ch 35 continued

Pulmonary Edema

• Defined as excess fluid in the lung.
• Normally, the lung is kept dry by lymphatic drainage, capillary hydrostatic pressure, capillary oncotic pressure and capillary permeability balance, and surfactant.
• Predisposing factors include left-sided heart disease, injury to pulmonary capillary endothelium, inhalation of toxic gases, lymphatic obstruction, and rapid pulmonary re-expansion.

Pulmonary Edema Causes and Treatment

• Left-Sided Heart Disease:
  • Pathophysiology involves left ventricle failure, increased filling pressures on the left side of the heart, and increased pulmonary capillary hydrostatic pressure.
  • When hydrostatic pressure exceeds oncotic pressure, fluid moves into the interstitium and alveolar flooding occurs.
  • Pulmonary edema develops at a wedge pressure or left atrial pressure of 20 mmHg.
  • Decreased capillary oncotic pressure can cause pulmonary edema at lower hydrostatic pressures.
  • Treatment includes diuretics, vasodilators, and medications to improve heart muscle contraction.
• ARDS or Inhalation of Toxic Gases:
  • Injury to alveolocapillary membrane increases capillary permeability, causing water and plasma protein leakage into the lung interstitium.
  • Interstitial and capillary oncotic pressure equalize, leading to water moving into the lung.
  • Treatment involves removing the offending agent and providing supportive therapy for oxygenation, ventilation, and circulation.
• Obstruction of the Lymphatic System:
  • Edema, tumors, fibrotic tissue, or increased systemic venous pressure compresses lymphatic vessels, causing obstruction.
  • Treatment varies depending on the cause of obstruction.
• Post Obstructive Pulmonary Edema (POPE):
  • Occurs after relief of upper airway obstruction.
  • Attempted inspiration against an occluded airway leads to excessive intrathoracic negative pressure, increased venous return and pulmonary blood volume.
  • Treatment involves positive end-expiratory pressure ventilation (PEEP).
• High-Altitude Pulmonary Edema (HAPE):
  • Occurs at altitudes typically >8000-10,000 feet associated with a hypobaric hypoxic environment.
  • Hypoxic pulmonary vasoconstriction and increased pulmonary capillary permeability are possible mechanisms.
  • Prevention involves medications, slow ascent, and descent to lower altitudes when symptoms occur.
• Clinical Manifestations:
  • Symptoms include dyspnea, hypoxemia, and increased work of breathing.
  • Physical exam may reveal inspiratory crackles, dullness to percussion over the lung bases, and ventricular dilation.
  • Severe edema can manifest as pink, frothy sputum, worsening hypoxemia, and hypoventilation with hypercapnia.

Pulmonary Fibrosis

• Defined as excessive fibrous or connective tissue in the lung.
• Etiology includes scar tissue formation after active pulmonary disease (ARDS, tuberculosis), autoimmune disorders (rheumatoid arthritis, systemic sclerosis, sarcoidosis), or inhalation of harmful substances (coal dust, asbestos).
• Pathophysiology involves loss of lung compliance leading to hypoxemia, and chronic inflammation resulting in alveolar epithelialization and myofibroblast proliferation.
• A complication is a poor prognosis in diffuse pulmonary fibrosis.

Idiopathic Pulmonary Fibrosis (IPF)

• Diagnosed when no specific cause can be identified.
• Most common idiopathic interstitial lung disorder affecting men over 60 years. Median survival is 2-5 years after diagnosis.
• Pathophysiology is characterized by chronic inflammation from multiple injuries at different lung sites with aberrant alveolar wound healing.
• Alveolar collapse and a fibroproliferative response thickens the alveolocapillary membrane leading to decreased oxygenation and hypoxemia.
• Progression involves decreased lung compliance, increased work of breathing and decreased tidal volume, leading to hypoventilation with hypercapnia.
• Acute exacerbations can cause rapid decompensation with a high mortality rate.
• Clinical manifestations include increasing dyspnea on exertion and diffuse inspiratory crackles.
• Diagnosis is confirmed by pulmonary function testing (decreased FVC), high-resolution CT, and lung biopsy.
• Treatment involves oxygen, corticosteroids, and cytotoxic drugs with low success rates.
• Additional therapies include antifibrotic drugs, inhaled interferon, anticoagulation therapy, and lung transplantation.

