonia increases. Factors that can compromise lung defenses or increase the likelihood of overwhelming them include:
Aspiration: Inhaling food, liquid, vomit, or other substances into the lungs can lead to aspiration pneumonia, especially in individuals with impaired swallowing reflexes.
Tracheal Intubation: The use of ventilators and the process of intubation can bypass some of the body’s natural defenses and introduce pathogens directly into the lower respiratory tract.
Air Pollution and Smoking: These can damage the mucociliary escalator and impair the function of alveolar macrophages, making the lungs more susceptible to infection.
Viral Upper Respiratory Infections (URI): Infections like the common cold or influenza can damage the respiratory tract’s lining, making it easier for bacteria to invade and cause pneumonia.
Aging: The immune system and lung function can decline with age, reducing the effectiveness of the lungs’ defense mechanisms.
Chronic Diseases: Conditions such as COPD, asthma, and heart disease can compromise lung function and the body’s ability to fight off infections.
Pneumonia: How Organisms Reach Lungs
3 ways organisms reach lungs:
1. Aspiration of normal flora from nasopharynx or
oropharynx
2. Inhalation of microbes present in air
3. Hematogenous spread from primary infection
elsewhere in body
Classifications of Pneumonia
No universal classification system
May be classified according to causative pathogens,
disease characteristics, or appearance on CXR (chest X-ray)
**Most effective classification:
Community-acquired (CAP) or
Hospital-acquired (HAP)
* Helps identify most likely organism and antimicrobial
therapy
CAP (community acquired pneumonia)
Community-acquired pneumonia (CAP)
Acute infection in patients who have not been
hospitalized or resided in a long-term care facility
within 14 days of the onset of symptoms
Can be treated at home or hospitalized dependent on
patient’s age, VS, mental status, comorbidities, and
condition
Assessment: Expanded CURB-65 scale to support
clinical judgment
The CURB-65 scale is a widely used clinical tool for assessing the severity of pneumonia and guiding decisions regarding the management and treatment of the condition, especially in adults. It helps in determining the need for hospitalization or intensive care admission. The CURB-65 score is based on five criteria, with each criterion scoring one point:
Confusion: New onset of confusion or altered mental status.
Urea: Blood urea nitrogen (BUN) level >7 mmol/L (>19 mg/dL).
Respiratory rate: ≥30 breaths per minute.
Blood pressure: Systolic <90 mm Hg or diastolic ≤60 mm Hg.
Age: ≥65 years
HAP (hospital acquired pneumonia)
Hospital-acquired pneumonia (HAP) or nosocomial
pneumonia
HAP: Occurs 48 hours or longer after hospitalization
and not present at time of admission
Ventilator-associated pneumonia —VAP: Occurs
more than 48 hours after endotracheal intubation
Both associated with
* Longer hospital stays
* Increased associated costs
* Sicker patients
* Increased mortality
Empiric Antibiotic Therapy
Empiric antibiotic therapy for pneumonia involves initiating treatment with antibiotics before a definitive diagnosis is made, based on the identification of the most likely causative pathogen and taking into consideration the patient’s clinical presentation, risk factors, underlying medical conditions, and hemodynamic stability. The goal is to start treatment promptly to reduce morbidity and mortality, especially in severe cases where waiting for confirmatory test results could lead to deterioration of the patient’s condition. Key considerations for empiric antibiotic therapy include:
Risk Factors: These can include age, smoking status, alcohol use, immunocompromised state (e.g., HIV, use of immunosuppressive medications), recent hospitalizations, and exposure to specific environments or populations that might increase the risk of certain infections.
Speed of Onset: Acute onset might suggest bacterial pneumonia, while a more gradual onset might indicate viral or atypical pathogens.
Clinical Presentation: Symptoms such as high fever, productive cough with purulent sputum, pleuritic chest pain, and physical exam findings like localized crackles or dullness to percussion can suggest bacterial pneumonia. Atypical presentations might suggest viral or other atypical pathogens.
Underlying Medical Conditions: Chronic conditions like COPD, asthma, heart disease, diabetes, and liver or kidney disease can influence the choice of empiric therapy, as certain pathogens might be more common or more severe in these patients.
Hemodynamic Stability: Patients with signs of sepsis or septic shock require immediate broad-spectrum antibiotics and possibly admission to an intensive care unit.
Most Likely Causative Pathogen: This is inferred based on the above factors, as well as community vs. hospital-acquired infection. For community-acquired pneumonia (CAP), typical pathogens include Streptococcus pneumoniae, Haemophilus influenzae, and atypical bacteria like Mycoplasma pneumoniae. For hospital-acquired pneumonia (HAP) or ventilator-associated pneumonia (VAP), more resistant bacteria like Pseudomonas aeruginosa and MRSA (Methicillin-resistant Staphylococcus aureus) may be more likely.
Based on these considerations, empiric antibiotic choices might include:
For CAP in outpatients without comorbidities: A macrolide (e.g., azithromycin) or doxycycline.
For CAP in outpatients with comorbidities or for more severe cases: A combination of a beta-lactam (e.g., amoxicillin-clavulanate) plus a macrolide, or monotherapy with a respiratory fluoroquinolone (e.g., levofloxacin).
For HAP or VAP: A broader spectrum antibiotic or combination therapy to cover for more resistant pathogens, tailored to the hospital’s antibiogram.
Types of Pneumonia
Viral—most common
May be mild or life-threatening
Bacterial
May require hospitalization
Mycoplasma—atypical
Mild; occurs in persons <40 years of age
Aspiration
Necrotizing
Opportunistic
Aspiration Pneumonia
Abnormal entry of oral or gastric material into lower
airway
***Major risk factors:
* Decreased level of consciousness
Depressed cough or gag reflex
* Difficulty swallowing
* Insertion of nasogastric tubes with or without tube
feeding
Aspirated material triggers inflammatory response
Primary bacterial infection most common
Empiric therapy based on probable causative
organism, severity of illness, and patient factors
Aspiration of acid gastric contents initially causes
chemical (noninfectious) pneumonitis results in
possible bacterial infection in 24 to 72 hour
Necrotizing Pneumonia
Rare complication of bacterial lung infection; often
happens with CAP
Common causative organisms are staph, Klebsiella,
strep
Signs and symptoms:
* Respiratory insufficiency/failure
* Leukocytosis (increased white blood cells in blood, sign of infection)
* Abnormalities on chest imaging
Treatment—long-term antibiotics; possible surgery
Opportunistic Pneumonia
Opportunistic pneumonia
Immunocompromised patients
* Severe protein-calorie malnutrition
* Immunodeficiencies
* Chemotherapy/radiation recipients
* Immunosuppression therapy; long-term corticosteroid
therapy
Caused by bacteria, virus, or microorganisms that do
not normally cause disease
Pneumocystis jiroveci pneumonia (PJP)
Pneumocystis jiroveci pneumonia (PJP)—fungal
infection; most common with HIV
Slow onset and subtle symptoms
* Fever, tachycardia, tachypnea, dyspnea, nonproductive
cough, and hypoxemia
* Chest x-ray - diffuse bilateral infiltrates to massive
consolidation
Can be life-threatening causing ARF, death
Spread to other organs
Treatment: trimethoprim/sulfamethoxazole
* Does not respond to antifungals
Cytomegalovirus (CMV) pneumonia
Cytomegalovirus (CMV) pneumonia
Herpes virus
Asymptomatic and mild to severe disease (impaired
immunity)
Most important life-threatening complications after
hematopoietic stem cell transplant
Treatment: antiviral medications and high-dose
immunoglobulin
Pathophysiology of Pneumonia
Atelectasis - pulmonary condition that affects lung function
Atelectasis - absence of gas or air in 1 or more
areas of the lung; may
Be asymptomatic
Be extremely SOB with severe chest pain
*need antibiotics
Consolidation - pulmonary condition that affects lung function
Consolidation – alveoli become filled with water,
fluid and/or debris
Typical with bacterial pneumonia
Can obstruct airflow, impair gas exchange, cause
significant respiratory insufficiency
*need antibiotics
Manifestations of Pneumonia
Most common
Cough: productive or nonproductive
Green, yellow, or rust-colored sputum
Fever, chills
Dyspnea, tachypnea
Pleuritic chest pain
Older or debilitated patients: confusion or stupor
* Older patients: hyperthermia, diaphoresis, anorexia,
fatigue, myalgias, headache
Physical examination
Fine or coarse crackles over affected region
Findings With consolidation:
* Bronchial breath sounds (These are louder, high-pitched sounds that are normally heard over the trachea. When heard over the lung periphery, they suggest consolidation, as sound travels more efficiently through solid or fluid-filled lung tissue)
* Egophony (This refers to a change in the quality of the voice sounds heard when the patient speaks. Typically, the patient is asked to say “E,” which will sound like “A” over an area of consolidation due to enhanced transmission of higher frequency sounds)
* Increased fremitus (Fremitus is the palpable vibration transmitted through the bronchopulmonary system to the chest wall when the patient speaks. It is increased over areas of consolidation because sound and vibrations travel better through solid or fluid media than through air)
Findings with Pleural Effusion
Dullness to Percussion: Normally, the chest produces a resonant sound when percussed. However, over an area with pleural effusion, the sound is dull due to the presence of fluid in the pleural space, which absorbs the sound waves.
Pleural effusion can mask the breath sounds and other characteristic sounds of lung tissue since the fluid separates the lung from the chest wall, making auscultation and percussion findings less clear.
