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Clubbing Causes

Causes of Clubbing
Clubbing involves an increase in the longitudinal curvature of the nail and nail plate
material. It is clinically characterized by:

Edema
Loss of the normal angle between the nail bed and nail fold.
Thickening of the whole distal part of the finger.
Hypertrophic osteoarthropathy

Radiographically, it presents as symmetrical clubbing of the terminal rufts

(acroosteolysis). There is no resorption of connective tissue.

Nail Bed Depth Ratio

The nail bed depth ratio is defined by the ratio of the digit's depth at the junction
between skin and nail (nail bed) and the depth at the distal interphalangeal joint.
Normally, the depth at the distal interphalangeal joint is more than the depth at the
nail bed. In clubbing, there is a reversal of this ratio, with a phalangeal depth ratio of
## Asthma Therapies

Methylxanthines
Methylxanthines such as aminophylline and theophylline can be administered once
or twice daily.

Administered via inhalation as a nebulizer or dry powder.

Long-acting theophylline preparations are used for maintenance therapy, with a
single daily dose in the evening to control nocturnal asthma.
Dosage varies from patient to patient.
Clearance is increased in smokers.

Beta-2 Adrenoreceptor Agonists

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Salmeterol and formoterol:

Highly selective, potent, long-acting B2-adrenoreceptor agonists.

Routinely used in place of short-acting B2-stimulants.

Theophylline is a medium-potency bronchodilator.

Used for acute attacks.

Inhaled Corticosteroids (ICS)

Inhaled corticosteroids (ICS) are the most effective controllers for asthma.

Examples include:
Beclomethasone dipropionate (200 ug)
Budesonide (200 ug)
Fluticasone (125 ug)
Ciclesonide (80-160 ug once a day)
Flunisolide
Mometasone
Administered twice daily as aerosols or dry powder, except for ciclesonide,
which is given once a day.

Advantages:

Effective in treating asthma of any severity and age.

Reduces the number of courses of oral corticosteroid therapy (OCS).
Can prevent irreversible changes in airway function in chronic asthma.
Effective in preventing asthma symptoms, exercise-induced asthma (EIA), and
nocturnal exacerbations and they also prevent severe exacerbations.

Mechanism of action:

Not bronchodilators, but the most effective anti-inflammatory agents.

Reduce the number of inflammatory cells and their activation in the airways.
Increase bronchial hyper-responsiveness and relieve or prevent airflow
obstruction.
Reverse B2-receptor down regulation produced by long-term use of B2-
agonists.

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Adverse effects:

Dysphonia (husky voice)

Oropharyngeal candidiasis
Minimized by using a spacing device with the metered-dose inhaler and
gargling with water after use.
Relatively free from systemic side effects at conventional doses.
Long-term use may result in osteoporosis, skin thinning, and adrenal
suppression.

Oral Corticosteroids (OCS)

Oral corticosteroids are necessary in patients not controlled by inhaled
corticosteroids.

Use at the lowest dose possible to minimize side effects.

Prednisolone is started as a single morning dose.
Dose is reduced by half every 6 hours.
Methylprednisolone is given at 40-60 mg orally per day.

Parenteral Corticosteroids:

Hydrocortisone: Loading dose of 4 mg/kg intravenously, followed by 2-3 mg/kg

every 6 hours.
Methylprednisolone: 40-125 mg every 6 hours.

Indications for corticosteroids in bronchial asthma:

Acute asthma that does not respond despite bronchodilator therapy.

Severe acute asthma (status asthmaticus).
Worsening asthma.
Patients who require continuing treatment with oral corticosteroids.

Steroid-Sparing Agents
Immunomodulatory treatments can be used in patients with severe asthma who have
serious side effects, in order to reduce the dose of oral steroids needed to control the
disease.

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Methotrexate (15 mg weekly)

Cyclosporine

Anti-IgE Monoclonal Antibodies

Omalizumab neutralizes/chelates free circulating IgE and decreases release of
mediators.

Mechanism:

Prevents the binding of circulating IgE to receptors on mast cells and basophils,
thus inhibiting IgE-mediated reactions.

Leukotriene Modifiers
Leukotriene modifiers are add-on therapies useful in persistent asthma.

Leukotriene receptor antagonists (LTRAs): montelukast, zafirlukast, and

pranlukast.
Montelukast: 10 mg once daily in the evening.
Zafirlukast: 20 mg BID
5-lipoxygenase inhibitors: zileuton
Zileuton may cause liver damage.

Cromones
Cromones are anti-inflammatory drugs for prophylactic use.

Sodium cromoglycate, cromolyn, and nedocromil.

Inhibit the degranulation of mast cells, thereby preventing the release of
mediators.
Useful in children with atopic asthma.

Anticholinergics
Anticholinergics are less effective than B2-agonists in asthma therapy but may be
used as additional bronchodilators.

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Examples:
Ipratropium bromide
Tiotropium

Uses:

Asthma not controlled by inhaled corticosteroids (ICS) and LABA combinations.

Useful during asthma exacerbations but less useful in stable asthma.

Dose:

Ipratropium: Two puffs of 20 ug each, four times/day, or 250-500 ug

nebulization.
Tiotropium: Two puffs of 9 ug each, once a day.

Side Effects:

Dryness of mouth and bitter taste.

General Measures in Asthmatics

Measures to Avoid
Opiates, sedatives, and tranquilizers in acutely ill patients with asthma.
B-blockers and parasympathetic agonists in asthmatics.
Expectorants and mucolytic agents.

Assessment of Asthma Control

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Controlled Partly controlled

Characteristics Uncontrolled asthma
asthma asthma

Any 1 or 2 Any 3 or more

Daytime symptoms more
No characteristics characteristics partly
than twice/week
present controlled asthma
Limitation of activities due to
No
asthma
Nocturnal
symptoms/awakening due to No
asthma
Need for reliever/rescue
medicine more than No
twice/week

Bronchial Thermoplasty
Bronchial thermoplasty is a procedure for severe asthma.

Delivers controlled radiofrequency energy to the airway wall via bronchoscopy.

Results in a prolonged reduction in airway smooth muscle.
Most patients will need to use asthma maintenance medications after the
procedure.

Risks:

Lung collapse
Bleeding
Additional breathing problems

Benefits:

Patient may use rescue inhalers less often.

Able to engage in more physical activity than before.

Severe Asthma Phenotypes

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This chart summarizes asthma severity, management strategies, and treatment

options for various levels of severity. It also illustrates the stepwise management of
chronic asthma, detailing progression from one step to the next based on patient
response to treatment.

Asthma is divided into phenotypes:

Type 2 inflammation
Non-type 2 inflammation

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Phenotypes shown in Flowchart 6.3.

Several factors may influence asthma, including:

Incorrect diagnosis
Incorrect inhaler technique
Poor adherence
Comorbidities

Targeted Therapy

The image above presents a detailed flowchart for managing asthma in adults and
adolescents aged 12 years and above, outlining treatment approaches based on the
severity of symptoms.

Targeted treatment for difficult-to-treat asthma:

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Allergic asthma IgE:

Characterized by Total serum ge

Demonstrated Igt-mediated
Add a anti-gge biologic

Omalizumab OCS in eosinophils:

past year or >300 2150 cells/uLand 2 ora more exacerbations requiring

Add a antii-5biologic

Mepolizumab Reslizumab Bervalizumab Neutrophilic:

OCS in past year cells/at and: 3ar more exacerbations requiring

Add: anti-l--41--11 biclogic

Airways smooth muscle (IASM) hypertrophy Patient tried who does not quallyy
forr other:

Duptiumab neutrophils inp patients who doi not respond tol

Cortioottrolids and dor not hawer other type

Management of Acute Severe Asthma (Status

Asthmaticus)
Term used for an exacerbation of asthma that has not been controlled by the
use of standard medication

Treatment at home:

Give high concentrations of oxygen (40-60%) through a mask, if available

Bronchodilator therapy: Any one of the following should be given,
Salbutamolterbutaline orterbutaline 10 mg every 201 minutes for 3doses 4-81
puffs every: 2-41 hours through metered-dose inhalers four to eight puffs with
a spacer every 201 minutes Corticosteroids: for: 3 doses), followedby

Management in hospital:

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Initial assessment: Take brief history, perform rapid examination of the

concentration of oxygen (40-60%).

Administer

Assess the: severity Table 6.21).

Give high concentrations of oxygen (40-60%) Bronchodilators

Acute Asthma Algorithm

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This medical chart details the assessment and management of asthma. It categorizes
asthma severity into mild, moderate, severe, and respiratory arrest imminent, with
corresponding symptoms and characteristics, and provides a step-by-step guide for
managing acute asthma, including baseline treatment and management strategies
for varying severities.

Exacerbations of Asthma
Assessment of severity of asthma.

Respiratory arrest
Mild Moderate Severe
imminent

Respiratory rate Increased Usually increased Increased Decreased or absent

Use of accessory Often
Usually not Usually present May be absent
muscles present
Wheezing Moderate Loud Loud Absent
Pulse rate 100-120 >120 >120 Bradycardia
Approximately
PaO2 >80% 60-80% <60
90%
Possibly
Mental status Usually agitated Drowsy Confused
agitated

Factors of Exacerbations
Viral infections (most common).
Molds
Pollens
Air pollution.

