Pneumonia Lesions: CT Quantification and Impact on COVID-19 Progression

19.03.202316.07.2023 by alexxlab

How does CT quantification of pneumonia lesions predict COVID-19 severity. What are the types of pneumonia and their causes. How can healthcare professionals effectively manage pneumonia cases. What role does imaging play in pneumonia diagnosis and prognosis.

Содержание

Understanding Pneumonia: Types, Causes, and Clinical Significance

Pneumonia is a complex respiratory condition characterized by infection of the lung parenchyma. Rather than a single disease entity, it encompasses a group of syndromes caused by various organisms, resulting in diverse manifestations and outcomes. Healthcare professionals must approach pneumonia with a nuanced understanding of its multifaceted nature to ensure optimal patient care.

Types of Pneumonia

The American Thoracic Society classifies pneumonia into three main categories:

Community-Acquired Pneumonia (CAP): Infections acquired outside of a hospital setting
Hospital-Acquired Pneumonia (HAP): Infections developing 48 hours after hospital admission
Ventilator-Associated Pneumonia (VAP): Infections occurring 48 hours after endotracheal intubation

This classification system aids in identifying common causative organisms and formulating effective treatment guidelines for both inpatient and outpatient management.

Patterns of Lung Involvement

Historically, pneumonia has also been categorized based on the pattern of lung involvement:

Focal non-segmental or lobar pneumonia: Affecting a single lung lobe
Multifocal bronchopneumonia or lobular pneumonia
Focal or diffuse interstitial pneumonia

Understanding these patterns is crucial for accurate diagnosis and treatment planning.

Etiology of Pneumonia: Unraveling the Microbial Culprits

Identifying the specific causative agent in pneumonia cases is essential for effective treatment and epidemiological tracking. However, pinpointing a single cause is often challenging in clinical practice. Studies have shown that a definitive etiologic agent is identified in less than 10% of patients presenting to emergency departments with pneumonia symptoms.

Common Causative Organisms in Community-Acquired Pneumonia

CAP can be caused by a variety of microorganisms, broadly categorized as bacterial, viral, and fungal:

Bacterial Causes

Bacterial agents are further classified as “typical” and “atypical” based on their ease of culture positivity:

Typical organisms:
- Streptococcus pneumoniae (Pneumococcus)
- Haemophilus influenzae
- Moraxella catarrhalis
- Group A Streptococcus
- Aerobic and anaerobic gram-negative organisms
Atypical organisms:
- Legionella species
- Mycoplasma pneumoniae
- Chlamydia species

In the United States, the most prevalent bacterial causes of CAP include Streptococcus pneumoniae, Staphylococcus aureus, Mycoplasma pneumoniae, and gram-negative enteric bacilli.

Viral Causes

Viral agents often colonize the nasopharynx of CAP patients. While their role as primary causative agents or contributors to secondary bacterial infections is still under investigation, common viral culprits include:

Influenza virus (most frequent)
Respiratory syncytial virus
Parainfluenza virus
Adenoviruses

Fungal Causes

Fungal pneumonia is typically associated with immunocompromised states, such as HIV infection or organ transplant recipients. However, certain fungal species can cause pneumonia in immunocompetent individuals, often leading to delayed diagnosis due to oversight.

The Role of CT Imaging in Pneumonia Management

Computed Tomography (CT) plays a crucial role in the diagnosis, assessment, and prognosis of pneumonia cases, particularly in the context of COVID-19. The quantification of pneumonia lesions through CT imaging has emerged as a valuable tool for predicting disease progression and severity.

CT Quantification of Pneumonia Lesions

CT scans provide detailed imaging of lung parenchyma, allowing for precise quantification of pneumonia lesions. This quantification process involves:

Identifying areas of lung opacity or consolidation
Measuring the volume and distribution of affected lung tissue
Assessing the density and characteristics of pneumonia lesions
Tracking changes in lesion size and appearance over time

How does CT quantification contribute to patient care? By providing objective measurements of disease extent and progression, CT quantification enables healthcare professionals to make more informed decisions regarding treatment strategies and patient management.

Predictive Value in COVID-19 Progression

Recent studies have highlighted the significance of early CT quantification in predicting the progression of COVID-19 to severe illness. What specific findings indicate a higher risk of severe disease?

Extensive ground-glass opacities
Rapid progression of lesion size and number
Involvement of multiple lobes
Presence of consolidations

By identifying these high-risk features early in the disease course, clinicians can implement more aggressive treatment protocols and closer monitoring for patients at risk of developing severe COVID-19.

Diagnostic Approaches in Pneumonia: Beyond Imaging

While CT imaging provides valuable insights, a comprehensive diagnostic approach to pneumonia involves multiple modalities. What other diagnostic tools and techniques are essential in pneumonia management?

Clinical Assessment

A thorough clinical evaluation remains the cornerstone of pneumonia diagnosis. Key components include:

Detailed patient history, including onset and progression of symptoms
Physical examination, with particular attention to respiratory findings
Assessment of vital signs and oxygenation status

Laboratory Tests

Various laboratory investigations aid in diagnosis and guide treatment decisions:

Complete blood count (CBC) to assess for leukocytosis or leukopenia
C-reactive protein (CRP) and procalcitonin levels as markers of inflammation
Blood cultures to identify bacteremia
Sputum gram stain and culture for pathogen identification
Molecular tests for viral and atypical pathogens

Radiographic Imaging

While CT provides detailed information, chest X-rays remain a valuable initial imaging modality:

Faster and more readily available than CT
Useful for identifying lobar consolidations and pleural effusions
Allows for monitoring of treatment response

Management Strategies for Pneumonia: A Tailored Approach

Effective management of pneumonia requires a tailored approach based on the type of pneumonia, causative organism, and patient factors. What are the key considerations in developing a comprehensive treatment plan?