How Different Disease Processes Cause Hypoxemia

• Hypoxemia is reduced oxygenation of arterial blood (PaO2).
• Caused by respiratory alterations that can lead to tissue hypoxia.
• Factors include oxygen delivery to the alveoli, ventilation of the alveoli, diffusion of O2 into the blood, and perfusion of pulmonary capillaries.
• Hypoxia is reduced oxygenation of cells in tissues.
• Cyanosis, hypoxemia, and hypoxia can exist independently but are interrelated.
• Hypoxemia often leads to compensatory hyperventilation and respiratory alkalosis.
• Results in widespread tissue dysfunction and organ infarction in severe cases.
• Can cause hypoxic pulmonary vasoconstriction leading to increased pulmonary artery pressure and right-sided heart failure (cor pulmonale).
• Clinical manifestations include cyanosis, confusion, tachycardia, edema, and decreased renal output.

Causes of Hypoxemia

• Decreased Inspired Oxygen (Decreased FiO2)
  • High altitude, low oxygen content of gas mixture, enclosed breathing spaces.
• Hypoventilation of the Alveoli
  • Lack of neurologic stimulation, defects in chest wall mechanics, large airway obstruction, increased work of breathing.
• Ventilation-Perfusion Mismatch
  • Asthma, chronic bronchitis, pneumonia, ARDS, atelectasis, pulmonary embolism.
• Alveolocapillary Diffusion Abnormality
  • Edema, fibrosis, emphysema.
• Decreased Pulmonary Capillary Perfusion
  • Intracardiac defects, intrapulmonary arteriovenous malformations.

Oxygen Delivery to the Alveoli

• The amount of oxygen in alveoli is the PaO2 dependent on:
  • Minute ventilation.
  • Oxygen content of the inspired air (FiO2).
• Definition of ventilation: The amount of air you breathe in and out (minute ventilation). The product of tidal volume and respiratory rate.
• Shallow or slow breathing (hypoventilation) results in less oxygen in the alveoli and more CO2 buildup, leading to hypoxemia, hypercapnia, and respiratory acidosis.
• FiO2 is the fraction of inspired oxygen. Normal FiO2 at sea level is 21% or 0.21. Lower FiO2 decreases oxygen content in the alveoli.

Diffusion of Oxygen from Alveoli to Blood

• Depends on ventilation and perfusion.
• V/Q ratio is the balance between air and blood. Normal V/Q ratio is 0.8-0.9 with more air entering the lungs than the blood supply.
• Abnormal V/Q ratio is the most common cause of hypoxemia.
• A V/Q mismatch, caused by inadequate ventilation in well-perfused areas leads to wasted perfusion.
• Shunting happens when blood passes through parts of the lung with no ventilation.

V/Q Imbalance Types

• Low V/Q ratio: Areas with good blood supply aren’t getting enough air. Common in asthma, pneumonia, atelectasis which leads to shunting.
• Shunting: Blood flows to areas without enough oxygen, resulting in wasted blood flow.
• Hypoxic Pulmonary Vasoconstriction: Blood vessels in poorly oxygenated areas constrict to reduce blood flow to better-functioning parts of the lungs, improving oxygenation.
• Large imbalance can lead to increased pressure in lung blood vessels and right heart failure (cor pulmonale) over time.

Diffusion of Oxygen Across the Alveolocapillary Membrane

• The alveolocapillary membrane is the barrier between the alveoli and the capillaries
• Oxygen needs to move from the alveoli into the blood, and this process is called diffusion.
• Thickened membrane can occur in conditions like edema or fibrosis slows the diffusion.
• Decreased surface area happens in diseases like emphysema reduces the area for oxygen to pass into the blood.
• Carbon dioxide can still move easily across the alveolocapillary membrane even if oxygen diffusion is impaired.

Perfusion of Pulmonary Capillaries (Blood Flow)

• Decreased perfusion means less blood flow to the lungs.
• Causes include intracardiac defects, problems in the heart that cause blood to bypass the lungs and intrapulmonary arteriovenous malformations (abnormal connections between blood vessels in the lungs).
• Bypassing the lungs leads to low oxygen in the blood that can not be improved with oxygen.