Treatment
Treatment of mild-to-moderate exacerbation

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Patient is reassessed every hour

Check response to treatment is done bynoting the patient distress, respiratory
rate, FEV, heart rate, presence of pulsus paradox studies. noninvasive
ventilation) using continuous positive pressure of BIPAP machines and tight
fitting face mask reduces the work without intubation.

Respiratory System
Administer nebulized (in be repeated after a few oxygen) salbutamol(5 mg) or
terbutaline (10mg) or levosalbutamol(1.257mu mg) immediately and B,-agonist
minutes, if there is no response. (subcutaneously or moribund. intravenously)
are: indicated in patients with excessive cough, too weak to inspire adequately.
Terbutaline is administered
Epinephrine subcutaneously (0.25-0.5 mg) or intravenously (0.1-10 ug/kg/min).
subcutaneously (adrenaline) may be administered in children and young adults.
Adult dose: is 0.2-0.5 mg as 1:1,000 every 20 minutes) solution.
Add nebulized ipratropium bromide 0.5 mg to
nebulizedsalbutamolsmg/tebbutalin to those within 15-30 minutes. It can be
10mg patients who repeated every 20 minutes for 3 doses. Aminophylline can
be given intravenously to those patients who do not respond to nebulized
bronchodilators. Give a of5 mg/kg/h as aninfusion. with 70-80% helium with
oxygen may be useful, since it reduces airway resistance and improves efficacy.
Cardiac or respiratory arrest, severe hypoxia (Pa0, <60 mmHg).hhpercaapna
(PaCO,> 50 mmHg), acidosi (pH <7:3),exnaastion,, or deterioration in mental
status patients, hydrocortisone sodium succinate 100 mg is administered
intravenously at repeated 4-6 hourly for 24 hours. presentation: and.

Role of Magnesium Sulfate

Either intravenously or by nebulization is not clear.
If no improvement with above measures, perform endotracheal intubation and
mechanical Indications forintubation: NIV breathing failure but require
Treatment bronchodilators
Assessment and serial arterial blood gas (ABG).

Bronchial Thermoplasty

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May be beneficial for moderate-to-severe persistent asthma.

Reduces the constriction in saturation mass of airway loading dose.

COPD and Emphysema Study Guide

Radiological Examination
Chest X-rays can help classify COPD types, but aren't reliable for determining
the severity of airflow limitation.

Emphysema Features:

Presence of bullae
Paucity of parenchymal markings or hyperlucency
Features of hyperinflation
Increased lung volumes
Flattening of the diaphragm

Chronic Bronchitis: No characteristic abnormality.

Crucial to identify complications like cardiac failure and other complications

from smoking like lung cancer.

Pathogenesis of Chronic Obstructive Pulmonary Disease

(COPD)

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The pathogenesis of COPD involves a complex interplay of environmental and host

factors. Cigarette smoking and air pollutants lead to airway inflammation and lung
damage. This damage is exacerbated by genetic predispositions like alpha-1
antitrypsin deficiency, which impairs the lung's ability to repair itself. The image
presents a flowchart illustrating the pathogenesis of complications of chronic
bronchitis. The flowchart, titled "Pathogenesis of complications of chronic bronchitis,"
outlines the consequences of chronic bronchitis, including central chronic bronchitis,
and branches out to various complications such as pulmonary vasoconstriction,
pulmonary hypertension, and cor pulmonale with right ventricular hypertrophy.
These complications can lead to severe outcomes, including respiratory failure,
desaturation of hemoglobin, secondary polycythemia, and eventually death. The
flowchart provides a clear visual representation of the potential consequences of
chronic bronchitis.

Environmental Risk Factors:

Cigarette smoke
Air pollutants (including those from industrial sources)
Respiratory tract infections

Host Factors:

Genetic factors, such as alpha-1-antitrypsin deficiency

Airway Inflammation: Leads to chronic inflammation and narrowing of the

airways.

Lung Damage: Oxidative stress and proteinases overwhelm repair

mechanisms, causing chronic obstructive pulmonary disease (COPD).

History and Symptoms of COPD

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Most Common Symptoms:

Sputum production
History of cough
Exertional dyspnea (breathlessness)

Cough:

Initially, occurs mainly in winter ("smoker's cough")

Later, increases in frequency, severity, and duration, especially in the
mornings

Sputum:

Usually in the mornings

May be purulent (mucopurulent relapse) or blood-stained (hemoptysis)

Breathlessness:

Insidious onset, aggravated by airflow obstruction, smoking, and infection

Severity assessed by the modified MRC dyspnea scale

Other Symptoms:

Fever during mucopurulent relapses

Wheezing
Chest tightness

Clinical Features and Comorbidities of COPD 🫁

Associated Comorbidities:

Muscle dysfunction
Osteoporosis
Lung cancer
Sleep disorders
Peptic ulcer
Glaucoma

Assessment of COPD

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Spirometry:

Reduced FEV1/FVC ratio

FEV1 to detect the severity of the defect

CT (HRCT): Useful for detection and characterization of diffuse emphysema.

BODE Index: A multidimensional prognostic index that accounts for:

Body mass index (BMI)

Obstruction (FEV1 percent predicted)
Dyspnea (Medical Research Council dyspnea scale)
Exercise capacity (6-minute walk test)

A BODE score greater than 7 is associated with a 80% 2-year

mortality, a score of 0-2 with 15%, and less than 5, less than 10%.

Arterial Blood Gases (ABG) Study: Demonstrates hypoxemia in patients with

exacerbation.

Measurement of Lung Volumes: Assesses hyperinflation.

Exercise Testing: Six-minute walk test assesses exercise tolerance and

response to pulmonary rehabilitation.

Blood Tests: Hemoglobin level and PCV may be elevated due to persistent
hypoxemia (secondary polycythemia).

Complications of COPD

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Macropurulent Relapse:

Develops due to infections by bacteria such as Streptococcus pneumoniae,

Haemophilus influenzae, or Moraxella catarrhalis.
Presents with fever and increased production of purulent sputum.

Carbon Dioxide Narcosis:

Persistent retention of CO2 (hypercapnia)

Manifests as altered behavior, drowsiness, headache, and papilledema.

Respiratory Failure:

Type I (low PaO2, normal PaCO2): Mild-to-moderate COPD

Type II (low PaO2, high PaCO2): Acute or chronic in severe COPD

Other Complications:

Secondary polycythemia
Pulmonary hypertension and right ventricular failure (cor pulmonale)
Pneumonia
Tuberculosis
Lung cancer
Pneumothorax
Deep vein thrombosis
Pulmonary embolism

Drug Therapy for COPD

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Used for short-term management of exacerbations and long-term relief of

symptoms.

None of the medications reduce the rate of decline of lung function.

General Measures:

Reduce exposure to smoke.

Avoid dusty and smoke-laden atmospheres.

Bronchodilators:

-adrenergic agonists:
Short-acting (e.g., salbutamol, terbutaline)
Long-acting (e.g., salmeterol, formoterol, indacaterol)
Antimuscarinic (anticholinergic) drugs:
Short-acting (e.g. ipratropium bromide)
Long-acting (e.g., tiotropium bromide, umeclidinium)
Oral theophylline or doxophylline

Phosphodiesterase Type 4 Inhibitors: Roflumilast can be used as an adjunct

therapy.

Inhaled Corticosteroids (ICS): May reduce the frequency and severity of

exacerbations in moderately severe COPD

Additional Treatments and Therapies

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Smoking Cessation: Aided by bupropion, nicotine replacement therapy, or

varenicline.

Pulmonary Rehabilitation: Individually designed program consisting of

education and cardiovascular conditioning.

Long-Term Oxygen Therapy (LTOT): Increases PaO2 and SaO2.

Indications:
PaO2 ≤ 55 mm Hg at rest
PaO2 between 56 and 59 mm Hg with secondary polycythemia.
Benefits:
Reduces mortality rates
Decreases pulmonary hypertension

Prevention of Infection: Vaccinations against pneumococcal and influenza

viruses.

GOLD Assessment and Therapy

ABCD assessment tool for COPD:
Assess airflow limitation (FEV1).
Assess symptoms and exacerbation risk.

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The GOLD (Global Initiative for Chronic Obstructive Lung Disease) assessment tool is
used to classify COPD severity and guide treatment decisions based on FEV1 (Forced
Expiratory Volume in 1 second), symptoms, and exacerbation risk. The image is a
detailed flowchart illustrating the impact of environmental and genetic factors on the
respiratory system, specifically the effects of cigarette smoke. The chart outlines how
exposure to toxic substances in cigarette smoke, such as those found in tobacco
smoke, fuels, and more, triggers an inflammatory reaction involving macrophage,
lymphocytes, and neutrophil activation. This reaction leads to the production of
cytokines, reactive oxygen species (ROS), and degradation of the extracellular matrix
(ECM), ultimately causing damage to alveolar cells through apoptosis and necrosis.
The flowchart also highlights genetic factors, including alpha-1 antiprotease
deficiency, polymorphisms of TGF-β receptor, and polymorphism of MMPs, which
increase susceptibility to oxidative stress and damage to epithelial cells. Overall, the
image provides a comprehensive visual representation of the complex interplay
between environmental and genetic factors that contribute to respiratory system
damage.