Complications of Pneumonia
Multidrug-resistant (MDR) pathogens—major
problem in treatment
Risk factors
Advanced age
Immunosuppression
History of antibiotic use
Prolonged mechanical ventilation
Antibiotic susceptibility tests (Antibiotic susceptibility tests are laboratory procedures used to determine the sensitivity of bacteria isolated from a patient to various antibiotics. In the context of pneumonia and its complications, these tests are crucial for guiding effective antibiotic therapy, especially when the infection is caused by bacteria that might be resistant to standard empirical antibiotic treatments)
Increase mortality from pneumonia
Other Complications:
Atelectasis
Pleurisy – inflammation of pleura
Pleural effusion – liquid in pleural space
Bacteremia – bacterial infection in the blood
Pneumothorax – lungs collapse from air in pleural
space
ARF – a leading cause of death in severe
pneumonia; ineffective O2 and CO2 exchange
Sepsis/septic shock – bacteria in alveoli enter
bloodstream; can lead to shock and MODS (multiple organ dysfunction syndrome)
Diagnosing Pneumonia
History and physical examination
Chest x-ray (CXR)
Thoracentesis and/or bronchoscopy
Pulse oximetry
Arterial blood gases (ABGs)
Sputum gram stain, culture & sensitivity
-Ideally before antibiotics started
Blood cultures
CBC with differential (looks at various types of cells in the blood)
Regular CBC Components:
WBC, RBC, Hemoglobin, Hematocrit, Platelets
With Differentials:
Neutrophils, Lymphocytes, Monocytes, Eisonophils, Basophils
CAP Drug Therapy
Initial empiric therapy
Gram-negative and gram-positive organisms
Infecting organism and risk factors for MDR (multiple drug resistant) organisms vary with local and institutional prevalence
and resistance patterns
Should see improvement in 3 to 5 days or need to
reevaluate
Antibiotics: IV, proceed to oral when stable; at least 5
days; afebrile 48 to 72 hours
Tuberculosis (TB)
Infectious disease caused by Mycobacterium
tuberculosis
Lungs most commonly infected
Can affect any organ
25% of world’s population has TB
Seeing increasing rates due to HIV and drug-resistant
strains of M. tuberculosis
Leading cause of mortality in patients with HIV
Risk Factors for TB
Poor, underserved, and minorities
Homeless
Residents of inner-city neighborhoods
Foreign-born persons
Living or working in institutions
IV drug users
Overcrowded living conditions
Poverty, poor access to health care
Immunosuppression
Etiology/Pathophysiology of TB
Gram-positive, aerobic, acid-fast bacillus (AFB)
Spread via airborne droplets, 1 to 5 um
Can be suspended in air for minutes to hours
Humans are only known reservoir for TB
Transmission requires close, frequent, or prolonged
exposure
NOT spread by touching, sharing food utensils,
kissing, or other physical contact
Number, concentration, length of time for exposure
and immunity influence transmission
Once inhaled, droplets lodge in bronchioles and
alveoli
Local inflammatory reaction occurs
Ghon lesion or focus—represents a calcified TB
granuloma—hallmark of primary TB infection
Granuloma—defense mechanism to wall off and
prevent spread
Only 5% to 10% of people with dormant TB will
develop active TB; may take months or years
M. tuberculosis
Aerophilic (oxygen-loving)—has affinity for lungs
Infection can spread via lymphatics and grow in other
organs
* Cerebral cortex, spine, epiphyses of the bone, liver,
kidneys, lymph nodes, adrenal glands
Multidrug-Resistant Tuberculosis
(MDR-TB)
Resistance to first-line drug therapy (isoniazid and
rifampin)
Extensively drug-resistant TB (XDR-TB) resistant to
any fluoroquinolone plus at least 1 2nd-line drug
**Several causes for resistance
Incorrect prescribing
Lack of case management
Nonadherence to prescribed regimen
TB Classification American Thoracic Society
Class
0 = No TB exposure
1 = Exposure, no infection
2 = Latent TB, no disease
3 = TB, clinically active
4 = TB, not clinically active
5 = TB suspect
TB - Another Classification System
Presentation
Primary, latent, reactivated
Whether pulmonary or extrapulmonary
**Primary TB infection
Starts when bacteria are inhaled, trigger inflammatory
reaction
Most people have effective immune response here
**Active TB infection
Primary TB – active disease within 2 years of
infection
* People co-infected with HIV at greatest risk
**Post-primary TB or reactivation TB
Occurs >2 years after initial infection
Patient infectious if site of TB is pulmonary or
laryngeal
**Latent TB infection (LTBI)
Occurs when there is not active TB disease
Positive skin test but asymptomatic
Cannot transmit TB; can develop active TB later
* Reactivation can occur with some diseases, stress
Treatment is as important as it is for primary TB
Clinical Manifestations of Pulmonary TB
Pulmonary TB
Takes 2 to 3 weeks to develop symptoms
Characteristic initial: dry cough that becomes
productive
Other symptoms: fatigue, malaise, anorexia, weight
loss, low-grade fever, night sweats
Late: dyspnea and hemoptysis (coughing of blood streaked sputum from lungs/brochial tissues)
Acute, sudden presentation of TB
High fever
Chills, generalized flulike symptoms
Pleuritic pain
Productive cough
ARF
Normal or adventitious breath sounds
Hypotension and hypoxemia may be present
Immunosuppressed (e.g., HIV) and older adults—
less likely to have fever and other signs of an
infection
HIV—carefully assess respiratory problems; rule out
PJP or opportunistic diseases
Older adult—change in cognitive function may be the
only initial sign
Extrapulmonary TB manifestations—depends on
organs infected
TB Complications - Miliary TB
Properly treated, TB heals without complications
**Miliary TB
Large numbers of organisms spread via the
bloodstream to distant organs
Occurs with primary TB or reactivation of LTBI (latent TB infection)
Fatal if untreated
Manifestations progress slowly and vary depending
on which organs are infected
* Fever, cough, and lymphadenopathy (swelling of lymph nodes)
* May include hepatomegaly (enlargement of the liver) and splenomegaly (enlargement of spleen)
TB Complications - Pleural TB
Pleural TB—extrapulmonary
Primary TB disease or reactivation of LTBI
Chest pain, fever, cough, unilateral pleural effusion
Empyema (accumulation of pus in pleural space); less common but occurs from large
numbers of TB organisms in pleural space
TB Complications Cont - Extrapulomary Complications
When Tuberculosis (TB) spreads beyond the lungs, it is referred to as extrapulmonary tuberculosis (EPTB), which can affect virtually any organ system in the body. The spread of TB to other organs can lead to various acute and long-term complications, depending on the organs involved. Here are some of the complications associated with TB infection in different parts of the body:
Spine (Pott’s Disease)
Description: Pott’s disease is TB of the spine, which is the most common form of skeletal tuberculosis. It involves the destruction of intervertebral discs and adjacent vertebrae, leading to the formation of a “cold abscess” that can spread along fascial planes.
Complications: Can result in severe back pain, deformity, and potential compression of the spinal cord, leading to paralysis (paraplegia or tetraplegia) if not treated promptly.
Central Nervous System (CNS)
Description: TB can affect the CNS, most commonly causing tuberculous meningitis, which is an infection of the membranes covering the brain and spinal cord.
Complications: Can lead to a range of severe neurological complications, including headaches, mental status changes, seizures, stroke, and permanent brain damage. It is considered a medical emergency.
Abdomen
Description: Abdominal TB can involve any abdominal organ, including the peritoneum, lymph nodes, gastrointestinal tract, liver, and spleen.
Complications: May cause abdominal pain, ascites (accumulation of fluid in the peritoneal cavity), intestinal obstruction, and generalized systemic symptoms like fever and weight loss. Peritonitis due to TB can lead to severe abdominal tenderness and guarding.
Other Organs
Kidneys and Urogenital Tract: Genitourinary tuberculosis can affect the kidneys, ureters, bladder, and reproductive organs, leading to chronic pain, hematuria (blood in urine), infertility, and, in severe cases, renal failure.
Adrenal Glands: Adrenal TB can lead to Addison’s disease, a condition where the adrenal glands do not produce enough steroid hormones, leading to weakness, weight loss, and electrolyte imbalances.
Lymph Nodes: TB can cause lymphadenitis, leading to swollen and sometimes draining lymph nodes. Scrofula is a term used for TB lymphadenitis of the neck.
Bones and Joints: Besides the spine, TB can affect other bones and joints, leading to chronic pain, swelling, and reduced mobility, most commonly in the hips and knees.
Diagnostic Studies of TB - TB Skin Test
Tuberculin skin test (TST)
AKA: Mantoux test
Screening for TB: Purified protein derivative (PPD)—
0.1 mL ID injection ventral forearm
* Inspect site for induration in 48 to 72 hours
* Induration—palpable, raised, hardened, or swollen
area (not redness)
Indicates development of antibodies following exposure to TB; occurs 2-12 weeks after initial exposure
Measure in mm and record
Positive
* Greater than or equal to 15 mm induration in low-risk
individuals
* Greater than 10 mm induration in high-risk
* Greater than or equal to 5 mm induration in
immunocompromised
False-positive and false-negative reactions may also
occur
Initial screening: 2-step testing
Recommended for health care workers and those
with decreased response to allergens
Initial injection; second injection in 1 to 3 weeks
* Initial positive—need further evaluation for active
disease, not 2nd injection
* Second positive—new infection or boosted reaction to
old infection
Negative 2-step testing ensures future positive results
accurately interpreted as new infection
TB Diagnostic Studies: Interferon-γ (INF-gamma) release assays (IGRAs)—
screening tool
Blood test detects INF gamma release from T-cells in
response to M. tuberculosis
* Includes QuantiFERON ®-TB Gold In-Tube (QFT-GIT)
and T-SPOT.TB® tests
* Rapid results
* Several advantages over TST but increased cost
LTBI can only be diagnosed by excluding active TB
TB Diagnostic Studies: Chest X Ray
Chest x-ray
Cannot make diagnosis solely on x-ray
May appear normal in a patient with TB
Suggestive findings
* Upper lobe infiltrates: TB bacteria thrive in areas of high oxygen concentration, making the upper lobes of the lungs a common site for TB infection. Infiltrates in these areas can be indicative of TB.
* Cavitary infiltrates (The formation of cavities, which are hollow spaces within the lung, is a hallmark of reactivation or post-primary TB. These cavities are formed due to the destruction of lung tissue by the bacteria)
* Lymph node involvement (Enlarged lymph nodes, particularly in the mediastinum (the central part of the chest separating the lungs), can be a sign of TB, especially in children and HIV-positive individuals)
* Pleural and/or pericardial effusion (TB can cause pleural effusion (fluid accumulation in the pleural space) and pericardial effusion (fluid around the heart), both of which can be seen on a chest X-ray)
Other diseases (i.e.; sarcoidosis) can mimic
appearance of TB
Limitations of Chest X-ray in TB Diagnosis
Cannot Confirm TB: A chest X-ray cannot distinguish TB from other diseases with similar radiographic appearances, nor can it determine if the disease is active or latent.
May Appear Normal: Some patients with active TB, particularly in the early stages or those with milder forms of the disease, may have a normal chest X-ray.
Mimicking Conditions: Diseases like sarcoidosis, fungal infections, and other bacterial pneumonias can have similar radiographic features, complicating the interpretation.
TB Diagnostic Studies: Bacteriologic Studies
TB sputum culture is gold standard
* 3 consecutive sputum samples at 8 to 24 hours
intervals; at least 1 specimen in early morning
* Initial test: stained sputum smears examined for AFB (acid-fast bacilli (AFB)
* Definitive diagnosis = mycobacterial growth—can take
up to 6 weeks
Treatment is started while waiting for culture results
when suspicion of TB is high
* Can also collect samples from other suspected TB site
Active TB Case: Drug Therapy
The treatment of active tuberculosis (TB) disease is a lengthy process that typically involves a two-phase approach with multiple antibiotics to ensure the elimination of the bacteria and to prevent the development of drug resistance.
