CAP and HAP Flashcards
what is pneumonia?
Inflammation of the lung parenchyma (lower respiratory tract) of infective origin characterized by consolidation (radiographic shadowing).
what is pneumonia caused by?
bacteria
what can it be treated with?
antibiotics
what are the 3 classifications of pneumonia?
- by aetiology - primary and secondary
- by the area of lung affected - bronchopneumonia, lobar, interstitial
- by location acquired - CAP and HAP
(By aetiology )
what is primary and secondary pneumonia ?
Primary pneumonia
NO apparent pre-existing conditions that may predispose to pneumonia
Secondary pneumonia
Risk factors predisposing for pneumoniaare present (e.g. COPD, CF, viral infection HIV, aspiration of gastric acid)
Secondary (complication of some other disease):
• Viral infection (influenza, measles)
• Aspiration of food or vomiting
• Obstruction of bronchus with foreign body, neoplasm and others.
• Inhalation of poisonous gases
• Major surgery
• Severe chronic diseases (tuberculosis), malnutrition
• Hipostatics – long lying after suffering stroke
By the area of lung affected
what is: Bronchopneumonia, Lobar, Interstitial
By the area of lung affected
Bronchopneumonia
at bronchioles
Bronchopneumonia Acute inflammation of the walls of the smaller bronchial tubes, with irregular areas of consolidation due to spread of the inflammation into the peribronchiolar alveoli . The disease is usually a result of the spread of infection from the upper to the lower respiratory tract, most common caused by the bacterium Mycoplasma pneumoniae, Staphylococcus pyogenes, or Streptococcus pneumoniae. Treatment includes administration of an antibiotic, oxygen therapy, supportive measures to keep the bronchi clear of secretions, and relief of pleural pain
Lobar
lower lung
Lobar : a severe infection of one or more of the five major lobes of the lungs that, if untreated, eventually results in consolidation of lung tissue.
Streptococcus pneumoniae is the usual cause; but Klebsiella pneumoniae, Haemophilus influenzae, and other streptococci can also produce the disease. If the diagnosis is made early, appropriate antibiotic therapy is highly successful.
Interstitial
between alveoli
Interstitial: a condition of diffuse, chronic inflammation of the lungs beyond the terminal bronchioles, characterized by fibrosis and collagen formation in the alveolar walls and by the presence of large mononuclear cells in the alveolar spaces. The disease may result from a hypersensitive reaction to chemotherapy drug busulfan chlorambucil (for leukemia) , or methotrexate. It may also be an autoimmune reaction, because it often accompanies celiac disease, rheumatoid arthritis, Sjögren’s syndrome, and systemic sclerosis. X-ray films of the lungs show patchy shadows and mottling, as in bronchopneumonia. Later stages of the disease reveal bronchiectasis, dilation of the bronchi, and shrinkage of the lungs. Treatment includes bed rest, oxygen therapy, and corticosteroids. Most patients die within 6 months to a few years, usually as a result of cardiac or respiratory failure.
By location acquired
what is CAP and HAP
Community-acquired pneumonia
Infection occurred during normal life (including nursing homes)
Hospital-acquired pneumonia
Infection acquired within the hospital
Ventilator-associated pneumonia
what are the risk factors for CAP?
Age: infants who are 2 years old or younger; 65-year-old or older
Living/working in nursing home or in contact with children
Smoking (including passive)
Preexisting pathological conditions
COPD, stroke, chronic cardiovascular diseases; neurological disorders e.g., dementia
Influenza
Hospitalisation in the previous 5 years
Older subjects: weakened immune system i.e., less able to fight off infections
Babies and young children : immune systems are not yet fully developed.
Smoking: it damages the tiny hairs in the lungs that help remove germs and bacteria.