Classification of Emphysema
Emphysema is a lung disease characterized by the abnormal, irreversible
enlargement of airspaces distal to the terminal bronchiole, accompanied
by the destruction of their walls.

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Centriacinar (Centrilobular) Emphysema:

Dilatation of the central or proximal parts of the acini

Common and severe in the upper lobes
Associated with heavy smokers and coal worker's pneumoconiosis

Panacinar (Panlobular) Emphysema:

Involves uniform dilatation of the airspaces

More common in the lower lobes
Associated with α1-antitrypsin deficiency

Paraseptal (Distal Acinar) Emphysema:

Dilatation at the periphery of the lobule

Found near the pleura
May cause spontaneous pneumothorax

Irregular (Scar/Cicatricial) Emphysema:

Irregularly involved
Associated with areas of fibrosis or scarring
Often asymptomatic

Etiology and Pathogenesis of Emphysema

The major event in emphysema is the destruction of the alveolar wall.

Mechanisms that Check Destruction:

Anti-elastases (e.g., α1-antitrypsin)

Antioxidants

Imbalance Leading to Destruction:

Protease-antiprotease imbalance (e.g., α1-antitrypsin deficiency)

Imbalance between oxidants and antioxidants

Genetic Factors: Influence susceptibility to emphysema.

Clinical Features of Emphysema

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Manifestations: Appear late, after significant lung damage.

Dyspnea: The most striking feature, progressing to breathlessness even at rest.
Cough: Expectoration of scanty mucoid sputum.
Other Symptoms: Weight loss, weakness, anorexia, and lethargy in advanced
disease.

Alpha-1-Antitrypsin Deficiency
α1-antitrypsin is a major inhibitor of proteases, particularly elastase, and
prevents proteolytic digestion of lung tissue.

Inherited as an autosomal recessive trait.

Deficiency results in proteolytic destruction of the lung, leading to severe
panacinar emphysema.

Physical Findings in Emphysema

General: Asthenic body build, short and thick neck, patient leaning forward.
Inspection: Distressed appearance, tachypnea, hypertrophy of accessory
muscles.
Chest: Cylindrical or barrel-like shape.
Percussion: Hyper-resonant sound over the lungs.
Auscultation: Diminished intensity of breath sounds, prolonged expiration.

Radiographic Findings in Emphysema

Chest X-ray: Low-set diaphragm, tubular heart, loss of peripheral vascular
markings, bullae.

Pulmonary Function Tests in Emphysema

Reduced FEV1, FVC, and FEV1/FVC ratio.
Increased TLC, RV, and RV/TLC ratio.
Reduced diffusing capacity for carbon monoxide.

Pulmonary Bullae

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Bullae are thin-walled air spaces produced due to the rupture of alveolar
walls.

May be single or multiple, small or large.

Located in the subpleural region along the borders of the lungs.
Complications include spontaneous pneumothorax and respiratory failure.

Blue Bloaters vs. Pink Puffers

Blue Bloaters:

Marked cyanosis and peripheral edema.

Associated with chronic bronchitis.

Pink Puffers:

Predominantly emphysema.

Cigarette Smoke Components and Diseases

Cigarette smoke contains gaseous and particulate compounds.
Consists of mainstream and sidestream smoke.
Diseases caused by smoking include COPD, lung cancer, cardiovascular
diseases, and various other respiratory and systemic conditions.

Differentiating Asthma and COPD

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Characteristics Bronchial Asthma COPD

Usually children and young

Age of onset Usually older individuals
adults
Family history of allergy, Smoking, atmospheric pollution, α1-
Risk factors
exposure to allergens antitrypsin deficiency
Wheezing, cough, and Chronic dyspnea and productive
Main symptoms
dyspnea cough
Nature of Vary from time to time and
Continuous symptoms
symptoms even over hours and days
Exercise, dust, or exposure to
Triggers Unrelated to triggers
allergens
Symptoms improve
Recovery of
spontaneously or with Slowly progressive despite therapy
symptoms
treatment
Often present (cardiovascular
Comorbidities Generally absent diseases, metabolic syndrome,
depression, osteoporosis)
Chest X-ray Normal Hyperinflation
Reversibility of airway
FEV1/FVC < 0.7 and persistent
Spirometry obstruction and normal
airflow limitation
between symptoms

Tuberculosis (TB)
Caused by Mycobacterium tuberculosis.

Transmission of TB
Inhalation of respiratory droplets from an active case of tuberculosis.

Epidemiology of TB
Common in countries like India and in parts of Africa.

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Determinants of Virulence in TB
Mycobacterium tuberculosis complex collectively causes TB.

Acid-Fast Bacilli (AFB)

Acid-fast bacilli are bacteria that resist decolorization by acid-alcohol after
being stained.

Mycobacterium tuberculosis is an acid-fast bacillus due to its high lipid content

in the cell wall.

NRAMP1 Gene and TB Resistance

NRAMP1 gene determines susceptibility to tuberculosis.

Sites of Infection
Primary focus always involves the small intestine.
Lung lesion (Ghon focus) is the hallmark of healing, with fibrosis.

Tuberculosis Study Guide

Primary Tuberculosis
Primary tuberculosis occurs upon initial exposure to Mycobacterium tuberculosis in
an unsensitized individual. The infection typically occurs during childhood.

Source: Usually from the lungs (exogenous), rarely from the tonsils, skin, or
intestines.
Inhalation: Tubercle bacilli are inhaled and deposited in the distal airspaces of
the lung, forming a small lesion.
Location: Commonly in the lower part of the upper lobe or upper part of the
lower lobe near the pleural surface.

Within 2-4 weeks post-infection, a gray-white area about 1-2 cm develops, known
as the Ghon focus, which undergoes caseous necrosis.

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Ghon Complex
The Ghon complex is the combination of the Ghon focus and regional lymph node
involvement. In most cases (about 95%), cell-mediated immunity controls the
infection, leading to healing via fibrosis and calcification.

Spread of Infection
In the initial weeks, spread can occur via lymphatic and hematogenous routes. In
some patients, the primary lesion can progress to progressive pulmonary
tuberculosis.

Bronchial Spread: Tuberculous lymph nodes may rupture into the bronchial
lumen, spreading the infection to other lobes or segments.

Hematogenous Spread:

Acute Form: More likely in infants, resulting in miliary tuberculosis or

tuberculous meningitis. Lesions may develop in the lungs, bones, joints,
liver, and kidneys.
Chronic Form: Secondary foci may remain dormant for months or years
after the primary infection.

Other Forms of Primary Tuberculosis

Can occur in the oropharyngeal and intestinal regions, especially the ileal area,
associated with mesenteric lymphadenitis, potentially from ingesting non-
pasteurized milk from infected cows.

Post-Primary (Secondary) Tuberculosis

Most patients do not show abnormal physical signs. If the lesion is severe, general
debility signs may be present.

Definition: Tuberculosis that develops in a previously sensitized individual. This

may occur shortly or many years after initial exposure.

Diagnosis

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Sputum examination for AFB is preferable, or laryngeal swabs/fasting gastric

washings.

Clinical Features of Primary Pulmonary Tuberculosis

Most patients are asymptomatic.
Some may have a self-limiting febrile illness lasting 7-14 days.
Progressive infection leads to reduced appetite and failure to gain weight.
Slight dry cough.
May be associated with fever or polyarthralgia.
Children: Enlargement of hilar lymph nodes is more prominent than the
pulmonary component.
Adults: Pulmonary component is more obvious.

Complications
Enlarged mediastinal lymph nodes may compress a bronchus, leading to middle
lobe collapse (middle lobe syndrome or Brock's syndrome).
Obstructive emphysema.
Broncholith: Calcification in a Ghon focus or node may be extruded into a
bronchus, potentially causing hemoptysis.

Source of Infection
Endogenous: Reactivation of a latent infection is the most common source.
Direct progression of a primary tuberculous lesion.

Physical Exam Findings

General: May reveal weakness or wasting in advanced cases
Respiratory System: Usually no abnormal signs unless there are complications;
crepitations may be heard.
Erythema nodosum may accompany primary pulmonary tuberculosis.

Clinical Features of Secondary Tuberculosis

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May remain asymptomatic.

Onset is usually insidious with symptoms developing slowly over weeks or
months.
Nonspecific symptoms: Malaise, low-grade fever (especially in the evenings),
anorexia, weight loss, and tiredness.
Respiratory symptoms: Chronic cough (most consistent), sputum (mucoid,
purulent, or blood-stained), chest pain (pleuritic or muscular).
Breathlessness in advanced cases or due to pleural effusion.
Localized wheeze due to local ulceration and narrowing of a major bronchus.

Spread Through the Body

Direct Spread: Along mucosal linings.
Lymphatic Spread: Along mucosal linings, regional lymph node involvement,
miliary disease.
Systemic Blood Vessels: Disseminated form (miliary tuberculosis).