- Intensive Phase
Duration: Usually the first 2 months of treatment.
Purpose: To rapidly kill the tubercle bacilli, thereby reducing the bacterial load and making the patient less infectious.
Drugs: A combination of four drugs is used during this phase:
Isoniazid: Effective against actively growing and dormant TB bacteria. It is known to increase the risk of hepatotoxicity (liver damage), so liver function tests are often monitored during treatment, especially in patients with pre-existing liver conditions, the elderly, and those with heavy alcohol use.
Rifampin (Rifampicin in some countries): Has a potent bactericidal activity and is effective against a broad range of bacteria including Mycobacterium tuberculosis. It can cause liver dysfunction and drug interactions by inducing liver enzymes that metabolize many other drugs.
Pyrazinamide: Its exact mechanism is not fully understood, but it’s particularly effective during the initial phase of treatment. It is contraindicated in pregnancy and in patients with acute hepatitis due to its potential hepatotoxic effects.
Ethambutol: Used to prevent the emergence of resistance. It can cause optic neuritis, leading to visual disturbances, so it’s often stopped if the TB strain is known to be susceptible to all four drugs, and the patient is not at high risk of drug resistance.
- Continuation Phase
Duration: Extends for an additional 4 months, making the total usual treatment duration 6 months.
Purpose: To eliminate any remaining bacteria and prevent relapse.
Drugs: The treatment is continued with two drugs:
Isoniazid
Rifampin
These drugs are continued to ensure the eradication of all TB bacteria and to minimize the risk of developing drug-resistant TB. The total duration of treatment may be extended in certain cases, such as TB meningitis, bone and joint TB, and in patients with drug-resistant TB or HIV co-infection.
Monitoring and Considerations
Monitoring: Patients on TB treatment require regular monitoring for drug efficacy, adherence, and potential side effects, including liver toxicity.
Directly Observed Therapy (DOT): To improve treatment adherence, the DOT strategy is often employed, where a healthcare provider or trained individual observes the patient taking each dose of medication.
Active TB Case - Drug Therapy
Active TB disease
Patients should be taught about adverse/side effects
and when to seek medical attention
Nonviral hepatitis is a major side effect for 3 of 4 first-
line drugs; liver function tests should be monitored
Alternatives are available for those who develop a
toxic reaction to primary drug
Drug Resistant TB Drug Therapy
MDR-TB
Sensitivity test determines drugs
Initial: Five drugs for at least 6 months after sputum
culture is negative
* 1-2 first-line, fluoroquinolone, injectable antibiotic and 1 or more second-line
Continuation: 4 drugs for 18 to 24 months
2 new drugs used in combination therapy
* Bedaquiline (Sirturo)
* Delamanid (Deltyba)
Latent TB Infection Treatment
Latent tuberculosis infection (LTBI)
Treatment easier due to fewer bacteria; usually 1
drug
Standard - Isoniazid for 9 months
* Inexpensive, effective, taken orally
* Can use 6-month plan if adherence issues
HIV patients and those with fibrotic lesions on chest x
-ray should take Isoniazid for 9 months
Alternative 3-month regimen of Isoniazid and
rifapentine for those not infected with MDR bacilli
4 months of rifampin for those resistant to isoniazi
Bacille-Calmette-Guerin (BCG) Vaccine
Live, attenuated strain of Mycobacterium bovis
Given to infants in parts of world with high prevalence
of TB
In United States, not recommended due to low risk of
infection except for select individuals
BCG vaccine can result in false positive TST
Acute Care: Airborne Isolation for TB Patients
Airborne isolation
* Single-occupancy room with 6 to 12 airflow
exchanges/hour
* Health care workers wear high-efficiency particulate air (HEPA) masks; fit tested
Atypical Mycobacteria - Pulmonary Issues
30+ varieties of acid-fast mycobacteria that
cause pulmonary disease, lymphadenitis (inflammation of lymph nodes), skin or
soft tissue (muscles, ligaments, fat) disease, or disseminated disease (a condition where an infection or other disease process spreads from the initial site to other parts of the body, often affecting multiple organ systems)
Found in tap water, soil, house dust, or bird feces
Symptoms: cough, shortness of breath, weight loss,
fatigue, blood-tinged sputum
Diagnosis: culture
Treatment: similar to TB
Pulmonary Fungal Infections
Caused by endemic or opportunistic fungi
May be life threatening
Transmission: inhalation of spores
Symptoms: similar to bacterial pneumonia
Diagnosis: skin testing, serology, biopsy
Treatment: antifungals
Lung Abscess
Etiology and pathophysiology
Necrosis of lung tissue from aspiration of bacteria from periodontal disease
* Other: IV drug use, cancer, PE, lung infarction, TB, parasitic and fungal diseases, sarcoidosis
Develops slowly; infection results in purulent fluid filled cavity with multiple microbes
Posterior upper lobes most often affected
* May erode into bronchi: foul-smelling sputum
* May grow into pleura: pleuritic pain
Multiple abscesses—necrotizing pneumonia
Clinical manifestations – occur slowly (weeks to
months):
Cough-producing purulent sputum; foul smell and
taste; hemoptysis
Other: fever, chills, night sweats, pleuritic pain,
dyspnea, anorexia, weight loss
Decreased breath sounds; crackles
Complications: pulmonary abscess (a localized collection of pus within the lung parenchyma (lung tissue), typically caused by a bacterial infection. It results from the necrosis (death) of lung tissue and the formation of a cavity filled with pus, dead cells, and other debris)
bronchopleural fistula (abnormal connection between the bronchial tubes and the pleural space (the thin fluid-filled space between the two layers of the pleura surrounding the lungs).
bronchiectasis: chronic condition characterized by permanent enlargement and scarring of the bronchial tubes. This leads to impaired clearance of mucus, resulting in frequent infections and blockages of the airways, often from CF
empyema (accumulation of pus in the pleural space, often arising as a complication of pneumonia, lung abscess, or thoracic surgery)
If antibiotics not effective—
* Percutaneous drainage of abscess
* Surgery: lobectomy or pneumonectom
Restrictive Respiratory Disorders
Disorders that impair movement of the chest wall
and diaphragm
2 categories:
Extrapulmonary—Lung tissue normal but caused by
issues in either CNS, neuro-muscular or chest wall disorders
Intrapulmonary— Abnormal pleural or lung tissue
disorders
Hallmark characteristic: reduced forced expiratory
volume (FEV1) on PFTs
FEV1: This measures the amount of air a person can forcefully exhale in one second after taking a deep breath. It is a critical measurement in assessing the presence and severity of airway obstruction.
PFTs best way to distinguish restrictive from
obstructive respiratory disorders
Atelectasis
Collapsed, airless alveoli
Decreased or absent breath sounds
Dullness on percussion
Caused by: secretions obstructing small airways
At risk: bedridden and postop surgery patients
Prevention and treatment
* Deep breathing exercises, incentive spirometry, early
mobility
Pleurisy
Inflammation of the pleura; AKA pleuritis
Etiology: infection, cancer, autoimmune disorders,
chest trauma, GI disease, and some medications
Manifestations
* Pain—sharp, worse with inspiration
* Breathing shallow—reduced movement
* Pleural friction rub—peak of inspiration
Treatment—underlying cause and pain management
* Teach splinting rib cage when coughing
Pleural Effusion
An abnormal collection of fluid in the pleural space, known as a pleural effusion, is indeed not a disease in itself but a sign or manifestation of other underlying conditions. The pleural space is a thin cavity between the lung and the chest wall, lined by the pleura (a membrane), and normally contains a small amount of lubricating fluid. Pleural effusions develop when there’s an imbalance between the production and absorption of this pleural fluid.
Causes of Pleural Effusion
The formation of a pleural effusion can be due to various mechanisms, including:
Increased Pulmonary Capillary Pressure: Often seen in heart failure, leading to fluid leakage from the capillaries into the pleural space.
Decreased Oncotic Pressure: Reduced protein levels in the blood, as seen in liver cirrhosis or nephrotic syndrome, can decrease the blood’s ability to retain fluid, leading to its accumulation in the pleural space.
Increased Pleural Membrane Permeability: Infections, inflammation, or injury can make the pleural membrane more permeable, allowing fluid to enter the pleural space more easily.
Lymphatic Flow Obstruction: Conditions that block or disrupt the normal flow of lymphatic fluid can lead to accumulation in the pleural space.
Types of Pleural Effusion
Based on the protein content and the underlying cause, pleural effusions are classified into two main types:
Transudative Effusions: These effusions are typically due to noninflammatory conditions that alter the pressure gradients and fluid balance, such as heart failure, liver cirrhosis, or nephrotic syndrome. Transudative effusions are characterized by low protein content and are generally not due to direct injury or inflammation of the pleura.
Exudative Effusions: Result from inflammatory conditions that increase the permeability of the pleural membrane, such as pneumonia, lung cancer, tuberculosis, or autoimmune diseases. Exudative effusions have a higher protein content and often contain inflammatory cells.
Empyema
Empyema, a specific type of exudative pleural effusion, involves the accumulation of pus in the pleural space, indicating a bacterial infection. This condition requires prompt and aggressive treatment, including antibiotics to combat the infection and drainage procedures (such as thoracentesis, chest tube insertion, or surgery) to remove the purulent fluid and alleviate symptoms.
Pleural Effusion Symptoms
Clinical manifestations:
Dyspnea, cough, sharp chest pain
Decreased chest movement; dullness, decreased
breath sounds on affected side
Chest x-ray and CT—location and volume
Empyema: above manifestation and fever, night
sweats, cough, weight loss
Interprofessional and nursing care
Treat underlying cause
Chemical pleurodesis – obliterate pleural space
Interstitial Lung Disease (ILD)
Diffuse parenchymal lung disease
More than 200 disorders caused by inflammation or
scarring (fibrosis) between air sacs (interstitium)
Cause often unknown
Known causes
* Inhalation of occupational and environmental toxins,
certain drugs, radiation therapy, connective tissue
disorders, infection, cancer
Treatment—reduce exposure or treat underlying
disease
* Corticosteroids, immunosuppressants; transplant
Idiopathic Pulmonary Fibrosis
Progressive disorder; chronic inflammation and scar
tissue in connective tissue; course is variable
Risk factors: smoking; wood & metal dust
Manifestations: exertional dyspnea (shortness of breath with exertion); dry,
nonproductive cough, clubbing (enlargement of fingertips and toes due to chronic low O2 levels), crackles
Progression: weakness, anorexia, weight loss
Diagnostic Studies:
* PFTs: Pulmonary Function Tests (PFTs): Typically show a reduced vital capacity (VC) and total lung capacity (TLC), indicating restrictive lung disease. There’s also impaired gas exchange, often assessed by reduced diffusion capacity for carbon monoxide (DLCO).
