VII. PATHOPHYSIOLOGYPLEURAL EFFUSION SECONDARY TO COMMUNITY ACQUIRED PNEUMONIA

Theoretically Based

Modifiable Factors:

Lifestyle: Smoking and Alcohol abuse Improper diet causing malnutrition

Environmental: Exposure to Pathogens: S. Pneumoniae, H. Influenza, Lagionella, P. Aureginosa, other gram (-) rods and viruses Exposure and inhalation of Secondhand smoke and other chemical pollutants

Genetics: The immunocompromised or immunosuppressed patients with low neutrophil count

Underlying Diseases: HIV/AIDS Diabetes Mellitus Cardiovascular Diseases Respiratory Diseases: Pulmonary tuberculosis and Chronic Obstructive Pulmonary Disease

Medication: Drugs that may cause Respiratory Depression: General Anesthetics, Opioids, Sedatives Drugs that may cause Immunosuppresion: Corticosteroids, Chemotherapeutic Drugs Self-medicating with antibiotics that may cause bacterial/viral resistance: Penicillin, Cephalosporins

Others: Depressed Cough Reflex

Non-Modifiable Factors:

Extremes of Age: The Very Young The Elderly (60 and Above)

Race or Ethnicity: Native Americans Native Alaskans

Gender: Male

Environmental: Inhalation of foreign materials into the lungs

Legend:

Modifiable and Non-Modifiable Risk Factors Clinical Manifestations/Signs and Symptoms

Susceptibility to bacterial invasion

Improper diet causing malnutrition

Drugs that may cause

Respiratory Depression and

Immuno-suppression:

General Anesthetics,

Opioids, Sedatives, Corticosteroids,

chemotherapeutic drugs

HIV/ADIS, DM, CVD, COPD, PTB

Excessive alcohol

intake and smoking

LIFESTYLE UNDERLYING DISEASES MEDICATIONGENETICSENVIRONMENTAL OTHERSGENDERAGERACE

Possible depressed cough and

glotic reflex More men smoke than

women

Exposure to 2nd hand

smoke and other

chemical pollutants

Exposure to pathogens:

S. Pneumoniae, H. Influenza,

Lagionella, P. Aureginosa, other gram (-) rods and

viruses

Self-medicating

with antibiotics that may

cause pathogenic resistance

The immuno-compro-mised or immuno-

suppressed patients with low

neutrophil count

MaleNative Americans and Native Alaskans

Impairment of host’s immune defenses

Highest morbidity

and mortality

rate Alterations in normal

flora

Inhalation of foreign materials

Decreased Immune response or immunesuppression

Decreased/Disruption of mucocilliary and macrophage activity

Decreased cough reflex

Bacterial invasion into the lungs and lower respiratory tract (trachea > bronchus > bronchioles > alveoli)

↑ WBC

Inflammatory response

Aspiration of bacteria in lower respiratory tract

Immune response triggered

FeverVasodilation and capillary permeability

Stimulate release of prostaglandinRelease of chemical mediators (Histamine, Bradykinin, etc.)

Lymphocytes produce cytokines

Release of killer T-Cells, macrophages, phagocytes and

anti-bodies

ChillsFluid shifting and edema Migration to alveoli

Alveolar O2 tension

Altered ventilation and diffusion

Exudate/Fluid accumulation in alveoli

Purulent exudate formation

Killer T-Cells, macrophages, phagocytes and anti-bodies take

effect to pathogens

Crackles

Cough with purulent yellowish secretions

Dyspnea

Filling of WBC in alveoli and the normally air containing space

Chest pain

Partial occlusion of bronchi and alveoli

Decrease oxygen level of blood that passes on the lungs

Venous blood entering pulmonary circulation passes unventilated area

Ventilation and Perfusion mismatch

Poorly oxygenated blood travels to the left side of the heart

Circulating O2

Hypoxia

Arterial hypoxemia

Oxygen demand

Altered Tissue Perfusion

Cerebral hypoxia

Headache, dizziness, fatigue, lethargy, restlessness,

confusion, irritability, loss of appetite, mood swings

Cyanosis

CNS AlterationsPallor

↑ Respiratory Rate

Hyperventilation↑ RBC

Difficulty of breathing and shortness of breath

Use of accessory muscles

↑ Heart Rate

Hemoptysis

Pulmonary consolidation

Alveolar collapse

Alveolar damage

Further damage to other lung parenchyma near the affected part

Atelectasis

Continuous exudates/fluid accumulation

Hypoventilation

Pulmonary neutrophilia

Apoptosis of other phagocytes

Secondary necrosis of other phagocytes

↑ Permeability of pleural capillary membrane

Inflammation

Altered fluid absorption

Empyema

Pale, Yellow, Cloudy Exudate; ↑Protein; ↑ WBC; ↓pH

Accumulation of fluid in pleural space

Ventilation-perfusion mismatch

Compromised cardiac output

Lung tissue compression

↑ Oncotic pressure

↑ Thoracic cavity size and ↓ lung size

↓ Lung expansion

Further accumulation of exudates in pleural space

↑Protein in Pleural fluid

Flattening or inversion of the diaphragm

Mediastinal compression

Chest pain

Arterial hypoxemia

Dullness in percussion

Irritation of pleural surfaces Non-productive cough

↓ or absent tactile fremitus

Dyspnea

> 150-200ml

↓ Total lung capacity, functional residual capacity,

force vital capacity

↓ Gas-exchange capacity

Compromised breathing

↓ Lung compliance

Atelectasis

↓ Breath sounds on affected area

Difficulty in taking deep breaths

Shallow breaths

Ventilatory restriction

Unmanaged effusion

Hypoxemia

Tachypnea

Hypoxia

Source:Focus on Pathophysiology by Bullock and Henze pp253-285 & 572-573Medical-Surgical Nursing by Brunner and Suddarth pp328-330 & 574