THE PNEUMONIAS BY DR A.O. ODEYEMI

OUTLINE

• Introduction

• Classification

• Epidemilogy

• Pathogenesis

• Pathology

• Risk factors

• Aetiology

• Clinical features

• Investigations

• Severity assessment

• Complications

• Differential diagnosis

• Treatment

• Prognosis

• Prevention

INTRODUCTION

• Pneumonia is defined as inflammation of the lung parenchyma

• It is an accumulation of inflammatory cells and secretions in the alveolar spaces of lung, caused by an infection.

• It is usually caused by bacteria but can also be caused by viruses and fungi.

• The infecting organism, the inflammatory response and the disturbance of gas exchange caused by alveolar involvement are responsible for clinical manifestations.

• The term pneumonia itself, however, includes other causes of inflammation of the lower respiratory air spaces, particularly the alveoli, such as acute or chronic eosinophilic pneumonia, cryptogenic organizing pneumonia, and usual interstitial pneumonia

CLASSIFICATION

• Pneumonia can be classified in various ways including; • Anatomic or radiologic distribution

• The setting or mechanism of acquisition

• The pathogen responsible

• Anatomic or radiologic distribution • Lobar pneumonia

• Bronchopneumonia

• Lobar pneumonia is a radiological and pathological term referring to homogeneous consolidation of one or more lung lobes, often with associated pleural inflammation.

• Bronchopneumonia refers to more patchy alveolar consolidation associated with bronchial and bronchiolar inflammation, often affecting both lower lobes.

CLASSIFICATION • The setting or mechanism of acquisition

• Community-acquired pneumonia (CAP)

• Health care-associated pneumonia (HCAP)

• Hospital-acquired pneumonia (HAP)

• Ventilator-associated pneumonia (VAP)

• Aspiration pneumonia

• Pneumonia in the immunocompromised host

• CAP is defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital

• HCAP is defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital in patients with increased risk of exposure to multidrug resistant (MDR) bacteria as a cause of infection.

• HAP is defined as pneumonia that develops at least 48 hours after admission to a hospital and is characterized by increased risk of exposure to MDR organisms as well as gram-negative organisms.

• VAP is defined as pneumonia that develops more than 48 hours after endotracheal intubation or within 48 hours of extubation.

• Aspiration pneumonia develops after the inhalation of oropharyngeal secretions and colonized organisms.

• The term aspiration pneumonia refers specifically to the development of an infectious infiltrate in patients who are at increased risk of oropharyngeal aspiration

• Risk factors for the development of aspiration pneumonia includes;

1) Decreased ability to clear oropharyngeal secretions due to; • Poor cough or gag reflex,

• Impaired swallowing mechanism e.g. dysphagia in stroke patients,

• impaired ciliary transport e.g. from smoking

2) Increased volume of secretions

3) Increased bacterial burden of secretions

4) Presence of other comorbidities - Anatomic abnormalities, gastroesophageal reflux disease (GERD), achalasia.

5) Critically ill patients

• Pneumonia is also sometime classifed based on the pathogen e.g • Mycoplasma pneumonia

• Viral pneumonia

• Bacterial pneumonia

EPIDEMIOLOGY • Pneumonia is a very common disease which occurs all over

the world.

• It is however most prevalent in South Asia and sub-Saharan Africa.

• In the United States, acute lower respiratory tract infections (LRTI) cause more disease and death than any other infection

• Worldwide acute (LRTI) cause a greater burden of disease than human immunodeficiency virus (HIV) infection, malaria, cancer, or heart attacks.

• It is the single largest infectious cause of death in children worldwide.

• It is responsible for the death of 920,136 children under the age of 5 in 2015, representing 16% of all deaths of children under five years old.

• The prevalence of various pathogens and epidemiology of disease vary widely between countries and regions

• Pneumonia occurs more commonly during winter and in colder climates.

• This is most likely to be due to increased frequency of viral upper and lower respiratory infections during winter with resultant impairement of host defenses leading to bacterial superinfection.

PATHOGENESIS • Pneumonia results from the proliferation of microbial

pathogens at the alveolar level and the host’s response to those pathogens.

• Although the lung (the organ with largest epithelial surface area) is in continous contact with the external environment, the lower respiratory tract remains sterile, under normal circumstances.

• Infectious organisms reaches the lower respiratory tract in one of the following ways • by aspiration of upper airway contents

• by aerosolisation

• through blood stream

• from adjacent structures

• Aspiration of upper airway content is the commonest in the pathogenesis of pneumonia

• Viruses, atypical bacterial, tuberculosis (TB) and fungal pathogens are examples of aerosol-caused infections.

• Haematogenous spread is possible in severe bacteraemia.

• In most cases, infections originate from heart valves or from thrombophlebitis.

• Colonisation of the upper airway by potential pathogens can occur in normal hosts, especially seasonally or during epidemics with typical bacterial pathogens (i.e. Streptococcus pneumoniae).

