Management of Pneumonia

Pneumonia is a common acute respiratory infection that affects the lung parenchyma, i.e. the alveoli and distal airways in the lower respiratory tract. Rather than a single disease, pneumonia is an umbrella term for a group of syndromes caused by a variety of microorganisms resulting in varied manifestations and sequelae. It is a major health problem globally, associated with high morbidity and short and long-term mortality in all age groups.

We recently spoke to Clinical Nurse Practitioner and Associate Lecturer South East Technological University Theresa Lowry Lehnen to find out more about this common respiratory condition.

Pneumonia is broadly divided into two categories; community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP). CAP can be defined as symptoms of an acute lower respiratory tract illness (cough and at least one other lower respiratory tract symptom); new focal chest signs on examination; and at least one systemic feature, either a symptom complex of sweating, fevers, shivers, aches and pains and/or temperature of 38°C or more. Any pneumonia acquired 48 hours after admission to an inpatient setting such as a hospital and not incubating at the time of admission is classed as HAP.

Theresa explains, “Pneumonia occurs more commonly in susceptible individuals. Children < 5 years and adults > 70 years are the populations most affected. Lower respiratory tract infections (LRTIs) including pneumonia and bronchiolitis affected 489 million people globally in 2019, according to data from the 2019 Global Burden of Diseases (GBD) study.

“Aspiration pneumonia contributes 5–15% of all cases of community acquired pneumonia and is associated with worse outcomes, especially in older patients with multiple comorbidities,” she explains.

There is a lack of data about the incidence of aspiration pneumonia in patients with hospital acquired pneumonia. However Theresa adds, “In Europe, the annual incidence of CAP is estimated at 1.07–1.2 cases per 1,000 people, increasing to 14 cases per 1,000 amongst those aged 65 years and over, with a higher incidence in men. The 2019 GBD study showed that LRTI was responsible for over 2.49 million deaths, with mortality highest amongst patients over 70 years of age (1.23 million deaths).

“Pneumonia is the single largest infectious cause of death in children worldwide. 740, 180 children under the age of 5 died as a result of pneumonia in 2019, accounting for 14% of all deaths of children under five years of age and 22% of all deaths in children aged 1 to 5.

“Development of pneumonia largely depends on the host immune response, with pathogen characteristics having a less prominent role. A large variety of microorganisms including

bacteria, respiratory viruses and fungi can cause pneumonia, and there are geographical variations in their prevalence. The causative microorganisms for CAP and HAP differ significantly. The most common causative microorganisms involved in community acquired pneumonia are Streptococcus pneumoniae, Respiratory viruses, Haemophilus influenzae and other bacteria such as Mycoplasma pneumoniae and Legionella pneumophila.

“The most frequent causative microorganisms in hospital acquired pneumonia are Staphylococcus aureus (including MSSA and MRSA), Enterobacterales, non-fermenting gram-negative bacilli example, Pseudomonas aeruginosa, and Acinetobacter spp.

“Fungal infections are usually implicated in patients with certain predisposing immunocompromised states like HIV and organ transplant recipients, among others. However, often overlooked, some fungal species can cause pneumonia in immunocompetent individuals which results in a delay in diagnosis and leads to unfavourable outcomes.”

Pathophysiology

There is an intricate balance between the organisms residing in the lower respiratory tract and the local and systemic defence mechanisms (both innate and acquired), which when disturbed gives rise to inflammation of the lung parenchyma (pneumonia), Theresa told us.

“The resident macrophages serve to protect the lung from foreign pathogens. Ironically, the inflammatory reaction triggered by these macrophages is what is responsible for the histopathological and clinical findings seen in pneumonia. The macrophages engulf these pathogens and trigger signal molecules or cytokines like TNF-a, IL-8, and IL-1 that recruit inflammatory cells such as neutrophils to the site of infection. They also serve to present these antigens to the T cells that trigger both cellular and humoral defence mechanisms, activate complement and form antibodies against these organisms.