Miliary Tuberculosis
Occurs when tubercle bacilli disseminate through the systemic arterial system,
frequently affecting the lungs.
Isolated organ tuberculosis can involve any organ, including the liver, bone marrow,
spleen, adrenals, meninges, and kidneys.

Radiological Findings of Pulmonary Tuberculosis

Ill-defined opacification in the upper lobes.
Features of consolidation, collapse, and cavitation.
Hilar and mediastinal shadows due to enlarged lymph nodes.
Diffuse small nodular shadows (miliary tuberculosis).

Common Radiological Manifestations

Parchely or nodular shadows in the upper zone on one or both sides Cavitation
(especially if more than one) Cavitation in the upper zone on one or both sides
Calafiedi lesion Pleurale effusion/thickeninng

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Antituberculous Drugs

Bactericidal vs. Bacteriostatic

Bactericidal: Kills bacteria.
Bacteriostatic: Inhibits bacterial growth.

Rifamycins

Rifapentine
Features: Lipophilic, longer duration of action.
Use: Pulmonary tuberculosis treatment (alternative to rifampicin).
Dose: 600 mg once or twice weekly.
Side Effects: Similar to rifampicin.
MOA: Inhibits arabinosyltransferase involved in arabinogalactan synthesis.
Excretion: Urine (dose reduction needed for creatinine clearance <50 mL/min).

Rifabutin
Related to rifampin.
Active against rifampicin-resistant M. tuberculosis.
More active than rifampin against Mycobacterium avium intracellulare
complex/NTM.
Dose: 150 mg daily.
Extent of absorption unchanged by food.
Adverse Effects: Similar to rifampin; recommended for HIV-infected patients on
protease inhibitors.

Ethambutol

Mechanism of Action

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Inhibits arabinosyl transferases, disrupting arabinogalactan synthesis.

Bacteriostatic.

Adverse Effects
Retrobulbar neuritis: Dose-dependent, reduced visual acuity, central scotoma,
red-green color discrimination issues; may lead to blindness if not discontinued.
Ototoxicity: Cochlear and vestibular damage, deafness.
Renal damage: Nephrotoxicity (nonoliguric renal failure); reduce dosage if
urinary output falls, albuminuria occurs, or tubular casts are detected.
Other: Hyperuricemia, peripheral sensory neuropathy.

Pyrazinamide
Effective in acidic pH (<6.0).
Bactericidal.
Inhibits mycolic acid synthesis.
Effective against slowly metabolizing bacilli in phagosomes.

Adverse Effects
Hepatotoxicity.
Hyperuricemia and arthralgias (especially shoulders).

Streptomycin
Aminoglycoside, bactericidal.
Derived from Streptomyces griseus.

Adverse Effects
Ototoxicity.
Renal damage.
Rare: Hemolytic anemia, aplastic anemia, agranulocytosis, thrombocytopenia.

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Short-Course Chemotherapy (SCC)

Regimens of 6-9 months duration.
Two phases:
Initial intensive phase: 2-3 months, rapidly kills majority of mycobacteria.
Continuation phase: 4-6 months, eliminates remaining bacilli.

Goals
1. Kill dividing bacilli.
2. Kill persisting bacilli.
3. Prevent emergence of resistance.

Treatment Regimens for Tuberculosis

Regimen Duration

A. DOTS (Directly observed treatment, short course)

For new TB cases: 2 months (HRZE) + 4 months (HRE) 6 months
B. DOTS PLUS
1. MDR TB: 6-9 months + 18 months 24-27 months
2. XDR TB: 6-12 months intensive + 18 months continuation 24-30 months

Monitoring Treatment
Serial sputum smear examinations: Assess progress.
Bacteriological assessment: Sputum smear microscopy and culture.
Radiological assessment: Chest radiographs.
ESR and body weight changes.

Drug-Resistant TB
Multidrug-resistant tuberculosis (MDR-TB): Resistance to at least
isoniazid (INH) and rifampicin.

Extensively drug-resistance TB (XDR-TB): Resistant to isoniazid,

rifampicin, fluoroquinolones, and at least one injectable aminoglycoside.

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Chronic cases and MDR-TB cases are not synonymous.

Causes
Inadequate treatment.
Drug-resistant organisms.
Non-compliance.

Forms of Drug Resistance

Initial drug resistance: Develops in patients who have not received prior
antituberculous chemotherapy.
Secondary or acquired drug resistance: Due to inadequate chemotherapy.
Mono-resistance (MR): Resistance to one first-line anti-TB drug only.
Polyresistance (PDR): Resistance to more than one first-line anti-TB drug
(other than both INH and rifampicin).
Rifampicin resistance (RR): Resistance to rifampicin.

Drug Susceptibility Testing (DST)

Methods:
Culture-based (e.g., on L-J medium): Takes 6-8 weeks.
Radiometric methods (e.g., BACTEC): Results within 10 days.
Molecular assays: Detect drug resistance.

Factors Contributing to Drug Resistance

Lack of good lab monitoring.
Drug shortages.
Poor quality drugs.
Inadequate treatment.

Principles for Managing MDR Tuberculosis

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Use at least 4 reliable drugs.

Avoid cross-resistance.
Monitor and manage side effects.
Never add a single drug to a failing regimen.
Provide 18-24 months' treatment with DOT therapy.

Extrapulmonary Tuberculosis (EPTB)

Tuberculosis occurring at body sites other than the lung.

Indications for Corticosteroids

Severe illness.
Severe hypersensitivity reactions to anti-TB drugs.
To prevent exudation and stricture formation.

Miliary Tuberculosis 🪨
Miliary tuberculosis results from widespread hematogenous
dissemination.

Clinically, miliary TB patients may be divided into three types:

1. Classical (acute) miliary tuberculosis

2. Cryptic (obscure) miliary tuberculosis, and
3. Nonreactive

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The image shows

the characteristic miliary shadows, called miliary mottling, in a chest X-ray. They are
small, diffuse shadows of 1-2 mm in diameter, evenly distributed throughout both
lung fields.

Types
Classical (acute) miliary tuberculosis:
More common in children and young adults.
Sudden or gradual onset.
High-grade fever, night sweats.
Cryptic (obscure) miliary tuberculosis:
Prolonged low-grade fever.
Lassitude, weight loss.
Chest X-ray usually normal.
Nonreactive miliary tuberculosis:
Usually in elderly patients.
Rare form of tuberculosis.

Bronchiectasis 🫁
Bronchiectasis is defined as an irreversible (permanent) dilatation or
destruction of the bronchial tree.

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Morphological Types
Tubular (cylindrical): Smooth dilation of the bronchi.
Varicose (bulbous): Dilated bronchi with multiple indentations.
Cystic (saccular/balloon appearance): Dilated bronchi terminate in blind-
ending sacs.

Etiology
Congenital/acquired.
Post-inflammatory.
Associated with cystic fibrosis.

Bronchiectasis

Clinical Features

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Severe persistent (chronic) productive cough:

Most common symptom.
Paroxysm of cough: Develops when the patient rises in the morning due
to postural changes draining pus and secretions into the bronchi.
Sputum:
Production varies with posture.
Characteristics: Foul-smelling (due to anaerobic infections), thick, copious,
tenacious, and continuously purulent, sometimes bloody.
Hemoptysis:
Breaks of blood are common with exacerbations of infection and are
commonly recurrent.
Rarely, hemoptysis occurs.
Cause: Rupture of thin-walled blood vessels on the walls of dilated
bronchi.
Pleuritic chest pain:
May be caused by infection of the pleura or segmental collapse caused by
retained secretions.
Infection exacerbation:
Increased sputum volume with fever, malaise, and anorexia precipitated
by upper respiratory tract infections.
General debility:
In severe/widespread bronchiectasis, the patient presents with difficulty
maintaining weight, anorexia, exertional breathlessness/dyspnea,
wheezing, and orthopnea.
Bronchiectasis sicca/dry bronchiectasis:
Occasionally, the patient is asymptomatic or has a nonproductive cough.
Commonly follows TB of the upper lobe.
Only manifestation will be hemoptysis.
Situs inversus: Found in 50% of cases of ciliary dyskinesia.

Associated Syndromes and Conditions:

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Brock's syndrome/middle lobe syndrome

ABPA
TB
Foreign body
Lady Windermere syndrome (LWS)
Voluntarily suppressing cough results in inability to clear secretions from
the middle lobe and lingula, leading to infection.
Congenital syndromes: yellow nails
Kartagener's syndrome
Young's syndrome
Chandra Khetarpal
Levocardia (immunodeficiency associated with bronchiectasis and paranasal
sinus anomalies)
Chediak-Higashi syndrome
Cystic fibrosis

Other Associations:

Pulmonary Suppurative pneumonia

Allergic bronchopulmonary aspergillosis (ABPA) complicating asthma
Post-obstructive bronchiectasis: Partial or total obstruction of the lumen
Examples: endobronchial tumors, foreign bodies, enlarged hilar lymph
nodes, tumor masses, bronchostenosis following endobronchial
tuberculosis
Autoimmune diseases: Rheumatoid arthritis, Sjogren's syndrome, systemic
lupus erythematosus, inflammatory bowel disease
Repeated aspiration of gastric juice
Inhalation of toxic gas (ammonia)
HIV infection
Interstitial lung fibrosis
Traction
Radiation fibrosis
Sarcoidosis
Chronic hypersensitivity pneumonitis
Bronchiolitis obliterans after lung transplantation
Collections
Persisting secretions cause mechanical obstruction and obstruction impairs
clearing mechanisms of the lung + resultsi in secretions distal to the
obstruction. leads to secondary infection
inflammation weakens and dilates airways.