• Once the colonisation occurs, aspiration of oropharyngeal secretion is the means by which the lower respiratory tract is inoculated.

• Aspiration of small quantities of oropharyngeal secretions occurs in approximately 50% of normal hosts during sleep and probably occurs more frequently in the setting of altered sensorium, alcohol or sedative drug use.

• The bacterial concentration of oropharyngeal secretions is very high, of the order of 10 organisms/mL, hence, aspiration of a small volume may provide a very high bacterial inoculum to the lung and once that occurs it depends on the efficiency of normal host defence mechanisms to prevent the development of pneumonia.

• Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest.

• In that situation, the alveolar macrophages initiate the inflammatory response to enhance lower respiratory tract defenses.

• The host inflammatory response, rather than proliferation of microorganisms, triggers the clinical syndrome of pneumonia.

• Inflammatory mediators released by macrophages and the newly recruited neutrophils create an alveolar capillary leak

• Even erythrocytes can cross the alveolar-capillary membrane, with consequent hemoptysis.

• The capillary leak results in a radiographic infiltrate and crackles detectable on auscultation, and hypoxemia results from alveolar filling.

• Decreased compliance due to capillary leak, hypoxemia, increased respiratory drive, increased secretions, and occasionally infection-related bronchospasm all lead to dyspnea.

• If severe enough, the changes in lung mechanics secondary to reductions in lung volume and compliance and the intrapulmonary shunting of blood may cause respiratory failure and the patient’s death.

PATHOLOGY • Classically, pneumonia evolves through four pathological

stages • Oedema

• Red hepatization

• Grey hepatization

• Resolution

RISK FACTORS • Recent influenza virus

infection

• Lung cancers

• COPD

• Bronchiectasis

• Chronic gingivitis and periodontitis

• Elderly

• HIV

• Cigarette smoking

• Upper respiratory tract infection

• Alcoholism

• Seizures

• Stroke

• Altered sensorium or coma

• Corticosteroid therapy

AETIOLGY • Potential aetiologic agents in CAP includes bacteria, fungi,

and viruses

• Pneumonia can be potentially caused by any bacteria particularly in the immunocompromised individual

• The most common cause of Pneumonia is Streptococcus pneumoniae

• Patients with HAP and VAP are more likely to be infected by an antibiotic resistant bacteria.

• HCAP represents a transition between classic CAP and typical HAP.

• Most cases of CAP are caused by relatively few pathogens including; • Streptococcus pneumoniae • Mycoplasma pneumoniae • Haemophilus influenzae • Chlamydia pneumoniae • Staphylococcus aureus • Legionella spp. • Gram-negative bacilli e.g Klebsiella Pneumoniae • Respiratory viruses e.g. Influenza A & B viruses, RSV, PIV e.t.c.

HOST FACTORS ASSOCIATED WITH SPECIFIC PATHOGENIC CAUSES OF PNEUMONIA UNDERLYING CONDITION ASSOCIATED MICROORGANISM

Active smoking/chronic obstructive lung disease

Streptococcus pneumoniae, Haemophilus influenzae, Legionella pneumophila, Moraxella catarrhalis, Pseudomonas aeruginosa, Chlamydophila pneumonia

Nursing home residents S. pneumoniae, gram-negative bacilli, H. influenzae, Staphylococcus aureus, Chlamydophila pneumonia, anaerobes, Mycobacterium tuberculosis

Alcoholism S. pneumoniae (including drug-resistant strains), gram-negative bacilli, anaerobes, Mycobacterium tuberculosis, Klebsiella pneumoniae, Acinetobacter species

Gross aspiration/poor dentition

Anaerobes, gram-negative enteric pathogens

Exposure to bats Histoplasma capsulatum

Exposure to birds Cryptococcus neoformans, Chlamydia psittaci, H. capsulatum

Exposure to rabbits Francisella tularensis

Exposure to farm animals Coxiella burnetii (Q fever), Viral influenza Influenza, S. aureus, S. pneumoniae, H. influenzae

Bronchiectasis, cystic fibrosis

Pseudomonas aeruginosa, Burkholderia cepacia, S. aureus, Aspergillus species, Mycobacterium avium complex

Lung abscess CA-MRSA, oral anaerobes, endemic fungal pneumonia, M. tuberculosis, atypical mycobacteria

Intravenous drug use S. aureus, anaerobes, M. tuberculosis, S. pneumoniae

Endobronchial obstruction Anaerobes

Recent antibiotic therapy Recent antibiotic therapy Drug-resistant S. pneumoniae, P. aeruginosa

HIV (early) S. pneumoniae, H. influenza, M. tuberculosis

HIV (late) The pathogens listed for early HIV infection, plus Pneumocystis jirovecii, Cryptococcus, Histoplasma, Aspergillus, atypical mycobacteria (especially M. kansasii and M. avium complex), P. aeruginosa, H. influenza

In the context of bioterrorism

Bacillus anthracis (anthrax), Yersinia pestis (plague), Francisella tularensis (tularemia)

CLINICAL FEATURES • Cough (with or without sputum production)

• Sputum may be mucoid, purulent, or blood-tinged sputum.