“This in turn, causes inflammation of the lung parenchyma, and makes the lining capillaries “leaky,” which leads to exudative congestion and underlines the pathogenesis of pneumonia.”

Histopathology in pneumonia can be broadly divided into bronchopneumonia/lobular pneumonia or lobar pneumonia.

Lobar Pneumonia is diffuse consolidation involving the entire lobe of the lung and its evolvement can be broken down into 4 stages:

• Congestion: This stage is characterised by heavy and wet spongy lung tissue, diffuse congestion, vascular engorgement, and the accumulation of alveolar fluid rich in infective organisms. There are few red blood cells and neutrophils at this stage.

• Red hepatisation: This stage is characterised by marked infiltration of red blood cells, neutrophils, and fibrin into the alveolar fluid. The lungs appear red and firm, similar in appearance to a liver, hence the term hepatisation.

• Gray hepatisation: The red blood cells break down and are associated with fibrinopurulent exudates causing a red to gray colour transformation.

• Resolution: This stage is characterised by clearing of the exudates by resident macrophages, with or without residual scar tissue formation.

“Bronchopneumonia is characterised by suppurative inflammation localised in patches around bronchi which may or may not be localised to a single lung lobe. Very rarely, severe forms of pneumonia may result in the formation of a lung abscess, a complete breakdown of tissue and formation of pus-filled pockets in focal areas of the lung. The infection may spread to the pleural space forming a fibrinopurulent exudate filling this space, known as empyema,” she says.

Risk Factors

CAP: Prematurity, malnutrition, household air pollution, ambient particulates or suboptimal breastfeeding are main CAPrelated risk factors in children. In adults, COPD, diabetes mellitus, cardiovascular disease and chronic liver disease are the most frequent comorbidities that increase the risk of CAP. Men have a higher risk than women, which may be explained by differences in anatomy, behavioural, socioeconomic and lifestyle factors. Immunocompromised patients have a higher risk of community acquired pneumonia than the general population. Several studies have demonstrated an association between lifestyle factors and the risk of CAP, including smoking, high alcohol consumption, being underweight due to poor-nutrition or underlying conditions that compromise the immune response, and poor living conditions.

HAP: Incidence of HAP is associated with various sociodemographic, clinical, and hospital environmental factors. Risk factors for hospital-acquired pneumonia include mechanical ventilation for > 48 h (VAP), residence in an ICU, duration of ICU or hospital stay, severity of underlying illness, and presence of comorbidities. Pseudomonas aeruginosa, Staphylococcus aureus, and Enterobacter are the most common causes of HAP.

Presentation and Diagnosis

Theresa continues, “The signs and symptoms of pneumonia are highly variable, and its clinical course can vary greatly between individuals. Symptoms may develop gradually over a number of days but may also appear much faster. Main presenting complaints include systemic signs such as fever with chills, malaise, loss of appetite, and myalgia. These findings are more common in viral compared to bacterial pneumonia.

“Pulmonary symptoms include cough with or without sputum production. Bacterial pneumonia is associated with purulent or rarely blood-tinged sputum. Viral pneumonia is associated with watery or occasionally mucopurulent sputum production. There may be an associated pleuritic chest pain with the concomitant involvement of the pleura.

“Dyspnoea and a diffuse heaviness of the chest are also occasionally seen. Common findings on physical examination include tachypnoea, tachycardia, fever with or without chills, decreased or bronchial breath sounds, egophony and tactile fremitus, both suggestive of a consolidative process, crackles on auscultation of the affected regions of the lung and dullness on percussion.”

Treatment

“Antibiotics are the mainstay therapy for pneumonia, however, the agents used depend on a variety of host and pathogen factors. Ideally, therapy should be pathogen-directed, even though a pathogen is often not identified. As therapy must be started promptly, empirical therapy directed at the most likely aetiological pathogens is required. Empiric therapy is guided by resistance patterns prevalent in the region as well as patient risk factors for multi-drug resistant organisms.