Dementia and pneumonia: The person’s ability to cope with infections and other physical problems will be impaired due to the progression of the disease, Ultimate CAP is cause of death in 2/3 of people with dementia
Aspiration pneumonia may be a devastating acute complication of stroke
Factors that after stroke may predispose to chest infection: neurological impairment, older age, unsafe swallow (difficulty with swallowing (food enter windpipe and then lung) oral health/oral pathogen ( dependence for oral care and alter oral flora leading to increased in concentration in saliva and bacteria colonization aspired into lungs), reduced mobility and have difficulty coughing
what are the common causes of pneumonia?
Streptococcus pneumoniae - gram positive (blue)
Viruses
Haemophilus influenza - gram positive (blue)
Influenza A and B
Gram Negative enteric bacilli (Escherichia coli) - pink
Mycoplasma pneumoniae
Staphylococcus aureus - gram positive (blue)
Legionella spp - gram positive (blue)
what is the pathogenesis of pneumonia? ( CAP)
1) arrival of pathogen at alveolar space
2) uncontrolled multiplication of pathogens
3) local production of cytokines primarily by alveolar macrophages
4) recruitment of neutrophils into the alveolar space and introduction of cytokines into systemic circulation
Traditional model:
CAP is thought to be caused byinhalation or aspiration of a respiratory pathogen into an otherwise sterile alveoli.
The local inflammatory response to the pathogen results inpulmonary signs and symptoms such as cough, sputum production, dyspnea, crackles, and hypoxemia.
Release of cytokines into thebloodstream leads tothe systemic signs or symptoms of pneumonia, which often include fever, fatigue, tachycardia,and leukocytosis.
Lung microbiome model:
With the discovery of the lung microbiome, the traditional model has evolved. When a respiratory pathogen arrives in the alveolar space, it likely has to compete with resident microbes to replicate.Additionally, resident microbes may also modulate the host immune response to the infecting pathogen.Hypothetically, CAP might also arise from uncontrolled replication of microbes that normally reside in the alveoli.
Full explanation:
Traditionally, CAP has been viewed as an infection of the lung parenchyma, primarily caused by bacterial or viral respiratory pathogens. In this model, respiratory pathogens are transmitted from person to person via droplets or, less commonly, via aerosol inhalation (eg, as withLegionellaorCoxiellaspecies). Following inhalation, the pathogen colonizes the nasopharynx and then reaches the lung alveoli via microaspiration. When the inoculum size is sufficient and/or host immune defenses are impaired, infection results. Replication of the pathogen, the production of virulence factors, and the host immune response lead to inflammation and damage of the lung parenchyma, resulting in pneumonia.
With the identification of the lung microbiome, that model has changed. While the pathogenesis of pneumonia may still involve the introduction of respiratory pathogens into the alveoli, the infecting pathogen likely has to compete with resident microbes to replicate. In addition, resident microbes may also influence or modulate the host immune response to the infecting pathogen. If this is correct, an altered alveolar microbiome (alveolar dysbiosis) may be a predisposing factor for the development of pneumonia.
In some cases, CAP might also arise from uncontrolled replication of microbes that normally reside in the alveoli. The alveolar microbiome is similar to oral flora and is primarily comprised of anaerobic bacteria (eg,PrevotellaandVeillonella) and microaerophilic streptococci [19-21]. Hypothetically, exogenous insults such as a viral infection or smoke exposure might alter the composition of the alveolar microbiome and trigger overgrowth of certain microbes. Because organisms that compose the alveolar microbiome typically cannot be cultivated using standard cultures, this hypothesis might explain the low rate of pathogen detection among patients with CAP.
In any scenario, the host immune response to microbial replication within the alveoli plays an important role in determining disease severity. For some patients,
a local inflammatory response within the lung predominates and may be sufficient for controlling infection.
In others, a systemic response is necessary to control infection and to prevent spread or complications, such as bacteremia.
In a minority, the systemic response can become dysregulated, leading to tissue injury, sepsis, acute respiratory distress syndrome, and/or multiorgan dysfunction.
what are the clinical symptoms of CAP?