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Pathogenesis Theories
Pressure of Secretion (Obstruction):

Obstruction of the airway leads to bronchiectasis.

Infection Theory:

Chronic persistent (recurrent) inflammation in the

bronchi/bronchioles weakens and dilates airway walls.

Traction Theory:

Traction of the bronchi walls due to fibrosis/scarring leads to

bronchial dilatation.

Physical Findings
Early Stages: May be normal.
Chronic:
Anemia
Raised ESR and leukocytosis indicating suppuration.
Respiratory alkalosis or hypoxemia.
Wheezing.
Bilateral, coarse leathery crepitations.

Sputum Examination
Collection: Collect in conical flask and allow to stand.
Layers: Forms three layers ("three-layered sputum").
Top: Mucoid layer.
Middle: Mucopurulent layer.
Bottom: Purulent layer.
Analysis:
Gram's stain.
Ziehl-Neelsen stain for acid-fast bacilli.
Culture and sensitivity (usually grows organisms in the nasopharyngeal
flora or Pseudomonas).

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Chest X-Ray (CXR)

Lacks sensitivity.
Signs:
Parallel linear densities ("tram-track opacities").
Ring shadows reflecting thickened and abnormally dilated bronchial
walls.

High-Resolution Computed Tomography (HRCT)

More specific and sensitive.
The imaging modality of choice for confirmation of bronchiectasis.
Specific criteria:
Thickened, dilated airways.
Parallel track sign or "tram track sign".
"Signet ring sign" (internal diameter of the bronchus is at least 1.5 times
more than that of the nearby vessel).
Absence of bronchial tapering in the periphery of the chest (presence of
tubular structures within 1 cm from the pleural surface).
Inspissated secretions.
Tree-in-bud pattern.

Pulmonary Function Tests

May detect mild to moderate airflow obstruction.
A restrictive pattern evolves with advanced disease.

Serum Immunoglobulins
Up to 10% of adults with bronchiectasis have antibody or subclass deficiency
(mainly IgA).
Useful when immunodeficiency is suspected.
About 30% have raised IgE.

Other Investigations

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Mucociliary clearance (saccharin):

Measures the time taken for a small pellet of saccharin placed in the
anterior chamber of the nose to reach the pharynx, where the patient can
taste it.
Prolongation of this time (>20 minutes) is found in patients with ciliary
dysfunction.
Bronchoscopy:
Identify the source of bleeding with hemoptysis.
Therapeutically to remove secretions.
Bronchography: Rarely indicated in advanced disease.
Urine examination: In advanced and chronic cases, proteinuria may develop due
to renal amyloidosis.
Echocardiogram: Usually normal, but right ventricular hypertrophy may be
detected when cor pulmonale develops.
Sweat electrolytes: Measurement of sodium and chloride concentrations in
sweat is useful in cystic fibrosis
Alpha-1 antitrypsin estimation is also done for primary
hypogammaglobulinemia.
Assessment of ciliary function:
Measurement of ciliary beat frequency: Assessed by using biopsies taken
from the nose.
Electron microscopy: It can detect structural abnormalities of cilia.
Sinus X-rays: For patients with rhinosinusitis. Does not establish the diagnosis.

Management

Goals of Treatment
Improvements in secretion.
Bronchial clearance.
Bronchial hygiene.

Bronchial Hygiene Methods

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Reduce the microbial load within the airways and minimize the risk of repeated
infections.
Techniques:
Chest physiotherapy (e.g., postural drainage, chest percussion).
Aerosolization of bronchodilators.
Hyperosmolar agents (e.g., hypertonic saline).
Postural drainage:
Patients must be trained by physiotherapists.
Performed at least three times daily for 5-10 minutes.
Involves adopting a position in which the affected lobe(s) to be drained
are uppermost.
Gentle mechanical chest percussion through hand clapping to the thorax
down is effective in most patients.
Bronchoscopic removal of inspissated secretions: Rarely necessary.

Antibiotic Therapy
Eradication of bacteria:
Suppress antibiotics: Daily for resolution of an acute infection in patients with
recurrences, the use of suppressive antibiotics may. minimize the microbial
Choice of antibiotic: Depends on the results of culture and sensitivity of
sputum.
If no specific pathogen is identified and the patient is not seriously ill, oral
agents like amoxicillin, ampicillin, cotrimoxazole, or tetracycline are
recommended.
More seriously ill patients with pneumonitis require parenteral antibiotics.
Duration of therapy:
Usually a 7- to 10-day course is sufficient.
Few patients may need prolonged therapy for several weeks.
Usually antibiotics used are amoxicillin, ampicillin, cotrimoxazole, or
tetracycline.
Inhaled antibiotics are safe and effective, e.g, tobramycin, gentamicin

Anti-inflammatory Therapy
Control of the inflammatory load in bronchiectasis.
Macrolide antibiotics have immunomodulatory action.
Inhaled corticosteroids may be useful in some patients.

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Other treatments
Bronchodilators (B-adrenoreceptor agonists, anticholinergics) improve
obstruction and help in clearance of secretion.

Surgical Treatment
Considered only in refractory cases.
Procedure: Excision of bronchiectatic areas.
Usually done in cases where the bronchiectasis is restricted to a single lobe or
segment.
Indications:
Children or young adults with localized lesions who fail to respond to
medical treatment.
Recurrent hemoptysis.
Recurrent localized pneumonias.
Reversal of airflow obstruction

Treatment of Hemoptysis
Bed rest and antibiotics.
Blood transfusion if necessary.
Bronchoscopy needed to detect the source of bleeding.
If hemoptysis continues, embolization of the bronchial artery is the treatment of
choice.

Lung Transplantation
Considered in patients with advanced disease and respiratory failure.

Management of Complications
Address each complication individually (e.g., antibiotics for infections).

Acute Lung Abscess

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Clinical Features
May present as acute (symptoms <1 month) or chronic (symptoms >1 month).
Acute presentation:
Dry cough
High-grade fever
Chills and rigors
After a few days, the abscess ruptures into a patent bronchus, leading to
expectoration of large amounts of foul-smelling purulent or sanguineous
sputum.
Sputum may often be blood-tinged
Expectoration varies with postures
General examination:
Anemia
Fever
Clubbing of the fingers and toes (may develop rapidly)
Halitosis
Oronasal fistulae
Signs of consolidation:
Dullness of percussion
Increased vocal fremitus and vocal resonance
Bronchial breathing
Crepitations
Pleural rub
Signs of cavitation:
Cavernous or amphoric breathing
Coarse post-tussive crepitations on auscultation

Pathogenesis

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Primary lung abscess:

About 80% of lung abscesses are primary (50% of these are aspiration
abscesses).
Predominant organisms are usually the mixed anaerobes found in the
oropharynx or nasopharynx
Infected material is bacteria aspirated

Secondary lung abscess:

Develops as a complication of several conditions.

Aspiration Abscesses:

Site and number:

Abscess cavities occur in those bronchopulmonary segments that
are most dependent at the time of aspiration.
Aspiration in the supine position produces abscess in the posterior
segment of the upper lobes or superior segment of the lower lobes
(bilateral).
Aspiration in the upright position produces abscess in the basilar
segments.
Amebic lung abscess typically occurs in the right lower lobe due to direct
extension of liver abscess through the diaphragm.
One-third of patients develop empyema (direct extension).
Depression of cough reflex favors aspiration from infected nasal sinuses
or gingivitis/periodontitis.

Causes of secondary lung abscess:

Pneumonia and necrotizing pneumonia.

Pulmonary TB.
Septic embolism: Important. The source of the embolus may be from
thrombophlebitis in any part of the systemic venous system or from vegetations
of infective bacterial endocarditis on the right side of the heart.
Bronchial obstruction by a bronchial cancer or foreign body.
Miscellaneous: Gastroesophageal reflux disease (chemical pneumonitis-
Mendelson's syndrome).
Primary cryptogenic lung abscesses: malignancy, pulmonary infarct.

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Investigations
Blood:
Normocytic anemia and/or raised inflammatory markers (ESR/CRP).
Leukocytosis.
Sputum:
Gram stain
Ziehl-Neelsen staining for acid-fast bacilli
Culture and sensitivity for aerobic and anaerobic organisms
Cytological examination for malignant cells.
Chest radiograph (Fig. 6.32):
Reveals a radiolucency in an opaque area of consolidation.
The wall of the abscess cavity completely surrounds the radiolucent area.
An air-fluid level may be seen in the abscess cavity.
CT scan of thorax: Shows lung abscess.
Bronchoscopy: Indicated:
To exclude malignancy.
To obtain specimens for studies.
For removal of secretions.

Treatment

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Postural drainage and chest physiotherapy.