Empyema

• An infected pleural effusion with pus in the pleural space.
• More common in older adults and children; develops as a complication of pneumonia, surgery, trauma, or bronchial obstruction from a tumor.
• Common infectious microorganisms: Staphylococcus aureus, Escherichia coli, anaerobic bacteria, and Klebsiella pneumoniae.
• Pathophysiology involves blocked pulmonary lymphatics resulting in outpouring of contaminated lymphatic fluid into pleural space.
• Progression occurs in three stages: exudative, fibrinopurulent, and organizing with pleural peel formation.
• Clinical manifestations include cyanosis, fever, tachycardia, cough, and pleural pain.
• Physical examination reveals decreased breath sounds directly over empyema.
• Diagnosis involves chest x-ray, thoracentesis, and sputum culture.
• Treatment includes antimicrobials and drainage of pleural space with chest tube.
• Severe cases may require ultrasound-guided pleural drainage, instillation of fibrinolytic agents, and/or injection of deoxyribonuclease into pleural space.
• Surgical debridement may be required.

Acute Respiratory Distress Syndrome (ARDS)

• Acute lung injury represents a spectrum of acute lung inflammation and diffuse alveolocapillary injury, with ARDS being the most severe form.
• Defined by:
  • Acute onset of bilateral infiltrates on chest x-ray not explained by cardiac failure or fluid overload (non-cardiogenic pulmonary edema).
  • A low ratio of the partial pressure of arterial oxygen to the fraction of inhaled oxygen.
• Affects over 190,000 people in U.S.
• Advances in medical care have decreased overall death rate
• Elderly, individuals with severe infections or immunocompromised have higher mortality
• Most common risk factors: genetic factors, sepsis, multiple trauma (especially when multiple blood transfusions are given) damages the alveolar capillary membrane
• Preventable factors: alcohol abuse and smoking
• Other causes include pneumonia, burns, aspiration, cardiopulmonary bypass surgery, oxygen toxicity, radiation therapy, and DIC.

Pathophysiology of ARDS

• Direct Causes: Aspiration of highly acidic gastric contents, inhalation of toxic gases, development of pneumonia.
• Indirect Causes: Circulating proinflammatory mediators released in response to systemic disorders (sepsis, trauma, and multiple transfusions).
• All disorders cause acute immune cell-mediated injury to the alveolocapillary membrane resulting in massive inflammation, alveolar flooding with protein-rich fluid that overwhelms ion channels and lymphatic removal of fluid.
• Pulmonary edema is associated with shunting, V/Q mismatch, reduced lung compliance, and hypoxemia.

ARDS Progressive Phases

• Exudative (Inflammatory) - within 72 hours
  • Releases inflammatory cytokines (IL-1B and IL-6) and endotoxins.
  • Macrophages release proinflammatory cytokines (IL-8), TNF-a, surfactant protein-D, and mitochondrial DNA.
  • Neutrophils release proteolytic enzymes, reactive oxygen species, nitric oxide, and arachidonic acid metabolites.
  • Platelet-activating factor damages the alveolocapillary membrane and increases capillary permeability.
  • Platelet / complement activation leads to a hypercoagulable state with intravascular microthrombus formation.
  • Platelets, neutrophils, and macrophages mediators cause pulmonary vasoconstriction and microthrombus formation, leading to pulmonary HTN / edema.
  • Alveoli and respiratory bronchioles fill with fluids.
  • Intraalveolar hemorrhagic exudate becomes cellular granulation tissue that appears as hyaline membranes leading to decreasing lung compliance, increased work of breathing, decreased alveoli ventilation, and hypercapnia.
• Proliferative - (overlaps fibrotic phase)
  • Resolution of pulmonary edema.
  • Proliferation of fibroblasts, myofibroblasts, and type II pneumocytes (with surfactant recovery).
  • Type I pneumocyte differentiation with epithelial cell regeneration.
• Fibrotic - 2 to 3 weeks post-initial injury
  • Remodeling (abnormal repair) and fibrosis occurs throughout lungs.
  • Fibrosis progressively obliterates alveoli, respiratory bronchioles, and interstitium which decreases functional residual capacity.
  • Causes continuing V/Q mismatch, severe right-to-left shunting, and respiratory failure.
  • Fibrosis of pulmonary capillaries causes pulmonary HTN.
  • Chemical mediators responsible for alveolocapillary damage of ARDS cause inflammation + endothelial damage + capillary permeability which leads to SIRS → MODS which contributes to mortality.