Typical symptoms : Cough* Temperature > 38°C* Sputum production Breathlessness*, wheeze* or chest discomfort* Feeling generally unwell Less frequent: Purulent/blood stained/rust colored sputum Pleural pain* Night sweats Dyspnea Fatigue Feeling confused and disorientated Chest X-ray shows consolidation
*= lower respiratory tract infection symptoms
what are the 4 stages of pneumonia?
and explain each one of them
Consolidation
Red hepatization
Grey hepatization
Resolution
Consolidation
Alveoli filled with mixture of inflammatory exudate, bacteria and white blood cells
Occurs in the first 24 hours
Cellular exudates containing neutrophils, lymphocytes and fibrin replaces the alveolar air
Capillaries in the surrounding alveolar walls become congested
The infections spreads to the hilum and pleura fairly rapidly
Pleurisy occurs marked by coughing and deep breathing (Atkuri & King, 2006; Steyl, 2007)
Red Hepatization
Occurs in the 2-3 days after consolidation
At this point the consistency of the lungs resembles that of the liver
The lungs become hypeaemic
Alveolar capillaries are engorged with blood
Fibrinous exudates fill the alveoli
This stage is “characterized by the presence of many erythrocytes, neutrophils, desquamated epithelial cells, and fibrin within the alveoli” exudate become/ is blood-stained(Atkuri & King, 2006; Steyl, 2007)
Grey Hepatization
Occurs in the 2-3 days after Red Hepatization (thus at the 1st week of the infection)
This is an avascular stage. The lung appears “gray-brown to yellow because of fibrinopurulent exudates, disintegration of red cells, and hemosiderin”
The pressure of the exudates in the alveoli causes compression of the capillaries. “Leukocytes migrate into the congested alveoli” (Atkuri & King, 2006; Steyl, 2007) exudate is beginning to degenerate prior to breaking down color is yellowish gray
Resolution (8-9 days after infection)
This stage is characterized by the “resorption and restoration of the pulmonary architecture“.
A large number of macrophages enter the alveolar spaces.
Phagocytosis of the bacteria-laden leucocytes occurs.
“Consolidation tissue re-aerates and the fluid infiltrate causes sputum”
“Fibrinous inflammation may extend to and across the pleural space, causing a rub heard by auscultation, and it may lead to resolution or to organization and pleural adhesions” (Atkuri & King, 2006; Steyl, 2007) Consolidated exudates undergo enzymatic and cellular degradation and clearance, leading to restoration of normal structure. The exudate digested by enzymatic activity, is cleared by macrophages and by cough mechanism.
CAP: Diagnosis and Severity Assessment In Primary Care (primary)
Diagnosis
Acute illness ≤21days
Cough
At least ONE ‘symptom’ of lower respiratory tract infections
Severity Assessment CRB65 score mortality risk assessment (1 point each) Confusion (≤8 points) Respiratory rate (>30bpm) Low Blood pressure (Syst < 90 OR Diast ≤ 60 mmHg) Age ≥ 65
1+ = need hospitalization
how can you differentiate covid 19 and pneumonia?
COVID-19 viral pneumonia
if patient:
history of typical COVID-19 symptoms for about a week has loss of sense of smell (anosmia) is breathless but has no pleuritic pain has a history of exposure to known or suspected COVID-19 COVID-19 rapid guideline: managing symptoms in the community. Managing breathlessness Managing cough Managing fever Managing anxiety, delirium and agitation
Bacterial pneumonia
if patient:
becomes rapidly unwell after only a few days of symptoms does not have a history of typical COVID-19 symptoms has pleuritic pain has purulent sputum
Assess severity Home treatment or hospital admission Antibiotic treatment unclear whether the cause is bacterial or viral symptoms are more concerning high risk of complications
how can you determine severity of CAP? (primary)
symptoms
Determining Severity
CRB65
Oxygen saturation levels (< 92%)
Symptoms and signs severe shortness of breath at rest or difficulty breathing coughing up blood blue lips or face feeling cold /clammy with pale or mottled skin collapse or fainting (syncope) new confusion becoming difficult to rouse little or no urine output