Antibiotic therapy:
Choice of drug depends on culture and sensitivity result.
Antibiotic treatment should be continued until there is either the
resolution of the lung abscess or the presence of a small stable lesion.
Aspiration Abscess:
Antibiotic therapy is similar to that of aspiration pneumonia.
Oral treatment:
The majority respond to oral treatment with ampicillin 500 mg four
times daily or cotrimoxazole 960 mg twice daily or clindamycin 300
mg thrice daily.
For anaerobic bacterial infection, patients with foul-smelling
sputum/oral metronidazole 400 mg 8 hourly should be combined
with the above oral treatment.
It should not be used alone.
Parenteral antibiotic therapy:
Required in seriously ill patients and consists of a beta-lactamase
inhibitor (e.g., ampicillin subactam) with clindamycin and
metronidazole or carbapenem (e.g., imipenem, meropenem)
intravenously every 6 hours.
Large lung abscess: Aspiration and placement of pigtail catheters may be
useful
Resectional surgery: Indicated in few cases. These include:
Massive hemoptysis.
Lung abscess associated with symptomatic bronchiectasis.
Lung abscess associated with localized malignancy.
Persistent lung abscess cavity with a large surgical cavities >8 cm.

Pleural Effusion

Definition
Excessive accumulation of serous fluid in the pleural cavity/space
(between parietal and visceral pleura).

Types of Effusion

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Empyema: Accumulation of purulent fluid (frank pus) within the pleural

cavity/space.
Hydrothorax: Passive transudation of fluid into the pleural cavity.
Hemothorax: Accumulation of blood within the pleural cavity/space.
Chylothorax: Accumulation of chyle within the cavity/space.

Composition of Pleural Fluid

Feature Normal Value

Volume 0.1-0.2 ml/kg

Cells 1,000-5,000/mm³
Mesothelial cells 3-70%
Monocytes 10-70%
Lymphocytes 2-30%
Granulocytes <10%
Eosinophils 0%
Protein 1-2 g/dl
Albumin 50-70%
Glucose ≈ plasma level
Lactate dehydrogenase (LDH) <50% plasma level

Classification and Causes

Types of
Causes
Effusion

Cardiac failure, Hypoproteinemia (e.g., nephrotic syndrome, cirrhosis

of liver, severe malnutrition), Constrictive pericarditis, Hypothyroidism,
Transudative
Meigs syndrome (benign ovarian tumors with ascites), Peritoneal
dialysis
Tuberculosis, Bacterial pneumonia, Malignancy, Pulmonary infarction,
Autoimmune diseases (e.g., rheumatoid arthritis, systemic lupus
Exudative
erythematosus), Acute pancreatitis, Postmyocardial infarction
syndrome

Mechanism

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Increased hydrostatic pressure

Decreased oncotic pressure
Decrease in pleural pressure
Increased permeability of microcirculation
Impaired lymphatic drainage from the pleural space
Movement of fluid from abdomen to pleural space

Clinical Features
Symptoms depend on the size and rate of accumulation of fluid.
Pleuritic chest pain (sharp pain on inspiration and coughing).
Breathlessness (dyspnea).
Inspection:
Tachypnea
Reduced chest movements on the affected side
Bulging of the intercostal spaces
Palpation:
Shift of trachea to the opposite side
Reduced vocal fremitus
Measurements: Diminished chest expansion, increase in the size of the
affected hemithorax, and an increase in spinoscapular distance.
Percussion:
Stony dullness over the fluid.
Upper level of the dullness is highest laterally in the axilla and is lower
anteriorly and posteriorly (Ellis S-shaped curve).
Small effusions may be detected as obliteration of Traube's space on
percussion.
Auscultation:
Breath sounds are markedly diminished or absent over the fluid.
Vocal resonance is markedly diminished over the fluid.
Occasional findings: Egophony and enhanced breath sounds can often be
appreciated at the superior border of the effusion because of underlying
atelectatic lung tissue.
Grocco's sign (Grocco's triangle; paravertebral triangle of dullness): It is a
triangular area of paravertebral dullness on the side opposite a pleural
effusion.

Causes of pleural effusion without tracheal/mediastinal shift:

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Underlying lung disease

Bilateral effusion
Loculated effusion
Effusion with fixed mediastinum (collapse/fibrosis)

Radiological Investigations
Chest X-Ray (CXR):
Significant pleural fluid >10 mm wide on lateral decubitus views.
Upright chest radiograph requires 175 mL to obscure the lateral
costophrenic sulcus, 500 mL of fluid will obscure the diaphragmatic
contour, and 1,000 ml of effusion reaches the level of the 4th anterior rib.
Decubitus radiographs and CT scans: Can identify effusions as little as 10ml .

Causes of Left-Sided Pleural Effusion

Pancreatitis
Pericardial inflammation
Rupture of the esophagus
Left-sided sub-diaphragmatic abscess
Thoracic duct involvement above D.I.

Pneumothorax

Definition
Presence of air/gas in the pleural cavity/space.

Classification

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Spontaneous
Primary (simple)
Secondary
Traumatic
Open
Closed
Tension
Iatrogenic
Non-iatrogenic

Etiology
Primary (Simple) Pneumothorax: Occurs in the absence of overt lung disease.
Commonly occurs between the ages of 20-40 years.
Risk factors: Smoking, tall stature, and the presence of apical subpleural
blebs (mostly familial).
Secondary Spontaneous Pneumothorax: Occurs in the presence of underlying
lung disease.
Most common causes are COPD (chronic bronchitis and emphysema) and
cavitary active pulmonary TB.
Other causes include bronchial asthma, cystic fibrosis, and Pneumocystis
jirovecii pneumonia.
Traumatic Pneumothorax: Results from penetrating or nonpenetrating injuries
to the chest.
Iatrogenic Pneumothorax: Following diagnostic or therapeutic interventions.
Most occur in the presence of an underlying lung disease.
Examples: transthoracic needle aspiration/biopsy, subclavian vessel
puncture, thoracocentesis, transbronchial needle aspiration, pleural
biopsy, and mechanical ventilation.

Clinical Features

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Symptoms:
Sudden onset unilateral pleuritic chest pain.
Breathlessness.
General examination:
Patient will be cyanosed.
Tachypneic
Peripheral pulses may be feeble.
Hypotension may be present.
Physical Signs:
Markedly diminished/absent breath sounds.
Absence of adventitious sounds.
Fullness of the chest
Diminished chest size
Movement of air.

Types of Spontaneous Pneumothorax

Tension
Feature Closed Pneumothorax Open Pneumothorax
Pneumothorax

The pleural tear acts

The pleural tear
Pleural tear The pleural tear is sealed. as a one-way valve
remains open.
mechanism.
Pleural Pressure is less than Pressure is equal to Pressure is more than
cavity atmospheric pressure. atmospheric pressure. atmospheric pressure.
Air continuously enters Air enters but cannot
The lung seals off and
Mechanism and leaves the pleural leave the pleural
does not reopen.
cavity/space. cavity/space.
The trapped air is slowly Infection of the pleural Trachea and
reabsorbed and the lung cavity is common due to mediastinal (apex
Result
re-expands completely in the broncho-pleural beat) shift to the
2-4 weeks. fistula. opposite side.

Types of Spontaneous Pneumothorax

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Closed Pneumothorax Open Pneumothorax Tension Pneumothorax

Acts as a ball and valve

Pleural Tear Sealed Open
mechanism
Pleural Less than atmospheric Equal to atmospheric More than atmospheric
Pressure pressure pressure pressure

Tension Pneumothorax
A valvular type of pneumothorax where air is trapped in the pleural space.
Air is drawn into the pleural space during inspiration, coughing, or sneezing but
cannot be expelled during expiration.
This causes a large quantity of air to accumulate, raising the intrapleural
pressure.
The high intrapleural pressure compresses the underlying lung, shifts the
mediastinum to the opposite side, and decreases venous return to the heart by
compressing the vena cava.
Clinical Features:
Rapidly progressive breathlessness
Central cyanosis
Rapid, thread-like pulse
Signs of circulatory collapse
Emergency Treatment:
Insertion of a large-bore needle into the pleural space through the second
anterior intercostal space.
Cover the open end of the needle with a glove finger to allow air to
escape.
Other methods include insertion of a wide-bore plastic cannula or an
intercostal catheter connected to a water-seal drainage system.

Catamenial Pneumothorax

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A rare condition occurring in females, typically above 25-30 years of age.

Presents with repeated attacks of spontaneous pneumothorax, usually on the
right side, associated with menstruation.
Attacks usually occur within 2 days before or after the onset of menstruation.
Hemoptysis may also develop.
Most frequently associated with endometriosis of the thorax.
Treatment: Ovulation-suppressing drugs, surgical exploration, and pleurodesis.

Clicking Pneumothorax
A small, left-sided pneumothorax localized in front of the pericardium.
Produces an alteration of heart sounds, making them loud and resonant.

Recurrent Spontaneous Pneumothorax

After a primary spontaneous pneumothorax, recurrence occurs within a year in
about 25% of patients.
Recurrence is common with emphysematous bullae or
lymphangioleiomyomatosis (LAM).
Recurrences usually occur on the same side.
Treatment: Obliteration of the pleural space by artificial pleurodesis, achieved
by intrapleural instillation of an irritant like tetracycline or talc powder,
pleurectomy at thoracotomy, pleural abrasion, or parietal pleurectomy at
thoracoscopy. Pleurodesis is recommended after a second pneumothorax.