• Frank haemoptysis

• Pleuritic chest pain

• GI symtoms such as abdominal pain, nausea, vomiting, and/or diarrhea.

• Other symptoms may include fatigue, headache, myalgias, and arthralgias.

• Hyperthermia (fever, typically >38°C) or hypothermia (< 35°C)

• Tachypnea (>18 cycles/min)

• Use of accessory respiratory muscles

• Tachycardia (>100 bpm) or bradycardia (< 60 bpm)

• Central cyanosis

• Altered mental status

• Adventitious breath sounds, such as crackles, rhonchi, or wheezes

• Decreased intensity of breath sounds

• Egophony

• Whispering pectoriloquy

• Dullness to percussion

• Tracheal deviation

• Lymphadenopathy

• Pleural friction rub

INVESTIGATIONS • To confirm the diagnosis of pneumonia

• To identify the aetilogic agent

• Anxillary investigations

• To detect complications

• Diagnosis of pneumonia is confirmed by imaging studies

Imaging studies

• Chest radiography: The criterion standard for establishing the diagnosis of pneumonia

• Chest computed tomography scanning

• Chest ultrasonography

CXR images

AETIOLOGIC DIAGNOSIS

• Except for patients admitted to the ICU, treatment directed at specific pathogen has not been shown to be superior to empirical treatment

• Hence the benefit of establishing a microbial etiology can therefore be questioned, particularly in light of the cost of diagnostic testing

• Identifying the aetologic agent however has several benfits including;

• Identification of an unexpected pathogen allows narrowing of the initial empirical regimen, thereby decreasing antibiotic selection pressure and lessening the risk of resistance.

• Pathogens with important public safety implications, such as influenza virus, may be found in some cases.

• Culture and susceptibility data helps in monitoring trends in resistance and the development of appropriate empirical therapeutic regimens.

• Sputum M/C/S

• Bronchoscopy plus bronchoalveolar lavage

• Thoracocentesis

• Blood cultures

• Urinary antigen test (pneumococcal and legionella)

• Polymerase chain reaction

• Serology

ANCILLARY INVESTIGATIONS • E,U + Cr

• Arterial blood gas (ABG) determination

• Full blood count (FBC) with differential

• Serum free cortisol value

• Serum lactate level

• C-reactive protein (CRP)

• Procalcitonin (PCT)

SEVERITY ASSESSMENT • This uses theCURB-65 score

• One point is given for the presence of each of the following:

• C onfusion – Altered mental status

• U remia – Blood urea nitrogen (BUN) level greater than 20 mg/dL (7mmol/L)

• R espiratory rate –30 breaths or more per minute

• B lood pressure – Systolic pressure less than 90 mmHg or diastolic pressure less than 60 mmHg

• Age older than 65 years

• Patients may be treated in an outpatient setting or may require hospitalization according to their CURB-65 score, as follows:

• Score of 0-1 – Outpatient treatment

• Score of 2 – Admission to medical ward

• Score of 3 or higher – Admission to intensive care unit (ICU)

COMPLICATIONS • Destruction and fibrosis of

lung parenchyma with scarring

• Bronchiectasis

• Necrotizing pneumonia

• Frank cavitation

• Parapneumonic effusion and empyema

• Lung abscess

• Respiratory failure

• Acute respiratory distress syndrome

• Ventilator dependence

• Superinfection

• Meningitis

• Death

DIFFERENTIAL DIAGNOSIS

• Asthma

• Atelectasis

• Bronchiectasis

• Bronchiolitis

• Bronchitis

• Chronic Obstructive Pulmonary Disease (COPD)

• Foreign Body Aspiration

• Lung Abscess

TREATMENT • Antibiotics is the mainstay of therapy in bacterial pneumonia

• Intravenous fluids (and, conversely, diuretics), if indicated

• Pulse oximetry

• Oxygen supplementation

• Positioning of the patient to minimize aspiration risk

• Ventilation in patients requiring mechanical ventilation

• Antifungal (if neccessary)

• Appropriate treatment of complications

PROGNOSIS

• Prognosis depends on the patient’s age, comorbidities, and site of treatment (inpatient or outpatient).

• Young patients without comorbidity do well and usually recover fully after ~2 weeks.

• Older patients and those with comorbid conditions can take several weeks longer to recover fully

PREVENTION

• The main preventive measure is vaccination

• A pneumococcal polysaccharide vaccine (PPV23) and a protein conjugate pneumococcal vaccine (PCV13) are available for use

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