High-Resolution Computed Tomography (HRCT): HRCT scans of the chest are crucial for diagnosing IPF and other ILDs, showing characteristic patterns such as reticular abnormalities, honeycombing, and traction bronchiectasis.
Open Lung Biopsy (VATS): Video-Assisted Thoracoscopic Surgery (VATS) for lung biopsy is considered the “gold standard” for definitive diagnosis when non-invasive methods are inconclusive. It allows direct visualization and sampling of lung tissue, which is then examined histologically for signs of fibrosis and other abnormalities.
Prognosis is poor; no known cure
Median survival rate 2.5 to 3.5 years after diagnosis
**Treatment
Corticosteroids and other immune suppressants
Kinase inhibitor drugs
Oxygen
Pulmonary rehabilitation
Lung transplant
Sarcoidosis
Chronic, multisystem granulomatous disease
*“Granulomatous” refers to a type of inflammation characterized by the formation of granulomas, which are small, localized nodular inflammations. Granulomas typically form when the immune system attempts to isolate and wall off substances that it perceives as foreign but is unable to eliminate. These substances can include infectious agents like bacteria, fungi, and parasites, as well as non-infectious agents such as foreign materials or certain inflammatory diseases.
Primary affect on lungs
* Dyspnea, cough, chest pain; many are asymptomatic
Other: skin, eyes, liver, kidney, heart, lymph nodes
Cause unknown
At risk: blacks and family history
Treatment—suppress inflammation
Follow 3 to 6 months: PFTs, chest x-ray, and CT scan
for progression
Chest Trauma
Traumatic injuries to chest contribute to many
traumatic deaths
Range of injuries
Simple rib fractures to cardiorespiratory arrest
Classify primary mechanisms of injury as either
blunt or penetrating trauma
Chest Trauma: Mechanisms of Injury
Mechanisms of Injury
Blunt
* Chest strikes or is struck by an object
* Shearing and compression injuries of chest structures
* External appearance may be minor but may have
severe internal organ damage
Penetrating
* Foreign object impales or passes through body tissues
creating an open wound
Fractured Ribs
Blunt trauma
Most common ribs 5 through 9 – least protected by
chest muscles
Can damage pleura, lungs, heart, and other internal
organs
**Manifestations
Pain with inspiration and coughing
Splinting
Shallow respirations
Fractured Ribs Complications
Complications
Atelectasis and pneumonia
Taping, using a thoracic binder not recommended
Treatment
Reduce Pain: NSAIDs, opioids, nerve blocks
Patient teaching
* Deep breathing and coughing
* Incentive spirometry
* Appropriate use of analgesics
* Early mobility when appropriate
Flail Chest
3 or more consecutive fractured ribs in 2 or more
places or fractured sternum and several consecutive
ribs
Causes unstable chest wall and paradoxical
movement with breathing
Flail segment moves opposite
Inspiration—sucked in
Expiration—bulges out
Inadequate ventilation; increased work of breathing (WOB)
Physical examination
Rapid, shallow respirations
Asymmetric and uncoordinated chest movement
Inadequate ventilation
Splinting
Crepitus near fractures
-Diagnostic study
Chest x-ray
Treatment
Ensure adequate ventilation/lung expansion
Adequate oxygenation
Pain management
Other, if needed:
* Intubation and mechanical ventilation
* Surgical fixation
Pneumothorax
Caused by air entering pleural cavity
Positive pressure in pleural space causes lung to
partially or fully collapse
Increased air in pleural space equals reduced lung
volume
Open: opening in chest wall
* Penetrating trauma—sucking chest wound
Closed: no external wound
Suspect pneumothorax with chest wall trauma
Manifestations
Small pneumothorax
* Mild tachycardia and dyspnea
Large pneumothorax
* Respiratory distress
Short, shallow, rapid respirations, dyspnea, low O2
saturation
* Absent breath sounds over affected area
Diagnostic Study: Chest x-ray
Shows air or fluid in pleural space and reduced lung volume
Pneumothorax Types
Types
Spontaneous—happens without trauma or a known cause; two types:
Primary Spontaneous Pneumothorax: This form typically occurs in healthy individuals without underlying lung disease. It is often attributed to the rupture of small air-filled blisters (blebs) on the lung’s surface. Risk factors include being a tall, thin male, smoking, a family history of pneumothorax, and a previous history of spontaneous pneumothorax.
Secondary Spontaneous Pneumothorax: This type occurs in individuals with underlying lung conditions such as chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis, and pneumonia. The diseased lung tissue is more prone to rupture, leading to a pneumothorax.
Iatrogenic — This form is caused by medical procedures and is considered an accidental complication. Common procedures that can lead to an iatrogenic pneumothorax include:
Biopsies: Particularly transthoracic needle biopsies of the lung.
Central Venous Catheter Insertion: Especially subclavian catheter placement, where the needle or catheter may inadvertently puncture the lung.
Mechanical Ventilation: High airway pressures can lead to alveolar rupture and pneumothorax, especially in patients with acute respiratory distress syndrome (ARDS) or other severe lung conditions.
Esophageal Procedures: Procedures involving the esophagus, such as endoscopy or surgery, can sometimes lead to pneumothorax due to the close anatomical relationship between the esophagus and the pleural space.
Tension Pneumothorax
Tension pneumothorax
**Tension pneumothorax is a severe and life-threatening type of pneumothorax where air accumulates in the pleural space and cannot escape, leading to progressively increasing intrapleural pressure. This condition is an emergency because of its rapid impact on respiratory and cardiac function.
Mechanism: In a tension pneumothorax, the mechanism often involves a one-way valve effect, where air enters the pleural space during inspiration but cannot exit during expiration. This leads to a continuous buildup of air, causing the affected lung to collapse fully and exert pressure on the mediastinum (the central compartment of the thoracic cavity), which includes the heart and major blood vessels.
Consequences
Mediastinal Shift: The increasing pressure pushes the mediastinum towards the unaffected side, which can compress the opposite lung and further impair respiratory function.
Hemodynamic Instability: The shift and the increased intrathoracic pressure reduce venous return to the heart, leading to decreased cardiac output and potentially rapid cardiovascular collapse.
Causes
Tension pneumothorax can occur in various contexts:
Trauma: Chest injuries that result in a pneumothorax can progress to a tension pneumothorax, especially if the chest wall is breached (open pneumothorax) or if lung tissue is torn (closed pneumothorax).
Iatrogenic: Medical procedures, such as central venous catheter insertion or positive pressure ventilation, can inadvertently cause a tension pneumothorax.
Spontaneous: Rarely, a primary or secondary spontaneous pneumothorax can evolve into a tension pneumothorax, particularly if a bleb ruptures and creates a one-way valve mechanism.
Symptoms and Signs
Severe shortness of breath
Hypotension and tachycardia
Tracheal deviation away from the affected side (a late and ominous sign)
Distended neck veins
Hyperresonance on the affected side with diminished or absent breath sounds
Management
Immediate recognition and treatment are crucial to prevent death. Management typically involves the urgent decompression of the pleural space to release the trapped air and relieve the pressure. This is often initially achieved with needle decompression, followed by the placement of a chest tube to continuously evacuate the air and allow the lung to re-expand. Emergency medical intervention is required, and in hospital settings, this condition is treated as a “do not pass go” scenario, meaning immediate action is taken without waiting for imaging confirmation.
Hemothorax
Blood in pleural space
* Injury to chest wall, diaphragm, lung, blood vessels,
mediastinum
Treat with chest tube
Hemopneumothorax – occurs with pneumothorax
Chylothorax
Chylothorax refers to the accumulation of lymphatic fluid, specifically chyle, in the pleural space. Chyle is a milky fluid rich in fats, which is transported by the lymphatic system from the digestive system to the venous blood circulation. A chylothorax occurs when this fluid leaks into the pleural cavity, often due to damage or obstruction of the thoracic duct or its tributaries.
Causes
The causes of chylothorax can vary and include:
Trauma: Surgical procedures in the chest or neck, or chest injuries, can damage the thoracic duct.
Malignancy: Lymphomas, lung cancer, or other cancers that metastasize to the lymph nodes can obstruct or invade the thoracic duct.
Idiopathic: In some cases, the cause of chylothorax remains unknown.
Treatment Approaches
Conservative Management:
Dietary Modification: A low-fat diet with medium-chain triglycerides (MCTs) can reduce chyle production. MCTs are absorbed directly into the portal system, bypassing the lymphatic system.
Fasting and Total Parenteral Nutrition (TPN): In some cases, temporarily stopping oral intake and providing nutrients via TPN can allow the thoracic duct to heal.
Thoracentesis: Repeated drainage of the chylous fluid can relieve symptoms and prevent respiratory compromise.
Medical Therapy:
Octreotide: This somatostatin analogue can reduce lymph production and is used to treat chylothorax by decreasing the flow of chyle, potentially allowing the site of leakage to seal.
Refractory Cases:
Surgery: Surgical options include repair or ligation of the thoracic duct, pleuroperitoneal shunting, or other procedures aimed at directly addressing the leak or bypassing the damaged section of the thoracic duct.
Pleurodesis: This procedure involves the introduction of a substance (e.g., talc) into the pleural space to induce inflammation and fibrosis, causing the pleural layers to adhere to each other and eliminating the space where chyle can accumulate. Pleurodesis is generally considered when other treatments have failed and the chylothorax is recurrent.
Considerations
The choice of treatment depends on the cause of the chylothorax, the volume of chyle leakage, and the patient’s overall health and underlying conditions. Conservative management is often the first line of treatment, with more invasive procedures reserved for cases where conservative measures fail or when there’s a significant or persistent chyle leak. The management of chylothorax often requires a multidisciplinary approach, including input from thoracic surgeons, oncologists, dietitians, and other specialists as needed.