Clinical Manifestations of ARDS

• Dyspnea and Hypoxemia with Poor Response to O2 Supplementation.
• Hyperventilation and Respiratory Alkalosis.
• Decreased Tissue Perfusion, Metabolic Acidosis, and Organ Dysfunction.
• Increased Work of Breathing, Decreased Tidal Volume and Hypoventilation.
• Hypercapnia, Respiratory Acidosis and Worsening Hypoxemia.
• Decreased Cardiac Output, Hypotension, and Death.

Berlin Definition of ARDS

• Mild: 200 mmHg < PaO2/FiO2 ≤ 300 mmHg.
• Moderate: 100 mmHg < PaO2/FiO2 ≤ 200 mmHg.
• Severe: PaO2/FiO2 ≤ 100 mmHg with bilateral infiltration on chest imaging not explained by cardiac failure or fluid overload.

Complications of ARDS

• Worsening hypoxemia and hypercapnia can cause respiratory failure, decreased O2 delivery, metabolic acidosis, organ dysfunction, decreased cardiac output, and hypotension, leading to death.

Diagnosis of ARDS

• Based on history of lung injury, physical examination, analysis of ABG, and chest x-ray.
• Initial physical examination reveals fine inspiratory crackles.
• Interstitial and alveolar infiltrates appear on chest x-ray post-injury.
• Serum biomarkers are studied for ARDS prediction / treatment outcomes.

Treatment of ARDS

• Early detection and management of contributing etiologies, supportive therapy to prevent progression of lung injury, and prevention of complications.
• No FDA-approved treatments.
• Modes of protective ventilation are used, including:
  • Low-tidal volume ventilation.
  • Noninvasive positive-pressure ventilation.
  • Permissive hypercapnia.
  • Prone positioning.
  • Neuromuscular blockade (paralytics).
  • Extracorporeal lung assistance.
• Investigation into use of Aspirin.
• Corticosteroids may be beneficial in persistent ARDS.

Prognosis of ARDS

• Survivors often have near-normal pulmonary function tests 12 months post-recovery.
• Others have persistent pulmonary dysfunction, reduced exercise capacity, and long-term neurocognitive impairment.

ARDS in Childhood

• Mortality is lower in children than adults.
• Survival rates are higher in children < 5 years old.
• Infants have more compliant chest walls, decreased hematocrit levels, increased baseline airway resistance, and decreased functional residual capacity requiring different management strategies.
• The maturing lung is at greater risk of ventilator-induced lung injury.
• Goal of treatment is to preserve and restore O2 delivery, minimize acute lung injury, and reduce morbidity and mortality.
• Use of corticosteroids is controversial.
• Surfactant therapy improves oxygenation and increases survival time ages 1 week to 21 years.
• Extracorporeal membrane oxygenation (ECMO) has improved survival time in some centers.

How Cigarette Smoking Causes/Exacerbates Pulmonary Disease Processes

• Tobacco smoke directly injures airway epithelial cells.
• Leads to chronic bronchial inflammation with bronchial edema, and increase in size & number of mucous glands & goblet cells in airway.
• Results in thick, tenacious mucus due to impaired ciliary function.
• Compromised lung defense mechanisms increases susceptibility to pulmonary infections & airway injury.

Lung Cancer & Tobacco Smoke

• Cigarette smoking is the #1 risk factor for lung cancer.
• Environmental tobacco smoke (secondhand smoke) also increases risk.
• Tobacco smoke contains lung carcinogens + genetic predisposition + epigenetic changes initiate tumor development.
• Tumor progression is promoted by growth factors, and inflammatory cells/products modify cell development and differentiation altering the immune response.
• Repetitive exposure to tobacco smoke and carcinogenic “hits.” causes visible epithelial cell changes on biopsy.
• Heavy smokers are at a higher risk of lung cancer death.

Pulmonary Hypertension

• Defined: Mean pulmonary artery pressure (mPAP) > 25 mmHg at rest. Normal is 15–18 mmHg.