“CAP management involves initial risk assessment of the patient and clinical findings to decide whether to manage the patient at home in the community, or in a hospital setting. Health professionals should take into account disease severity and how ill the individual is; clinical observations; social circumstances including the availability of support at home; comorbidities; age; and risk of non-adherence to medication.

“While often conceptualised as an acute, completely reversible disease, numerous studies have documented that CAP patients continue to have significantly greater mortality than expected over the following 2 to 5 years, with some studies suggesting even longer-term adverse impacts and reduced quality of life. A significant proportion of the excess mortality may be due to cardiovascular disease, either myocardial infarction or stroke, and heart failure.”

Theresa adds, “The mechanisms driving the excess of cardiovascular and cardiac disease has not been definitively determined, but accelerated atherosclerosis and direct cardiac damage during acute pneumonia are both strong hypotheses. Observational studies have also demonstrated a greater burden of long-term cognitive impairment, functional impairment, and depressive symptoms after pneumonia or sepsis. In community acquired pneumonia (CAP), antibiotics are started immediately. If symptoms are not improving as expected with antibiotics, therapy should be reviewed and escalated, or hospital referral considered. Severity is assessed using the CRB-65 score.

“The need for hospital referral should be assessed, and at review, re-assessed using the CRB65 criteria. At convalescence, it is important to ensure COVID-19, influenza and pneumococcal vaccinations are up to date.”

*Alternative doxycycline dose: 100mg every 12 hours.

In non-severe infection, 200mg stat then 100mg every 24 hours can be considered.

• Pleuritic pain should be relieved using simple analgesia, and consider pulmonary embolism.

• Consider advising patients on hydration and smoking cessation where appropriate.

• Consider time off work for patients with CAP dependent on clinical assessment.

• Advise to consult pharmacist for symptom relief.

While patients should start to show improvement after 48 hours, complete recovery can be a long process and it is common for patients to experience symptoms for several weeks after treatment. Management of VAP and HAP is prolonged, complicated, and involves the use of broad-spectrum antibiotics. It involves early identification of signs of pneumonia and thorough evaluation before starting empiric therapy. In treating HAP and VAP major concerns include the high prevalence of multi-drug resistance in the implicated organisms isolated from such patients. Major risk factors to take into consideration while estimating the risk for drug resistance include patient comorbidities, recent receipt of antibiotics, functional status, and severity of illness.

Outlook

Perspective on the pathogenesis of pneumonia is changing due

to advances in microbial detection and clinical epidemiology. Theresa concludes, “Previously thought to be a sterile space, the lung is now recognised as a complex ecosystem of microbes, with equally complex relationships to their host and each other. Widespread availability of rapid molecular diagnostic testing has provided a new insight into aetiologies of pneumonia that challenges paradigms set by earlier studies from microbiology cultures.

“Biomarkers, including C-reactive peptide, procalcitonin, and newer diagnostic technologies that combine microbial detection with inflammatory patterns are improving our understanding and refine the paradigm of lung infection, but to date have still to deliver meaningful clinical interventions.

“Ultrasound is an emerging technology that has expanded in its availability of point-ofcare testing with increasingly high quality. Several studies have suggested that lung ultrasound demonstrating airspace consolidation or focal distribution of B lines may have closer alignment with the clinician diagnosis of pneumonia or CT findings than chest radiographs. However, no studies currently exist that examine whether lung ultrasound improves diagnosis or outcomes. The perceived relative advantage over chest radiographs, degree of adoption, and consistency with this technique will influence the role of this technology in the future.

“Recent radiological and clinical research has questioned long standing concepts of pneumonia, especially community-acquired pneumonia, and challenged the radiological “gold standard” of a chest radiograph. Much work is being carried out to translate recent advances in understanding of lung infection, technological advances in diagnostic tools, and the leverage of clinical data into real improvements in management options and outcomes for patients with pneumonia. Substantial changes and improvements in diagnosis and treatment options can occur through challenging existing definitions, advancing technology, and adopting research designs that accommodate the complexity of patients and host–pathogen interactions.”

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