Treatment of Pneumothorax
Dependent on severity, underlying cause and
hemodynamic stability
Emergency treatment—Cover wound with dressing
secured on 3 sides
* Inspiration: pulls dressing against wound so air
cannot enter pleural space
* Expiration: dressing pushes out and air escapes
If impaled object in place, stabilize it with a bulky dressing but do not pull it out
Treatments
Chest tubes with water-seal drainage
Other: partial pleurectomy, stapling, or pleurodesis
Tension pneumothorax
Needle decompression— immediate
Chest tube and water-seal drainag
Pulmonary Edema
Abnormal accumulation of fluid in alveoli and
interstitial spaces
Complication of heart and lung problems
Most common cause: left-sided HF
Can be a life-threatening medical emergency if
severe
* Dyspnea, diaphoresis, wheezing
* 3rd heart sound may be present
* Blood-tinged, frothy sputum
CXR is best option for confirming diagnosis
Treatment focuses on
Find underlying cause of edema
Reduce amount of fluid in lungs
Care
Place in semi or high Fowler’s
O2 to keep SpO2 greater than 90%
IV diuretics or nitroglycerine
Monitor vs, WOB, breath sounds, output, electrolyte
balance, response to treatment
Pulmonary Embolism
Etiology and Pathophysiology
Blockage of 1 or more pulmonary arteries by
thrombus, fat or air embolus, or tumor tissue
Clot in venous system into pulmonary circulation then
lodges in small blood vessel and obstructs alveolar
perfusion
Most often affects lower lobes
Most PEs arise from deep vein thrombosis (DVT)
Venous thromboembolism (VTE) – preferred term to
describe spectrum from DVT to PE
Origination: deep veins of legs, femoral or iliac veins,
right side of heart (atrial fibrillation) and pelvic veins
(especially after surgery or childbirth)
* Other: central venous catheters or arterial lines; fat
(fractured long bones); air (IV), vegetation on heart
valves, amniotic fluid, and cancer
A saddle embolus refers to a large thrombus (blood clot) that lodges at a bifurcation (branching point) of a major artery, most commonly the pulmonary artery. This type of embolus is termed “saddle” because it straddles the bifurcation, resembling a saddle on a horse. In the context of pulmonary embolism (PE), a saddle embolus sits at the junction where the main pulmonary artery divides into the left and right pulmonary arteries.
Risk Factors for PE
Immobility or reduced mobility
Surgery within 3 months (especially pelvic and lower extremity)
History of VTE
Cancer
Obesity
Oral contraceptives/ hormone therapy
Smoking
Prolonged air travel
Heart failure
Pregnancy
Clotting disorders
PE Clinical Manifestations
Depend on type, size, and extent of emboli
Appear suddenly or begin slowly
Dyspnea most common; mild-moderate hypoxemia
Other: tachypnea, cough, chest pain, hemoptysis,
crackles, wheezing, fever, tachycardia, syncope,
pulmonic heart sound
Massive PE: change in mental status, hypotension,
feeling of impending doom, cardiorespiratory
arrest/death
PE Complications
About 10% with massive PE die within 1st hour
Pulmonary infarction – death of lung tissue
Occlusion of medium or large-sized vessel,
inadequate collateral blood flow, and preexisting lung
disease results in alveolar necrosis and hemorrhage
which may result in abscess and pleural effusion
Pulmonary hypertension
- condition characterized by increased blood pressure in the pulmonary arteries. In the context of PE, PH can result from the obstruction of pulmonary vessels by emboli, which increases vascular resistance and pressure within the pulmonary artery system.
-Results from hypoxemia associated with massive or
recurrent emboli which can cause chronic
thromboembolic pulmonary hypertension
Right ventricular hypertrophy
-Over time, the increased workload on the right ventricle can lead to right ventricular hypertrophy (RVH), where the muscle of the right ventricle thickens. This can progress to right ventricular failure, characterized by symptoms such as leg swelling, increased abdominal girth due to fluid accumulation, and fatigue.
PE Diagnostic Study: D-Dimer
D-Dimer Test
Description: The D-dimer test measures a specific type of protein fragment that is produced when a blood clot is degraded by fibrinolysis. Elevated levels of D-dimer can indicate the presence of an active clotting and dissolution process within the body.
Usefulness: The D-dimer test is particularly valuable in ruling out PE in patients with a low clinical probability. A normal D-dimer level can be a strong indicator that a PE is unlikely in patients deemed to be at low risk based on clinical assessment and risk stratification tools.
Limitations:
Sensitivity and Specificity: While D-dimer levels are often elevated in the presence of PE, they can also be elevated in many other conditions, such as recent surgery, trauma, infection, pregnancy, and cancer, making the test less specific. The sensitivity of the test can be limited, particularly for small PEs, leading to false negatives in up to 50% of such cases.
False Positives: Due to its lack of specificity, a positive D-dimer test is not diagnostic of PE and requires further investigation with imaging studies, especially in patients with a moderate to high clinical probability of PE.
PE Test: Spiral (helical) CT scan/CT angiography or CTA
CT Pulmonary Angiography (CTA)
Description: CTA is a specialized form of CT scan that uses intravenous contrast material to visualize the pulmonary arteries. It is currently the most commonly used diagnostic imaging study for suspected PE.
Advantages: CTA provides a detailed three-dimensional picture of the pulmonary vasculature, allowing for the direct visualization of clots within the arteries. It is highly sensitive and specific for diagnosing PE.
Requirements: The test requires the administration of iodinated contrast material, which can be contraindicated in patients with allergies to the contrast medium or those with significant renal impairment.
Considerations: While CTA is highly effective in diagnosing PE, the need for contrast material and radiation exposure are important considerations, especially in pregnant women, individuals with renal insufficiency, or those with a known contrast allergy.
PE Test: Ventilation-perfusion (V/Q) scan
**nuclear medicine test used to assess the circulation of air and blood within the lungs
Components of a V/Q Scan
Perfusion Scanning:
Involves the intravenous injection of a radiolabeled isotope (commonly technetium-99m-labeled macroaggregated albumin).
The isotope travels through the bloodstream and lodges in the small capillaries in the lungs.
A gamma camera captures images of the distribution of the radioisotope, reflecting blood flow (perfusion) to various parts of the lung.
Areas that do not receive blood flow due to blockages (such as those caused by a pulmonary embolism) will appear as defects or “cold spots” on the scan.
Ventilation Scanning:
The patient inhales a radioactive gas (such as xenon or technetium-99m-labeled aerosol) which distributes throughout the lungs.
The gamma camera again captures images, this time of the distribution of the inhaled gas, reflecting ventilation (airflow) in the lungs.
Areas that do not receive airflow will show up as defects on the scan.
Interpretation
A normal V/Q scan indicates both ventilation and perfusion are uniformly distributed throughout the lungs.
A mismatch, where ventilation is normal but perfusion is impaired (ventilated but not perfused), is suggestive of a pulmonary embolism. This is because the blood clot blocks blood flow, but air can still enter the lung segment.
V/Q scans are typically reported as having a low, intermediate, or high probability of PE based on the pattern and extent of mismatches.
Limitations and Considerations
While V/Q scans are less invasive than CTA and avoid the use of iodinated contrast, their interpretation can be more complex, especially in patients with pre-existing lung diseases such as COPD, which can also cause mismatches.
The specificity of the V/Q scan can be lower than that of CTA, particularly in patients with abnormal chest radiographs or underlying lung conditions. In such cases, the result might be reported as non-diagnostic or of intermediate probability, necessitating further testing.
Important Tests, Not Diagnostic for PE
Arterial Blood Gases (ABGs)
Findings: In PE, arterial blood gases often show low PaO2 (hypoxemia) due to impaired gas exchange.
However, the pH is often normal because respiratory compensation (increased breathing rate) helps to maintain the acid-base balance.
Limitations: Hypoxemia can result from various respiratory and cardiac conditions, not just PE, making this finding non-specific.
Chest X-ray
Findings: May show signs such as atelectasis (collapse of part of the lung), pleural effusion (fluid in the pleural space), or elevated hemidiaphragm, but these findings are not specific to PE. In many cases of PE, the chest X-ray can be normal or nearly normal.
Limitations: While helpful in ruling out other causes of the patient’s symptoms, such as pneumonia or pneumothorax, a chest X-ray alone cannot diagnose PE.
Electrocardiogram (ECG)
Findings: ECG changes in PE can be varied and nonspecific, including tachycardia (fast heart rate), nonspecific ST-segment and T-wave changes, and, in more severe cases, signs of right heart strain such as the S1Q3T3 pattern.
Limitations: These changes are not specific to PE and can be seen in many other cardiac and pulmonary conditions.
Serum Troponin Levels
Findings: Troponin levels may be elevated in PE, indicating right ventricular strain or myocardial injury due to the increased workload on the right side of the heart.
Limitations: Elevated troponin levels can also occur in various cardiac conditions, including myocardial infarction, and are not specific to PE.
B-type Natriuretic Peptide (BNP) or N-terminal pro b-type Natriuretic Peptide (NT-proBNP)
Findings: These peptides can be elevated in cases of significant PE that leads to acute right heart strain or failure, as they are released by the ventricles in response to excessive stretching of heart muscle cells.
Limitations: Elevated BNP or NT-proBNP levels can also be seen in other conditions that cause cardiac strain, such as heart failure, and are not specific for PE.
While these tests contribute valuable information to the overall clinical assessment, they must be interpreted in the context of the patient’s history, physical examination, and other diagnostic findings. The definitive diagnosis of PE typically requires imaging studies such as CT pulmonary angiography (CTA) or a ventilation-perfusion (V/Q) scan.
Care for PE
Initial Management
Stabilization: In cases of massive PE with hemodynamic instability, immediate measures to stabilize the patient include oxygen supplementation to relieve hypoxemia and intravenous fluids to support blood pressure. In severe cases, advanced life support measures may be necessary.
Anticoagulation Therapy
Heparin: Initial anticoagulation often starts with the administration of heparin (unfractionated heparin or low molecular weight heparin) to prevent further clot formation. Heparin acts quickly and can be adjusted based on the patient’s response.
Oral Anticoagulants: Transition to oral anticoagulants, such as warfarin, direct oral anticoagulants (DOACs) like rivaroxaban, apixaban, or edoxaban, usually follows. The duration of anticoagulation therapy depends on the individual’s risk factors for recurrence and the presence of reversible risk factors at the time of the initial event.
Thrombolytic Therapy
Indications: Thrombolytic (fibrinolytic) therapy is reserved for patients with high-risk (massive) PE with hemodynamic instability, as it can rapidly dissolve the thrombus and restore pulmonary circulation. However, it carries a significant risk of bleeding and is contraindicated in certain patients.
Surgical and Interventional Procedures
Embolectomy: In cases where thrombolytic therapy is contraindicated or has failed, or in patients who continue to deteriorate hemodynamically, surgical removal of the clot (pulmonary embolectomy) may be necessary.