Clinical Classification of Pulmonary Hypertension

• Idiopathic Pulmonary Arterial Hypertension (IPAH):
  • Rare, primarily affects women ages 20–40.
  • Endothelial dysfunction causes increased vasoconstrictors, decreased vasodilators, proinflammatory cytokines, abnormal potassium channels, phosphodiesterases, serotonin and adrenomedullin, as well as growth factor release, leading to intimal and medial hypertrophy, intimal fibrosis, abnormal angiogenesis, and in situ thrombosis.
• Heritable Pulmonary Hypertension (Familial Pulmonary HTN):
  • BMPR2 gene mutation, intracellular signaling abnormalities lead to vascular proliferation.
• Drug- and Toxin-Induced Pulmonary HTN:
  • Linked to certain medications/toxins.
• Pulmonary HTN Associated with Other Diseases (APAH):
  • Common Associated Conditions: Connective tissue disease (e.g., scleroderma), HIV infection, Portal hypertension, Congenital heart disease, COPD, Chronic hemolytic anemia.
• Pulmonary HTN Due to Left-Sided Heart Disease (Most Common Cause):
  • Left ventricular dysfunction and Valvular heart disease.
• Pulmonary hypertension with unclear multifactorial mechanisms:
  • Hematologic disorders: Myeloproliferative disorders, splenectomy, and chronic hemolytic anemia Metabolic disorders: Glycogen storage disease, Gaucher disease, and Thyroid disorders Systemic disorders: Sarcoidosis, Pulmonary Langerhans cell histiocytosis, Lymphangioleiomyomatosis, Neurofibromatosis and Vasculitis
  • Others: Tumoral obstruction, Fibrosing mediastinitis, Chronic renal failure on dialysis, Segmental PH and Recurrent pulmonary embolism (PE)
• Risk factors: Diet, drugs, amphetamines, and cocaine

Causes of Pulmonary HTN

• Elevated left ventricular pressure, Increased blood flow through the pulmonary circulation, Obliteration or obstruction of the vascular bed and Active constriction of the vascular bed caused by hypoxemia or acidosis

Pathophysiology of Pulmonary HTN

• Idiopathic Pulmonary Hypertension:
  • Overproduction of vasoconstrictors, decreased vasodilators, and growth factor release causes vascular remodeling, narrowed lumens & abnormal vasoconstriction, increased resistance to pulmonary artery blood flow.
  • Increased pulmonary artery pressure leads to increased right ventricle workload, right ventricular hypertrophy, progressing to right-sided heart failure (cor pulmonale) that can cause death.
• Hereditary Pulmonary Hypertension:
  • Mutation in the BMPR2 gene which leads to abnormal vascular proliferation worsening pulmonary hypertension.
• Gas Exchange & Lung Function Impact:
  • Reduced gas exchange due to restricted lung volumes.
• Pulmonary Hypertension & Associated Respiratory Diseases:
• Often a serious complication of acute or chronic lung conditions: COPD or Obesity Hypoventilation syndrome
• Hypoxic Pulmonary Vasoconstriction worsens the condition increases pulmonary artery pressures (PAP).

Clinical Manifestations of Pulmonary HTN

• May not be detected until it becomes severe, symptoms often masked by primary pulmonary or cardiovascular disease.
• First indication: abnormality noted on chest x-ray , EKG, enlarged pulmonary arteries and right heart border showed right ventricular hypertrophy
• Fatigue, progressive SOB with exertion, chest discomfort, tachypnea, palpitations, and cough are common.
• Physical Examination: peripheral edema, jugular venous distention, enlarged right ventricle, and splitting of the second heart sound.

Diagnosis and Treatment of Pulmonary HTN

• Diagnosis of disease severity is quantified using New York Heart Association/WHO classification.
• Diagnosis and accurate assessment of PAP can be made ONLY WITH RIGHT-SIDED HEART CATHETERIZATION.
• Studies used chest x-ray, echocardiogram and CT-scan Additional underlying cause studies using ABGs, liver function testing, HIV serology, EKG, polysomnography, and ventilation-perfusion scanning is needed to rule out all other causes of hypertension.
• Treatment: General therapy O2, diuretics, and anticoagulants with avoidance of air travel, decongestant medications, tobacco use and pregnancy.
• Medications: Prostacyclin analogs, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and calcium Channel Blockers that fail medical therapy may require lung transplant.
• Treat the underlying disorder in secondary pulmonary HTN.
• Persisted pulmonary HTN that causes hypertrophy of medial smooth muscle = is no longer reversible but is treated with supplemental O2 to reverse hypoxic vasoconstriction.