Open Pneumothorax
Communication between the pleural cavity and the atmosphere.
The pleural cavity develops secondary to rupture of an emphysematous bulla or
a small pleural bleb.
Clinical features:
Infection of the pleural space
Fever
Tension pneumothorax

Bronchopleural Fistula

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Abnormal connection between the bronchial tree and pleural space.

Results in atmospheric pressure throughout the respiratory cycle, preventing
lung re-expansion and facilitating infection into the pleural space, causing
empyema.
May also lead to a lung abscess.
Treatment: Requires drugs, surgical exploration and pleurodesis.

Pneumonia

Definition
Inflammation of the lung parenchyma causing acute respiratory illness.
Characterized by exudative solidification of alveoli filled with
inflammatory exudates, resulting in consolidation.

Classification

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Classification Description

Anatomic Distribution
Infection involves many contiguous alveoli. Radiologically
Lobar Pneumonia
appears as nonsegmental consolidation.
Inflammation involves conducting airways, bronchioles, and
Bronchopneumonia
surrounding alveoli.
Inflammation is confined to interalveolar septa. X-ray shows
Interstitial Pneumonia
a reticular pattern.
Clinical Setting
Community-Acquired
Infection acquired in the community.
Pneumonia
Nosocomial Pneumonia Infection acquired in a hospital setting.
Pneumonia in
Immunocompromised Occurs in patients with weakened immune systems.
Host
Infections acquiredi in the course ofal hospital stay
(development of pneumonia: after 248 hours of
Health Care-Associated hospitalization). Most of this pneumonia occurs outside
Pneumonia intensive care units, However, thet highest riskis observed
in patientsgd mechanical ventilation veniiattrrassociatedd
pneumonia
Etiological
Caused by a specific pathogenic organism without pre-
Primary Pneumonia
existing respiratory system abnormality.
Secondary Pneumonia Occurs secondary to other factors, including aspiration.
Suppurative Pneumonia Necrotizing pneumonia.

Community-Acquired Pneumonia (CAP)

Acute pulmonary infection in a patient not hospitalized or living in a long-term
care facility for 14 days or more before presentation.
Includes both immunocompetent and immunocompromised patients.

Causative Agents

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Common Less Common

Streptococcus pneumoniae Enterobacteriaceae (Klebsiella)

Haemophilus influenzae Streptococcus pyogenes
Moraxella catarrhalis Pseudomonas aeruginosa
Mycoplasma pneumoniae Coxiella burnetii (Q fever)
Viruses (RSV, influenza) Chlamydia pneumoniae, C. trachomatis, C. psittaci
Adenovirus

Predisposing Conditions

Risk Factors

Extremes of age
Upper respiratory tract infections
Comorbidities (chronic kidney disease, congestive heart failure, diabetes)
Malnutrition
Cigarette smoking
Alcohol
Corticosteroid therapy
Congenital or acquired immune deficiencies (HIV)
Decreased or absent splenic function
Other respiratory conditions (cystic fibrosis, obstructing lesions)
Indoor air pollution

Clinical Features

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Vary according to the immune status of the patient and the infecting agent.

Pulmonary Symptoms:

Cough (may be productive with purulent or rusty sputum)

Chest pain (pleuritic)
Breathlessness

Systemic Features:

Sudden onset of fever, rigors, shivering, and malaise

Delirium
Loss of appetite
Headache
Tachypnea

Extrapulmonary Features:

Extrapulmonary Symptoms Infectious Agent

Myalgia, arthralgia, malaise Legionella and Mycoplasma

Myocarditis and pericarditis Mycoplasma pneumoniae
Headache, abdominal pain, diarrhea, vomiting Legionella pneumoniae
Labial herpes simplex reactivation Pneumococcal pneumonia
Skin rashes (erythema multiforme) Mycoplasma pneumoniae

Types of Presentation

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Classical (e.g., S.
Feature Atypical (e.g., Mycoplasma)
pneumoniae)

Onset Sudden Gradual and insidious

Fever High, shaking chills Low-grade
Chest Pain and
Pleuritic, sudden onset Dry cough, no blood tinge
Breathlessness
Cough Productive
Sputum Purulent, blood tinge
General Condition Poor
High (up to 20% in Low (1-2% except in
Mortality
bacteremia) Legionellosis)
Mycoplasma, Chlamydia,
Causative Organisms S. pneumoniae
viruses
Systemic manifestations
Yes
present

Chest Examination
Vary depending on the anatomy and distribution of infection.
May include:
Increased respiratory and pulse rate
Elevated temperature
Dullness on percussion
Enhanced conduction of sound
Bronchophony
Whispering pectoriloquy
Coarse crackles

CURB-65 Severity Assessment

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Factor Criteria Points

Confusion New mental confusion 1

Urea >7 mmol/L 1
Respiratory Rate >30 breaths/minute 1
Blood Pressure Systolic BP <90 mmHg or Diastolic BP <60 mmHg 1
Age ≥65 years 1
Risk
Assessment
0 or 1 point: low mortality (1.5%), suitable for home
Group 1
treatment
Group 2 2 points: mortality 9.2%, hospitalization for treatment
Group 3 ≥3 points: mortality 22%, requires ICU admission

Diagnostic Tests
Sputum Examination: Gram stain, culture, antimicrobial testing, Ziehl-Neelsen
staining.
Blood Cultures: Recommended, may identify causative organism.
Antigen Detection: For Legionella and Streptococcus pneumoniae.
Arterial Blood Gases: Assess ventilatory failure or acidosis.
HIV Test: Offer to all patients with pneumonia.
Chest X-Ray: Essential for confirmation, detection of complications.
Invasive Procedures: Percutaneous transtracheal aspiration, bronchoscopy.

Radiological Findings
Lobar Pneumonia: Patchy opacification evolves into homogenous consolidation
of affected lobe; air bronchograms may be present.
Bronchopneumonia: Patchy and segmental shadowing.
Multilobar Pneumonia: Multilobar shadowing, cavitation and abscesses.

General Complications

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Respiratory failure
ARDS
Bacteremic dissemination
Empyema
Lung abscess
Sepsis

Community-Acquired Pneumonia (CAP) Treatment

Administer antibiotics promptly, preferably within 4 hours of presentation.

Empiric antibiotic regimens (Table 6.74)

Duration of therapy: Minimum of 5 days (usually 7-10 days)

Switch to oral antibiotics when patients are afebrile and improving.

Provide oxygen and manage fluid balance.

Setting Therapeutic Options

Ambulatory, not requiring

Oral macrolide (erythromycin or
hospitalization, age under 60
azithromycin)
years
Ambulatory, not requiring Oral β-lactam/β-lactamase inhibitor +
hospitalization, comorbidity or macrolide or oral antipneumococcal
age over 60 years fluoroquinolone
β-lactam (cefoperazone or ceftriaxone) +
Requiring hospitalization macrolide or antipneumococcal
fluoroquinolone
β-lactam/β-lactamase inhibitor alone
Aspiration pneumonia requiring
(ampicillin/sulbactam,
hospitalization
piperacillin/tazobactam)

Unresolved/Slow-Resolving Pneumonia

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Considered unresolved if fever declines within 72 hours, temperature

normalizes within 5 days, and respiratory signs return to normal.
Slowly resolving CAP is defined as >50% clearing by 2 weeks or complete
clearing at 4 weeks.

Recurrent Pneumonias

Condition

Bronchial obstruction
Bronchiectasis
Immunocompromised state
Sequestration of lung
Ciliary dyskinesia
Multiple myeloma and other lymphoreticular malignancies

Prevention
Smoking cessation
Vaccination (influenza and pneumococcal)

Immunological Deficiency and Pneumonia

Defects Leading to Increased Susceptibility

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Innate immunity defects: Impact the body's first line of defense.

Humoral immunodeficiency: Affects complement or immunoglobulin function.
Cell-mediated immunity defects: Can be congenital or acquired.
HIV infection: Weakens the immune system.
Immunosuppressive agents: Treatment that suppresses the immune system.
Leukopenia: Reduced white blood cell count, increasing infection risk.
Age: Very young (under 2) and older adults (over 65) are more vulnerable.
Cigarette smoking: A strong risk factor for community-acquired pneumonia
(CAP).
Alcoholism (ALPS): Increases pneumonia risk, along with leukopenia and
pneumococcal sepsis.
Poverty and overcrowding: Associated with lowered host resistance.
Underlying conditions: Liver disease and chronic lung disease.
Asplenia/hyposplenia: Impaired splenic function.
Impaired local defenses: Due to anesthesia or drugs.

Characteristics of Pneumococcal Pneumonia 🫁

Mode of infection: Droplet infection.
Causative factors: Diminished respiratory movements.
Physical signs:
Dull percussion note.
No mediastinal shift.
Markedly increased vocal fremitus and resonance.
Bronchial breathing.
Bronchophony, egophony, and whispering pectoriloquy may be present.
Coarse crepitations during resolution.
Sputum:
Gram's staining may show Gram-positive, lancet-shaped diplococci.
Culture may show S. pneumoniae.