Catheter-Directed Therapy: Less invasive than surgery, this involves the use of catheters to deliver thrombolytic agents directly to the clot or to mechanically break up the clot.
Supportive Care
Compression Stockings: May be used to prevent the post-thrombotic syndrome, especially after deep vein thrombosis (DVT).
Monitoring: Regular follow-up and monitoring for the recurrence of symptoms or signs of bleeding due to anticoagulation therapy.
Prevention of Recurrence
Risk Factor Modification: Includes addressing modifiable risk factors such as smoking cessation, weight management, and avoiding prolonged immobility.
PE Management Cont. - Supporting Cardiorespiratory Status
Oxygen Therapy
Administration: Oxygen is administered via a nasal cannula or face mask to patients experiencing hypoxemia due to impaired gas exchange from the PE. The goal is to maintain adequate oxygen saturation and relieve symptoms of hypoxia.
Titration: The fraction of inspired oxygen (FiO2) is titrated based on arterial blood gas (ABG) analysis to achieve target oxygen saturation levels, usually above 90% or higher based on the patient’s underlying conditions.
Mechanical Ventilation: In cases of severe respiratory failure or when the patient’s work of breathing is excessively high, mechanical ventilation may be necessary to ensure adequate oxygenation and ventilation.
Pulmonary Hygiene
Purpose: Maintaining clear airways and preventing atelectasis (collapse of part of the lung) is essential for optimizing lung function, especially in immobilized patients or those with underlying lung disease.
Techniques: Include incentive spirometry, chest physiotherapy, and frequent repositioning to promote lung expansion and secretion clearance.
Shock Management
IV Fluids: Intravenous fluids may be administered cautiously to improve cardiac output and maintain blood pressure, particularly in hypotensive patients. However, fluid management must be carefully balanced to avoid fluid overload, which can worsen respiratory status.
Vasopressors: In cases of persistent hypotension despite adequate fluid resuscitation, vasopressors such as norepinephrine may be used to support blood pressure and maintain perfusion to vital organs.
Heart Failure (HF) Management
Diuretics: For patients showing signs of fluid overload or heart failure, diuretics can help reduce fluid accumulation, alleviate pulmonary congestion, and improve breathing.
Pain Management
Opioids: Pain, particularly pleuritic chest pain, can be significant in PE and may impair the patient’s ability to take deep breaths, leading to atelectasis. Opioids like morphine can relieve pain and reduce the sympathetic stress response, which can be beneficial in acute PE. However, care must be taken to avoid respiratory depression, especially in patients with compromised respiratory function.
PE Drug Therapy
Anticoagulation therapy is the cornerstone of treatment for pulmonary embolism (PE) and is typically divided into three phases: initial, longer-term, and extended. The choice of anticoagulant, the duration of therapy, and the addition of fibrinolytic agents depend on the severity of the PE, the risk of bleeding, and the patient’s overall health status.
Initial Phase (First 7 Days)
The goal during the initial phase is to rapidly anticoagulate the patient to prevent further clot formation.
Low-Molecular-Weight Heparin (LMWH): Preferred for its predictable pharmacokinetics and lower risk of heparin-induced thrombocytopenia (HIT). It is administered subcutaneously and does not usually require monitoring of the aPTT (activated partial thromboplastin time).
Unfractionated IV Heparin: Used in patients with severe renal impairment (where LMWH is contraindicated) or when rapid reversibility is required, such as in anticipation of surgery. It requires continuous intravenous infusion and regular monitoring of the aPTT to ensure therapeutic anticoagulation.
Longer-Term Phase (Up to 6 Weeks)
After the initial stabilization, the patient may transition to oral anticoagulation or continue on LMWH.
Warfarin (Coumadin): A vitamin K antagonist that requires monitoring of the INR (International Normalized Ratio) to maintain a therapeutic range. The initiation of warfarin overlaps with heparin or LMWH for at least 5 days and until the INR is therapeutic for 24 hours.
Direct Oral Anticoagulants (DOACs): Alternatives to warfarin include rivaroxaban, apixaban, edoxaban, and dabigatran. These agents have the advantage of fixed dosing and do not require routine monitoring of coagulation parameters.
Extended Phase (6 Months and Beyond)
Extended anticoagulation may be indicated in patients with recurrent PE, ongoing risk factors for venous thromboembolism (VTE), or unprovoked PE. The decision to continue anticoagulation beyond 6 months is based on weighing the risk of recurrent VTE against the risk of bleeding.
Fibrinolytic Therapy
Indications: Reserved for patients with massive PE and hemodynamic instability or those with a high risk of mortality, as fibrinolytic agents can rapidly dissolve blood clots.
Agents: Include tissue plasminogen activator (tPA) and alteplase (Activase). These drugs activate plasminogen to plasmin, which then degrades fibrin clots.
Considerations: Fibrinolytic therapy carries a significant risk of bleeding, including intracranial hemorrhage, and is contraindicated in patients with a high risk of bleeding.
PE Surgical Therapy
Pulmonary embolectomy is a surgical or interventional procedure considered for the treatment of massive pulmonary embolism (PE), especially in patients who are hemodynamically unstable and for whom thrombolytic therapy is contraindicated due to the risk of bleeding. There are two main approaches to embolectomy: surgical embolectomy and percutaneous catheter-based techniques.
Surgical Pulmonary Embolectomy
Indications: Typically reserved for patients with life-threatening, massive PE who are in shock or have persistent arterial hypotension, and in whom thrombolysis is contraindicated or has failed.
Procedure: Involves the surgical removal of the embolus from the pulmonary artery under general anesthesia, often requiring cardiopulmonary bypass.
Considerations: Given its invasive nature, surgical embolectomy is associated with significant risks and is usually considered a last resort. The decision to proceed with surgery is based on a careful assessment of the potential benefits and risks.
Percutaneous Catheter Embolectomy
Description: A less invasive alternative to surgical embolectomy, this procedure involves the use of catheters inserted through the veins to reach the pulmonary artery and mechanically remove or break up the clot.
Techniques: May include aspiration embolectomy, rheolytic thrombectomy (using high-velocity jets of saline to break up the clot), or rotational thrombectomy devices.
Advantages: The percutaneous approach generally has a lower risk compared to open surgery and can be performed more quickly, which is crucial in an emergency setting.
Endovascular Ultrasound Delivered Thrombolysis
Description: This is a novel technique where ultrasound waves are used in conjunction with catheter-delivered thrombolytic drugs to enhance the breakdown of the clot. The ultrasound helps to increase the penetration of the thrombolytic agent into the thrombus, potentially reducing the required dose and the risk of bleeding.
Application: This technique may be used in certain centers for patients with intermediate-risk or high-risk PE, particularly when conventional thrombolysis is contraindicated or needs to be used at reduced doses.
Inferior Vena Cava (IVC) Filter
Purpose: An IVC filter is a device placed in the inferior vena cava to catch and prevent large clots from the lower extremities or pelvis from reaching the lungs. It is considered in patients who have contraindications to anticoagulation or in whom anticoagulation has failed to prevent recurrent PE.
Considerations: The use of IVC filters is controversial due to potential long-term complications, including filter migration, fracture, and increased risk of deep vein thrombosis (DVT) at the filter site. The decision to place an IVC filter should be individualized, and in many cases, the filter is considered retrievable and may be removed once the risk of PE has diminished.
Pulmonary Hypertension
Elevated pulmonary artery pressure (> 20 mm Hg)
due to an increase in resistance to blood flow
through the pulmonary circulation
Mean pulmonary artery pressures
* Normal 12 to16 mm Hg
* Greater than 25 mm Hg at rest
* Greater than 30 mm Hg with exercises
May be primary disease or secondary complication
5 Classes of Pulmonary Hypertension
Five Classes (World Health Organization) based on
causes
Group 1: medication, specific disease, genetic link or
idiopathic
Group 2: left-sided heart failure
Group 3: lungs and hypoxia
Group 4: CV system and thromboembolism
Group 5: Multifactorial: hematologic, renal or
metabolic involvement
Idiopathic Pulmonary Arterial
Hypertension (IPAH)
Pulmonary hypertension without known cause
results in right HF and death if untreated
Previously known as primary pulmonary hypertension
Etiology and Pathophysiology
Uncertain; related to connective tissue disease,
cirrhosis, and HIV
Insult to pulmonary endothelium results in vascular
scarring, endothelial dysfunction, and smooth muscle
proliferation
Affects females more than males
Pathogenesis of Pulmonary
Hypertension and Cor Pulmonale
Clinical Manifestations of Pulmonary HTN
Pulmonary hypertension (PH) is a complex and serious condition characterized by high blood pressure in the arteries of the lungs, which can lead to right heart failure if untreated. The clinical manifestations of pulmonary hypertension can vary widely among individuals and typically progress as the disease advances.
Classic Symptoms
Dyspnea on Exertion: Shortness of breath during physical activity is one of the earliest and most common symptoms of PH, occurring due to the heart’s inability to pump enough blood through the lungs at increased rates required during exertion.
Fatigue: Patients often experience profound tiredness or weakness, which can be attributed to the reduced oxygen delivery to the muscles and organs.
Other Symptoms
Exertional Chest Pain: May occur due to the increased workload on the heart, particularly the right ventricle, as it struggles to pump blood through the narrowed pulmonary arteries.
Dizziness and Syncope (Fainting): These symptoms can result from reduced blood flow to the brain, especially during physical activity when the demand for blood flow is higher.
Abnormal Heart Sounds: An S3 heart sound, or “ventricular gallop,” can sometimes be heard in patients with PH and is indicative of increased fluid volume and pressure inside the heart.
Progression of Disease
Dyspnea at Rest: As PH progresses, shortness of breath can occur even at rest, indicating a significant impairment of pulmonary blood flow and cardiac function.
Right Ventricular Hypertrophy (Cor Pulmonale): Prolonged high blood pressure in the pulmonary artery places a chronic strain on the right ventricle, leading to its enlargement and thickening (hypertrophy).
Heart Failure (HF): Advanced PH can lead to right-sided heart failure, characterized by symptoms such as edema (swelling) in the ankles and legs, ascites (abdominal fluid accumulation), and fatigue.
Pulmonary HTN Diagnostics
Diagnostics
The diagnosis of pulmonary hypertension involves a combination of tests, often beginning with non-invasive methods and progressing to more definitive testing:
Right-Sided Heart Catheterization: The gold standard for diagnosing PH, this procedure measures the pressure in the pulmonary arteries directly and assesses the heart’s function.