Viral/Bacterial Pneumonia in Adults and Children

• Mechanisms of self-defense:
  • Upper airway: cough reflex and muco-ciliary clearance
  • Lower respiratory tract: alveolar macrophage (uses pattern recognition receptors)
  • Neutrophils: phagocytes kill microbes: neutrophil extracellular trap (NET)
  • Inflammatory mediators and immune complexes damages bronchial mucous membrane and alveolocapillary membrane filling with debris and exudate

Pneumonia (Adults)

• An infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites.
• Highest incidence and mortality is in the elderly.
• Risk factors include advanced age, compromised immunity, underlying lung disease (COPD), alcoholism, altered consciousness, chest trauma, impaired swallowing, smoking, endotracheal intubation malnutrition, immobilization, and underlying cardiac or liver disease.
• Categorized as community-acquired (CAP) OR healthcare-associated (HCAP)/hospital-acquired (HAP)/ventilator-associated (VAP).
• HAP has the greatest mortality
• VAP occurs in those requiring intubation and mechanical ventilation
• Characteristics of the individual is important to determine which etiologic microorganism is likely

Pathophysiology Adults

• Routes of infection: Aspiration of oropharyngeal secretions, inhalation and Endotracheal tubes and suctioning.
• Bacteria spread to lungs in the blood stream from bacteremia
• Healthy individuals:Pathogens that reach the lungs are expelled or controlled by mechanisms of self-defense.
• Bacteria spread to lungs in the blood stream from bacteremia
• Healthy individuals: Pathogens that reach the lungs are expelled or controlled by mechanisms of self-defense.
• Alveolar macrophage activates T cells and B cells with the induction of cellular and humoral immunity release TNF-α and IL-1.
• Mast cells and Fibroblasts release chemotactic signals inflammation in the lung the capillaries of the lungs into the alveoli neutrophils.
• Neutrophils critical phagocytes that kill microbes through the formation of phagolysosomes.
• The release of inflammatory mediators and immune complexes damage bronchial, mucosal, and alveolocapillary membranes terminal bronchioles and acini.
• Obstruction of bronchioles and accumulation of exudate in the acinus V/Q mismatching, hypoxemia, and dyspnea.

Pneumococcal Pneumonia (Bacteria)

• Infection is limited to one or two lobes
• Streptococcus pneumoniae most common cause of bacterial pneumonia S. pneumoniae initiate innate and adaptive immune responses & crucial for opsonizing the encapsulated bacterium
• Rapid lysis occurs with antibiotic treatment, release toxic pneumolysin to every cell in the lung results in worsening clinical symptoms in individuals after they begin antibiotic treatment
• Inflammatory cytokines and cells alveolar edema which spreads the infection into adjacent portions of the lung consolidation

Viral Pneumonia

• Seasonal, usually mild and self-limiting can lead to secondary bacterial infection by damaging ciliated epithelial cells creating bacterial infection
• A primary infection or as a complication of another viral illness.
• Influenza impairs antibacterial defense mechanisms .and sloughing of bronchial epithelial cells that prevents mucociliary clearance promoting bacterial attachment Bronchial walls allowing viruses to evade the protective effect of surfactant proteins in alveoli severe systemic illness and sepsis with many complications and high morbidity / mortality rate
• New / atypical forms can affect previously healthy populations threat for pandemics

Prevention of Pneumonia, Adults

• Prevention of aspiration, respiratory isolation, dental and endotracheal tube interventions.

Clinical Manifestations and Diagnosis of Pneumonia Adults

• May demonstrate signs of underlying systemic disease or sepsis
• Most cases of pneumonia precede an upper respiratory infection(cough, dyspnea, and fever)
• Physical Examination: pulmonary consolidation, inspiratory crackles, increased tactile fremitus and whispered pectoriloquy
• Diagnosis of Severe → blood and sputum cultures obtained before starting antibiotics
• Pathogen is identified by sputum characteristics
• Individuals is immunocompromised additional therapies are performed

Treatment Pneunomia Adults

• Management involves establishing adequate ventilation and oxygenation
• Individuals will most likely have hypoxemia with respiratory alkalosis
• Individuals with underlying lung disease may require mechanical ventilation
• Maintain Adequate hydration and pulmonary hygiene
• Treatment administered with Antibiotics and antivirals.