Clinical Features of Pneumonia 状

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Onset: Sudden, with high fever (up to 40°C) and chills.

Cough: Initially dry and painful, becoming productive with mucopurulent
sputum.
Sputum characteristics: "Rusty" or blood-stained.
Systemic symptoms: Loss of appetite, headache, body aches.
Chest pain: Pleuritic, may be referred to shoulder or abdomen, accompanied by
friction rub.
Breathing: Rapid and shallow due to pain.
Other: Flushed face.

Investigations for Pneumonia

Chest radiograph: Shows homogeneous radiopaque area with air
bronchograms, may detect parapneumonic effusion or empyema.
Sputum assays: Based on detecting nucleic acids or pneumococci.
Serological tests: Detect pneumococcal antigens in serum, urine, and sputum.
Urinary antigen detection: Remains positive for weeks after onset.
Blood culture: May show S. pneumoniae.

Signs of Consolidation
Signs of consolidation are minimal initially but progress to frank signs
after 2 days. These include diminished respiratory movements, slight
impairment of percussion, pleural rub, hot and dry skin, herpes labialis,
and fine crepitations.

Complications of Lobar Pneumonia

Neurological: Meningitis, mental confusion
Pulmonary: Parapneumonic effusion, empyema, pulmonary congestion and
edema, acute respiratory failure.
Cardiovascular: Acute pericarditis, endocarditis, circulatory failure
Spread of infection: To other lobes or pleural space

Respiratory Failure

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Types of Respiratory Failure

Type I (Hypoxemic):
Definition: PaO₂ < 60 mm Hg at sea level.
Cause: Failure of oxygen exchange due to alveolar flooding and increased
shunt fraction.
Response to Oxygen: Hypoxemia refractory to supplemental oxygen.
Type II (Hypercapnic):
Definition: PaCO₂ > 45 mm Hg.
Cause: Failure to exchange or remove carbon dioxide, decreased alveolar
minute ventilation.
Association: Accompanied by hypoxemia that corrects with supplemental
oxygen.
Type III (Perioperative):
Cause: Increased atelectasis due to decreased functional residual capacity,
often in the setting of abnormal abdominal wall mechanics.
Improvement Strategies: Anesthetic modifications, operative technique,
posture, incentive spirometry, postoperative analgesia.
Type IV (Shock):
Description: Occurs in patients in shock, necessitating resuscitation.
Goal of Ventilation: Stabilize gas exchange and unload respiratory
muscles.

Mechanisms Producing Respiratory Failure

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Mechanism Description

May be due to low tidal volume, impaired neuromuscular

transmission (e.g., Guillain-Barré syndrome, myasthenia gravis),
Hypoventilation
or reduced respiratory rate. PaCO₂ increases, PaO₂ decreases,
and alveolar-arterial oxygen gradient is normal.
Ventilation- The most common cause of hypoxemia; administration of 100%
Perfusion (V/Q) O₂ will markedly improve hypoxemia. Elevation of alveolar-
Mismatch arterial oxygen gradient.
Deoxygenated blood bypasses ventilated alveoli, mixes with
oxygenated blood, and produces hypoxemia. Hypoxemia
Shunt
persists even with 100% oxygen. Elevation of alveolar-arterial
oxygen gradient.
Diffusion
Uncommon cause of hypoxemia.
Abnormality
Decreased Inspired
High altitude.
Oxygen

Acute vs. Chronic Respiratory Failure

Feature Acute Chronic

PaCO₂ Increased Normal or slightly reduced

Bicarbonate
Normal Elevated due to renal compensation.
(HCO₃⁻)
Hypoxemia present, Patients may develop polycythemia,
Other may be transient or pulmonary hypertension, and cor pulmonale
persistent. due to chronic hypoxemia.

Sleep Apnea

Definitions

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Apnea: Cessation of airflow for at least 10 seconds.

Hypopnea: Reduction in airflow by ≥50% for ≥10 seconds, OR a smaller
reduction associated with oxygen desaturation ≥4% or arousal.
Respiratory Effort-Related Arousal (RERA): Increasing respiratory effort for
≥10 seconds leading to arousal from sleep, not meeting apnea or hypopnea
criteria.

Types of Sleep Apnea

1. Obstructive Sleep Apnea (OSA): Continued thoracoabdominal effort despite
airflow cessation.
2. Central Sleep Apnea: Lack of thoracoabdominal effort during airflow cessation.
3. Mixed Sleep Apnea: Features of both obstructive and central apnea.

Acute Respiratory Distress Syndrome (ARDS)

Definition
ARDS is a form of acute respiratory failure characterized by sudden and
progressive dyspnea, severe hypoxemia, and diffuse pulmonary infiltrates
due to increased permeability of the alveolar-capillary membrane.

Berlin Definition of ARDS

Timing: Within 1 week of a known clinical insult or new/worsening respiratory
symptoms.
Origin of Edema: Respiratory failure not fully explained by cardiac failure or
fluid overload. Objective assessment (e.g., echocardiography) needed to
exclude hydrostatic edema.
Oxygenation: Defined by PaO₂/FiO₂ ratio with PEEP ≥5 cm H₂O:
Mild: 200-300 mm Hg
Moderate: 100-200 mm Hg
Severe: <100 mm Hg

Direct Lung Injury Causes

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Pneumonia (viral, bacterial, fungal, Pneumocystis jirovecii, Mycoplasmal)

Aspiration of gastric contents
Inhalation of toxic gases (ammonia, chlorine, nitrogen dioxide, ozone, oxygen,
smoke)
Blunt chest trauma (pulmonary contusion, near drowning)

Indirect Lung Injury Causes

Systemic disorders: Shock, septicemia, uremia, eclampsia, severe trauma
Multiple bone fractures (fat embolism), flail chest, head trauma, burns
Blood: Multiple transfusions
Drug overdose (narcotics, barbiturates, thiazides, nitrofurantoin)
Others: Acute pancreatitis, cardiopulmonary bypass, Goodpasture's syndrome,
SLE

Contraindications to Extracorporeal Carbon Dioxide

Removal
Severe heart or lung failure with high oxygen requirements
Severe cardiac failure of any cause
Primary allograft failure after transplant
Conditions incompatible with survival (CNS status, end-stage malignancy)
High risk of systemic bleeding

Phases of ARDS

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1. Exudative Phase (1-7 days):

Diffuse alveolar damage with inflammation.
Increased capillary permeability, damage to alveolar cells.
Formation of hyaline membranes.
Loss of surfactant, alveolar collapse, hypoxemia.
2. Proliferative Phase (7-21 days):
Initiation of repair processes.
Alveolar exudate undergoes organization, neutrophils disappear.
Type II pneumocytes proliferate.
Fibroblast development.
3. Fibrotic Phase (later):
Proliferation of fibroblasts, interstitial fibrosis.
Lung function may improve over 6-12 months.

Pathophysiology
1. Lung Injury: Initiates inflammatory responses throughout the lung.
2. Alveolar Damage: Damage to Type I and II alveolar cells, surfactant disruption.
3. Inflammatory Mediator Release: Macrophages and neutrophils release
cytokines and vasoactive substances.
4. Pulmonary Vasoconstriction: Hypoxic pulmonary vasoconstriction and
microvascular thrombi.
5. Consequences:
Alveolocapillary membrane permeability increases, leading to pulmonary
edema.
Hyaline membrane formation.
Lung compliance decreases, and pulmonary hypertension results.
Hypoxemia due to V/Q mismatch.

Clinical Features
History: Development of dyspnea and hypoxemia within hours to days of an
inciting event.
Physical Examination: Tachypnea, tachycardia, cyanosis, use of accessory
muscles.

Investigations

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Chest Radiograph: Diffuse, bilateral alveolar infiltrates. Initially, patchy

peripheral distribution progressing to diffuse involvement.
Arterial Blood Gases: Hypoxemia, respiratory alkalosis initially, progressing to
respiratory acidosis.

ARDS Severity Assessment

Severity PaO₂/FiO₂ Ratio

Mild 200-300
Moderate 100-200
Severe <100

Management
Treat underlying cause.
Support organ system dysfunction.
Maintain adequate oxygenation using PEEP.
Lung-protective mechanical ventilation with low tidal volumes.
Permissive hypercapnia may be allowed.

Hemoptysis

Causes of Hemoptysis

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Common causes Uncommon causes

Bronchial carcinoma,
bronchiectasis, acute and chronic Bronchial adenoma, foreign body
bronchitis
Pulmonary tuberculosis
Parasites (e.g., hydatid disease, flukes), trauma,
(Rasmussen's aneurysm), lung
actinomycosis, mycetoma
abscess, pneumonia
Goodpasture's syndrome, polyarteritis nodosa,
Pulmonary infarction idiopathic pulmonary hemosiderosis, primary
pulmonary hypertension
Mitral stenosis, aortic aneurysm, pulmonary
Acute left ventricular failure
thromboembolism
Leukemia, hemophilia,
anticoagulants, hemorrhagic Other uncommon causes
diathesis

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