Electrocardiogram (ECG): Can show signs of right ventricular strain or hypertrophy.
Chest X-Ray: May reveal enlarged pulmonary arteries and changes in the size and shape of the right ventricle.
Pulmonary Function Tests (PFTs): Useful for evaluating lung function and ruling out other respiratory conditions.
Echocardiogram: Non-invasive ultrasound imaging that can estimate pulmonary artery pressures and assess right ventricular function.
CT Scan: Can provide detailed images of the lungs and pulmonary vasculature, helping to identify underlying causes of PH such as chronic pulmonary emboli.
Time to Diagnosis
The average time from symptom onset to diagnosis is approximately 2 years, often because the early symptoms of PH are nonspecific and can be attributed to other, more common conditions. By the time of diagnosis, the disease may be quite advanced, underscoring the importance of early recognition and intervention in symptomatic individuals.
Care for Pulmonary HTN
Early recognition—stop progression
Report: unexplained shortness of breath, syncope,
chest discomfort, edema of feet and ankles
Drug therapy
Pulmonary vasodilation, reduce right ventricular
overload, and reverse remodeling
Manage edema
Prevent thrombi
Prevent hypoxia
Goal – keep O2 saturation 90% or greater
Pulmonary HTN Surgical Interventions
Surgical interventions for pulmonary embolism (PE) and its complications, particularly pulmonary hypertension (PH), are considered when medical therapy is insufficient or when the condition is life-threatening. These interventions can range from procedures aimed at removing the obstruction in pulmonary arteries to palliative surgeries that alleviate symptoms and improve the quality of life.
Pulmonary Thromboendarterectomy (PTE)
Description: PTE, also known as pulmonary endarterectomy (PEA), is a complex surgical procedure designed to remove chronic thromboembolic material from the pulmonary arteries. This procedure is indicated for patients with chronic thromboembolic pulmonary hypertension (CTEPH), a form of PH that results from the organization and fibrosis of unresolved pulmonary emboli.
Outcome: PTE can be curative for patients with CTEPH, often resulting in significant improvements in symptoms, pulmonary hemodynamics, and exercise capacity. It is the treatment of choice for suitable candidates with this condition.
Atrial Septostomy (AS)
Description: AS is a palliative procedure performed to create a right-to-left shunt at the atrial level. By creating a small opening between the right and left atria, this procedure reduces right atrial pressure, decreases right ventricular afterload, and improves left ventricular preload.
Indications: AS is considered for patients with severe PH and right heart failure who are refractory to medical therapy and not candidates for PTE or lung transplantation. It can improve symptoms and exercise tolerance but is associated with significant risks.
Lung Transplant
Description: Lung transplantation involves replacing one or both diseased lungs with healthy lungs from a donor. It is a treatment option for advanced lung disease, including end-stage PH when other treatments have failed.
Outcome: Lung transplantation can significantly improve the quality of life and survival in selected patients. Recurrence of the original disease in the transplanted lungs is rare, but the procedure carries risks such as rejection and infection.
No cure
Treatment can relieve symptoms, improve quality of
life, prolong life
* Untreated, death can occur within a few years
Secondary Pulmonary Arterial
Hypertension (SPAH)
Chronic increase in pulmonary artery pressures from
another disease
Parenchymal lung disease, LV dysfunction,
intracardiac shunts, chronic PE, or systemic
connective tissue disease
Symptoms: dyspnea, fatigue, lethargy, chest pain; RV
hypertrophy and right-sided heart failure
Diagnosis—similar to IPAH
Treatment—treat underlying cause; if irreversible—
IPAH therapies
Cor Pulmonale
Enlarged right ventricle secondary to disorder of
respiratory system; COPD
Pulmonary hypertension preexists; HF
**Clinical manifestations
Subtle and often masked by lung symptoms
Exertional dyspnea, tachypnea, cough, fatigue, RV
hypertrophy (ECG), increased intensity in S2 heart
sound, polycythemia
HF: peripheral edema, weight gain, distended neck
veins, full, bounding pulse, enlarged liver
Cor Pulmonale Care
Early identification before irreversible heart changes
Determine and treat underlying cause
Long-term oxygen
Other individualized therapies
Environmental Lung Diseases
Environmental or occupational inhalation of dust or
chemicals
Lung damage depends on
* Toxicity of inhaled substance
* Amount and duration of exposure
* Susceptibility of individual
**Environmentally induced lung diseases includes
Pneumoconiosis
Chemical pneumonitis
Hypersensitivity pneumonitis
Pneumoconiosis
Pneumoconiosis—inhaled mineral or metal dust
particles
Classified by origin
* Silicosis—sand or rock
* Coal worker’s pneumoconiosis—“black lung” results in
pulmonary fibrosis
* Asbestosis results in mesothelioma; cancer occurs 15
to 19 years from exposure
Chemical pneumonitis
Inhalation of toxic chemical fumes
* Acute—diffuse lung injury; pulmonary edema
* Chronic—bronchiolitis obliterans
Hypersensitivity pneumonitis (extrinsic allergic
alveolitis
Extrinsic allergic alveolitis—inhaled allergic antigens
* Bird fancier’s lung (feathers and bird droppings)
* Farmer’s lung (hay dust)
* Acute, subacute, chronic forms
Environmental Lung Disorders, Clinical Manifestations
Clinical manifestations (10 to 15 years)
Dyspnea, cough, wheezing, weight loss
Pulmonary function tests: reduced vital capacity
Chest x-ray, CT scans—lung involvement
Cor pulmonale—right heart failure due to diffuse
fibrosis
Complication: COPD
Other: acute pulmonary edema, lung cancer,
mesothelioma, TB
Late: cor pulmonale
Environmental Lung Diseases
Lung Transplants
Lung transplantation is a viable treatment option for patients with end-stage lung disease when other treatments have failed to provide relief. It involves replacing one or both diseased lungs with healthy lungs from a deceased donor. Diseases that may lead to consideration for a lung transplant include:
Chronic Obstructive Pulmonary Disease (COPD): Advanced stage of the disease where medical therapy does not significantly improve symptoms or quality of life.
Idiopathic Pulmonary Fibrosis (IPF): A progressive and usually fatal lung disease with no known cause or cure.
Cystic Fibrosis (CF): A genetic disorder that damages the lungs and can lead to severe respiratory problems.
Idiopathic Pulmonary Arterial Hypertension (IPAH): A rare and progressive condition that increases the pressure in the pulmonary arteries.
Alpha-1 Antitrypsin Deficiency: A genetic condition that can cause liver and lung disease, leading to emphysema.
Preoperative Care and Evaluation
Before a lung transplant, a comprehensive evaluation is conducted to assess the patient’s overall health, the severity of lung disease, and suitability for transplantation. This evaluation includes:
Medical Assessment: Detailed review of the patient’s lung disease history, current lung function, and overall physical health.
Psychosocial Evaluation: Assesses the patient’s mental health, social support system, and ability to adhere to a complex postoperative care regimen.
Contraindications: Certain conditions can preclude a patient from being a transplant candidate, including active infections, certain cancers, severe heart, liver, or kidney diseases, and ongoing substance abuse.
United Network for Organ Sharing (UNOS) and Lung Allocation Score (LAS)
In the United States, the allocation of donor lungs is managed by the United Network for Organ Sharing (UNOS), which uses a Lung Allocation Score (LAS) to prioritize patients based on the severity of their disease and their projected survival without a transplant versus their expected survival post-transplant. The LAS is a numerical score that ranges from 0 to 100, with higher scores indicating a higher priority for transplant.
Postoperative Regimen
After a lung transplant, patients must adhere to a strict postoperative regimen that includes:
Immunosuppressive Medication: To prevent organ rejection, patients must take lifelong immunosuppressive drugs, which can have significant side effects and increase the risk of infections.
Regular Monitoring: Includes frequent check-ups, lung function tests, and monitoring for signs of rejection or infection.
Rehabilitation: Pulmonary rehabilitation is crucial for improving lung function, strength, and overall well-being after transplantation.
4 Types of Lung Transplant Surgeries
Surgical procedures
Four types
* Single-lung; thoracotomy incision on affected side while opposite lung is ventilated
* Bilateral lungs; incision across sternum; donor lungs
implanted separately
* Heart-lung; median sternotomy incision
* Lobes from living-related donor; reserved for those
unlikely to survive waiting for a donor to become
available; most have cystic fibrosis
Lung Transplant Post Op Care
Postoperative Care: ICU
Ventilator and hemodynamic support
IV fluids
Immunosuppression
* Tacrolimus, mycophenolate mofentil, and prednisone
Nutrition
High risk for multiple complications
Infections are leading cause of death, especially in 1st
year
Lung Transplant Complications
Rejection
Acute: 5 to 10 days
* Fairly common in 1st year after transplant
* Fever, fatigue, dyspnea, dry cough, O2 desaturation
Chronic: Bronchiolitis obliterans (BOS)
* Progressive airflow obstruction unresponsive to
bronchodilators and corticosteroids
Prevent/treat complications—infection
Discharge planning/Coordination of care
* Self-care, medication management, contacting
transplant team, pulmonary hygiene, rehabilitation
Lung Cancer
Leading cause of cancer-related deaths (25%) in
U.S.; more than breast, prostate, colon
combined
Estimated 235,000 new cases in 2021; 131,000
deaths expected
High mortality rate; low cure rate
Advances in treatment improving response
Gender considerations
Promoting health equity
Etiology of Lung Cancer
Smoking is 80-90% of them
Risk related to total exposure to tobacco smoke
Total number of cigarettes smoked
Age of smoking onset
Depth of inhalation
Tar and nicotine content
Use of unfiltered cigarettes
Sidestream (secondhand) smoke is also a health
risk
Other causes of lung cancer include exposure to:
Pollution
Radiation /radon
Asbestos
Industrial agents (radon, coal dust, asbestos,
chromium, silica, arsenic, diesel exhaust) increase
risk, especially in smokers
* Incidence, risk factors, survival vary between genders
* Incidence and survivability vary between racial and
ethnic populations
Pathophysiology of Lung Cancer
Arise from mutated epithelial cells
Tumor development promoted by epidermal growth
factor
It takes 8 to 10 years for a tumor to reach 1 cm
Smallest lesion detectable on x-ray
Occur primarily in segmental bronchi and upper
lobes
Primary lung cancers categorized into 2 subtypes
Non–small-cell lung cancer (NSCLC); 84%
Small-cell lung cancer (SCLC); 13%
Metastasis—direct extension and blood and lymph
system
Common sites: lymph nodes, liver, brain, bones,
adrenal glands
SCLC and NSCLC account for 97% of lung tumors;
other 3% include hamartomas, mucous gland
adenoma, mesotheliomas
Non–Small-Cell Lung Cancer
(NSCLC)
Squamous cell carcinoma
Slow growing
Early symptoms: cough and hemoptysis
Adenocarcinoma
Moderate growing
Most common in nonsmokers
Large-cell carcinoma
Rapid growing
Highly metastatic
Small-Cell Lung Cancer (SCLC)
Very rapid growth
Most malignant
Early metastasis
Associated endocrine disorders
Chemotherapy and radiation
Poor prognosis
Paraneoplastic Syndrome
Caused by hormones, cytokines, enzymes, or
antibodies that destroy healthy cells
May manifest before cancer diagnosed
Associated most with SCLC
Examples: hypercalcemia, SIADH, adrenal
hypersecretion, polycythemia, Cushing’s syndrome
Lung Cancer Clinical Manifestations
Symptoms nonspecific and appear late in
disease
May be masked by chronic cough
Depend on type of primary lung cancer, location,
and metastatic spread
Often presents as a lobar pneumonia that does
not respond to treatment
Persistent cough with sputum (most common)
Hemoptysis (Hemoptysis is the medical term for coughing up blood from the lower respiratory tract (bronchi and lungs)
Dyspnea
Wheezing
Chest pain
Localized or unilateral; mild to severe
Later manifestations
Anorexia, nausea/vomiting, fatigue, weight loss
Hoarseness
Unilateral paralysis of diaphragm
Dysphagia
Superior vena cava obstruction
Palpable lymph nodes
Mediastinal/cardiac involvement
Lung Cancer Diagnostic Studies
Chest x-ray (normal, mass or infiltrate, metastasis,
pleural effusion)
CT scan (location and extent of mass, mediastinal
involvement, lymph node enlargement)
Sputum cytology (rarely used)
Lung biopsy—definitive diagnosis
Pleural fluid analysis
Metastasis
Bone and CT scans—brain, abdomen, and pelvis
H & P
CBC with differential
Chemistry panel
Liver, renal, and pulmonary function tests
MRI
PET scan
Lung Cancer Staging - NSCLC
Lung cancer staging is crucial for determining the extent of the disease, guiding treatment decisions, and assessing prognosis. Non-small cell lung cancer (NSCLC), which accounts for the majority of lung cancer cases, is staged using the TNM system, developed by the American Joint Committee on Cancer (AJCC) and the Union for International Cancer Control (UICC). This system takes into account three key components: the size and extent of the primary tumor (T), whether the cancer has spread to nearby lymph nodes (N), and the presence of distant metastasis (M).