Complications and Pneumonia Childhood

• Severe pneumonia is a common cause of sepsis and septic shock

Pneumonia (Childhood)

• Major cause of morbidity and mortality in children especially in developing countries.
• Most common agents viruses and bacteria
• Risk Factors younger than 2 years, overcrowded living conditions, winter season, recent antibiotic treatment, attendance at daycare centers, and passive smoke exposure
• Nutritional status and underlying disease influences morbidity and mortality

Viral Pneumonia vs Bacterial Pneumonia Childhood

• Viral : Etiology is 2-3 times more likely in children Most common cause in infants and young children is RSV with a aquisition of droplets Causes the destruction of epithelial cells with mononuclear.

• Bacterial: Streptococcus pneumoniae past neonatal A viral ifection can set up the infection Bacteria defense vascular engorgement edema and a fibrinopurulent respiratory failure which sets up sepsis in the body

Clinical Presentation and Prevention of Pneunomia Childhood

• Viral: cough and no fever; normal WBC count and Mild to high fever Physical Examination: respiratory rate and oxygen saturation

• Bacterial: Preceding viral illness -Elevated temperature, absolute neutrophil counts and Followed by fever with chills and rigors, shortness of breath

Clinical : childhood Childhood immunization and segmental or lobar Procalcitonin MOST SPE

ATYPICAL PNEUMONIA in Childhood

• Most common cause of CAP for school-age children and transmission is from person-to-person.
• Children are increasingly showing to be macrolide-resistant
• Mycoplasma microorganisms lack cell walls
• Symptoms typically resamble upper respiratory = LOW grade fever

Pleural Effusions

• Defined presence of fluid in the pleural space.
• Source of fluid is from blood vessels or lymphatic vessels occasionally an abscess will drain into pleural space.

TRANSUDATIVE vs EXUIDATIVE Pleural effusion

• Transudative : is clean fluid from the blood vessels
• EXUDATIVE responds to inflammation by incresing permeation due high concentration
• Transudative* examples: heart failure and Liver/kidney disorders hypoproteinemia
• EXUDATIVE* examples:high concentrations of WBC and plasma proteins parapneumonic effusions

Clinical Manifestations and Diagnosis/Treatment of Pleural Effusion

• may not affect lung function once resolved.
• Dyspnea, compression atelectasis, and pleural pain with large pleural effusions.
• Mediastinal shift and cardiovascular symptoms
• Physical Examination: decreased breath sounds, dullness to percussion on the affected side.
• Diagnosis is confirmed by chest imaging and thoracentesis that determines the type.
• Large effusions may require surgery.

Squamous Cell Cancer of Lung

• Arise from the cells that line the bronchi from mutated epithelial stem cells
• NSCLC (85%) and neuroendocrine tumors (such as small cell carcinoma
• NSCLC divided into 3 groups SCC, adenocarcinoma, largest cell

Squamous association

• Slow growing
• Pneumonia and atelectasis
• With smoking!
• Tumor location centrally - common blood in sputum.
• Tumor remain small - Tend not to metastisize to late stages if treated
• Chest pain is a LATE symptom indicating a large tumo

Tuberculosis

• Caused by Mycobacterium tuberculosis and airborne droplets Risk factors: Prolonged communicstion with HIV

Pathophysiology of TB

• Transmission of TB spreads through air with living condition
• Immunocompetent individual spreads the infection latently without knowing.

1. Person transfers airborne
2. Polymorphism 3 Immunocompetent Individual is is asymotioic 4 settings living setting After M TB, non specific and Migratory

Prevention, clinical manifestations and Diagnosis of TB

Isolated or by Screening Latent TB is asympromafic Weight lose, fever cough, loss Meningingits, Bone Pain or neurlogic Sputom Cultures Skin test xray

Treatment and Complications of TB

Mechanisms of drig exist from inconsistently and MTR

• In conclusion...* MDT are resistant 2 different drugs XDR are at least 3-4