TNM System
T (Tumor): Describes the size of the original tumor and whether it has grown into nearby areas. T is classified from TX (primary tumor cannot be assessed) to T4, based on the size of the tumor and the extent of invasion into surrounding structures.
N (Node): Indicates whether the cancer has spread to nearby lymph nodes and how many. N is classified from NX (regional lymph nodes cannot be assessed) to N3, based on the location and number of lymph nodes involved.
M (Metastasis): Describes whether the cancer has spread to other parts of the body. M0 means that no distant metastasis is found, while M1 indicates the presence of metastasis.
Staging Groups
Based on the TNM classifications, NSCLC is grouped into stages I through IV, which may have A or B subtypes to further define the extent of the disease:
Stage I: The cancer is confined to the lungs and has not spread to any lymph nodes. This stage is further divided into IA and IB based on the size of the tumor.
Stage II: The cancer has spread to nearby lymph nodes or has grown into surrounding structures. This stage is divided into IIA and IIB.
Stage III: More extensive lymph node involvement or larger tumor size. Stage III is subdivided into IIIA (limited to one side of the chest and may still be considered for surgery) and IIIB (more extensive disease, generally not considered operable).
Stage IV: The most advanced stage, indicating that cancer has spread beyond the lung to other parts of the body. This stage is often associated with a poor prognosis.
Treatment Implications
Stages I, II, and IIIA: Patients with NSCLC in these stages may be candidates for surgical resection, possibly combined with chemotherapy, radiation therapy, or targeted therapy, depending on specific tumor characteristics and patient health.
Stage IIIB and IV: These stages are usually considered inoperable due to extensive local spread or distant metastasis. Treatment typically focuses on systemic therapies such as chemotherapy, targeted therapy, immunotherapy, and palliative care measures to relieve symptoms and improve quality of life.
Lung Cancer Staging - SCLC
Small Cell Lung Cancer (SCLC) is an aggressive form of lung cancer characterized by rapid growth and early spread to distant sites. Due to its aggressive nature, the traditional TNM staging system (which considers Tumor size, lymph Node involvement, and Metastasis) used for non-small cell lung cancer (NSCLC) is not typically applied to SCLC. Instead, SCLC is classified into two main stages for the purpose of treatment planning and prognosis:
Limited Stage
Definition: Limited-stage SCLC is defined as cancer that is confined to one side of the chest and can be reasonably encompassed within a single radiation therapy field. This includes the primary tumor and regional lymph nodes.
Treatment: Patients with limited-stage disease may be candidates for more aggressive treatments aimed at cure, which can include combinations of chemotherapy, radiation therapy, and in some cases, surgery. Despite the aggressive nature of SCLC, treatment at the limited stage can lead to significant responses, although the risk of recurrence remains high.
Extensive Stage
Definition: Extensive-stage SCLC refers to cancer that has spread beyond the limits of a single radiation field, including cancer that has spread to the other lung, distant lymph nodes, or other organs (metastasis).
Treatment: For extensive-stage SCLC, the treatment primarily involves systemic therapies such as chemotherapy and immunotherapy. The focus is usually on controlling the disease, alleviating symptoms, and improving quality of life, as the prospects for cure are significantly lower compared to limited-stage disease.
Prevalence at Diagnosis
At the time of diagnosis, most patients with SCLC have extensive disease due to the cancer’s rapid growth and tendency to metastasize early in its course. This extensive spread at diagnosis is a major factor in the overall prognosis and treatment strategy for SCLC patients.
Screening for Lung Cancer
Annually in adults ages 50 to 80 with a history of
smoking
20 pack-year history
Current smoker
Quit less than15 years ago
Completed with low dose CT
Lung Cancer Surgical Therapy - NSCLC
For early-stage Non-Small Cell Lung Cancer (NSCLC) (Stages I to IIIA) without mediastinal lymph node involvement, surgical resection offers the best chance for a cure. The choice of surgical procedure depends on various factors, including the size and location of the tumor, the patient’s lung function, and overall health status.
Surgical Procedures for NSCLC
Segmental or Wedge Resection:
These are limited resection procedures where only a small, localized part of the lung is removed.
Segmental Resection: Involves removing a larger portion of the lung tissue, including one or more segments (subdivisions of the lung lobes).
Wedge Resection: The removal of a small, wedge-shaped portion of lung tissue that contains the tumor along with a margin of healthy tissue.
These procedures are typically considered for smaller tumors or for patients whose lung function may not tolerate more extensive surgery.
Lobectomy:
The removal of an entire lobe of the lung. Since the lungs are divided into lobes (three on the right and two on the left), a lobectomy can remove a significant portion of lung tissue while leaving the rest intact.
Lobectomy is generally the preferred surgical procedure for NSCLC when feasible because it offers a balance between removing all of the cancerous tissue and preserving lung function.
Pneumonectomy:
Involves the removal of an entire lung and is usually reserved for tumors that are centrally located or involve the main bronchus where less extensive surgery is not possible.
Given the significant reduction in pulmonary function, pneumonectomy is considered only when absolutely necessary and after careful evaluation of the patient’s ability to tolerate the loss of an entire lung.
Video-Assisted Thoracoscopic Surgery (VATS):
A minimally invasive surgical technique where the surgery is performed using small incisions and guided by a thoracoscope (a small camera) inserted into the chest.
VATS can be used for lobectomies and smaller resections and is associated with less pain and a shorter recovery period compared to traditional open surgery.
VATS is particularly useful for tumors located near the outer edges of the lungs.
Considerations for Surgery
Assessment of Cardiopulmonary Reserve: Prior to surgery, a thorough assessment of the patient’s cardiopulmonary function is essential to ensure they can tolerate the loss of lung tissue. Tests may include pulmonary function tests, echocardiography, and sometimes cardiopulmonary exercise testing.
Comorbidities: The presence of other medical conditions can impact the choice of surgical procedure and the overall prognosis. Conditions that affect the heart, lungs, or other major organs are particularly important to consider.
Adjuvant Therapy: Depending on the specific stage and histopathological findings, adjuvant chemotherapy or radiation therapy may be recommended after surgery to reduce the risk of recurrence.
Radiation Therapy for Lung Cancer
NSCLC and SCLC
Used as curative, palliative, or adjuvant therapy
Combined with surgery, chemo, targeted therapy
Primary therapy for those who are not surgical
candidates due to co-morbidities
Relief of symptoms: dyspnea, hemoptysis, SVC
syndrome, and pain
Preoperative to reduce tumor mass
Monitor for complications
Stereotactic Body Radiotherapy
(SBRT)
Stereotactic radiosurgery (SRS)
High dose of radiation accurately delivered to
tumor (outside CNS)
Smaller part of healthy lung exposed
Damages tumor DNA
Therapy is given over 1 to 3 days
Option for nonsurgical, early stage lung cancer
Chemotherapy for Lung Cancer
Primary treatment for SCLC
Treatment of nonresectable tumors or adjuvant
to surgery in NSCLC
Variety of drugs and protocols
Typically combination of 2 or more drugs
etoposide, carboplatin, cisplatin, paclitaxel,
vinorelbine, docetaxel, gemcitabine, and pemetrexed
(Alimta)
Targeted Therapy for Lung Cancer
Block tumor growth; less toxic than chemotherapy
Tyrosine kinase inhibitors—block signals for growth
in cancer cells
cetuximab (Erbitux), erlotinib (Tarceva), afatinib
(Gilotrif), gefitinib (Iressa), osimertinib (Tagrisso),
necitumumab (Portrazza)
Kinase inhibitor—inhibits kinase protein responsible
for cancer development and growth
Angiogenesis inhibitor—inhibits growth of new blood
vessels
Immunotherapy for Lung Cancer
Targets PD-1, a protein on T cells that normally
helps keep these cells from attacking other cells
in the body
Nivolumab (Opdivo), atezolizumab (Tecentriq),
pembrolizumab (Keytruda)
Boosts immune response against cancer cells
Shrink tumor cells or slow growth
Can be used in people with squamous cell
NSCLC whose cancer progressed after other
treatments