Antimicrobial Therapy

The choice of antimicrobial agents depends on several factors:

Suspected or confirmed pathogen
Local antimicrobial resistance patterns
Patient’s risk factors and comorbidities
Severity of illness

For community-acquired pneumonia, empiric therapy often includes:

Beta-lactam antibiotics (e.g., amoxicillin, ceftriaxone)
Macrolides (e.g., azithromycin) for atypical coverage
Fluoroquinolones in select cases

Supportive Care

Alongside antimicrobial therapy, supportive measures play a crucial role:

Oxygen therapy to maintain adequate oxygenation
Fluid management to ensure proper hydration
Antipyretics for fever control
Chest physiotherapy to promote airway clearance

Monitoring and Follow-up

Regular assessment of treatment response is essential:

Clinical evaluation of symptom improvement
Serial chest imaging to track resolution of infiltrates
Laboratory tests to monitor inflammatory markers
Adjustment of therapy based on clinical course and culture results

Pneumonia in the Context of COVID-19: Special Considerations

The COVID-19 pandemic has brought unique challenges to pneumonia management. How does the approach to COVID-19 pneumonia differ from traditional pneumonia cases?

Distinct Pathophysiology

COVID-19 pneumonia often presents with:

Bilateral, peripheral ground-glass opacities on imaging
Rapid progression to acute respiratory distress syndrome (ARDS)
Potential for cytokine storm and multisystem involvement

Treatment Modalities

Management of COVID-19 pneumonia may include:

Antiviral agents (e.g., remdesivir)
Corticosteroids for severe cases
Immunomodulatory therapies in selected patients
Anticoagulation to prevent thrombotic complications

Infection Control Measures

Strict infection prevention protocols are crucial:

Isolation of confirmed and suspected cases
Use of appropriate personal protective equipment (PPE)
Implementation of airborne precautions during aerosol-generating procedures

Future Directions in Pneumonia Research and Management

As our understanding of pneumonia continues to evolve, what emerging trends and technologies are shaping the future of pneumonia care?

Advanced Imaging Techniques

Innovations in imaging technology promise more precise diagnosis and monitoring:

Artificial intelligence-assisted image analysis for faster and more accurate lesion quantification
Dual-energy CT for improved characterization of lung pathology
Functional imaging techniques to assess lung perfusion and ventilation

Personalized Medicine Approaches

Tailoring treatment based on individual patient characteristics and pathogen profiles:

Genomic sequencing of pathogens for targeted antimicrobial therapy
Host biomarker profiling to predict disease severity and treatment response
Immunomodulatory therapies based on patient’s immune status

Novel Therapeutic Strategies

Ongoing research is exploring innovative treatment modalities:

Development of new antimicrobial agents to combat resistant pathogens
Inhaled antibiotics for direct delivery to the site of infection
Immunotherapy approaches to enhance host defense mechanisms
Microbiome modulation to prevent and treat pneumonia

As we continue to advance our understanding of pneumonia pathophysiology and leverage cutting-edge technologies, the future holds promise for more effective, personalized approaches to pneumonia management. The integration of advanced imaging techniques, such as CT quantification of pneumonia lesions, with comprehensive clinical assessment and emerging therapeutic strategies, will undoubtedly lead to improved outcomes for patients affected by this complex respiratory condition.

Pneumonia Pathology – StatPearls – NCBI Bookshelf

Continuing Education Activity

Pneumonia is an umbrella term for a group of syndromes caused by a variety of organisms that result in infection of the lung parenchyma. Classification schemata have helped establish the common organisms responsible for each type of pneumonia and helped to formulate treatment guidelines for efficient management, in both inpatient and outpatient settings. Optimize interprofessional team strategies to improve care coordination and communication to enhance outcomes for patients affected by pneumonia.

Objectives:

Identify the types of pneumonia.
Describe the typical exam findings in a patient with pneumonia.
Outline considerations that influence the management of pneumonia.
Summarize interprofessional team strategies for improving care coordination and communication to enhance outcomes for patients affected by pneumonia.

Access free multiple choice questions on this topic.

Introduction

Pneumonia has been defined as an infection of the lung parenchyma. Rather than looking at it as a single disease, health care professionals must remember that pneumonia is an umbrella term for a group of syndromes caused by a variety of organisms resulting in varied manifestations and sequelae.[1]

There have been many attempts to classify pneumonia based on the etiology, clinical setting in which the patent acquired the infection, and the pattern of involvement of lung parenchyma, among other classifications. This article reviews pneumonia based on the classification followed by the American Thoracic Society.

Community-Acquired Pneumonia (CAP)

Any pneumonia acquired outside of a hospital in a community setting.[2]

Hospital-Acquired Pneumonia (HAP)

Any pneumonia acquired 48 hours after being admitted in an inpatient setting such as a hospital and not incubating at the time of admission is considered as HAP. This classification helps clear the confusion surrounding the terms healthcare-associated and hospital-acquired pneumonia. Now all pneumonia acquired in the setting of assisted-living facilities, rehabilitation facilities, and other healthcare facilities have been included under community-acquired pneumonia, and a hospital setting is necessary for classifying pneumonia as HAP.[3]

Ventilator Associated Pneumonia (VAP)

Any pneumonia acquired 48 hours after endotracheal intubation is considered as VAP.[4]

These categories have helped establish the common organisms responsible for each type of pneumonia and helped to formulate treatment guidelines for the efficient management in both in-patient and out-patient setting.

Depending on the pattern of involvement, pneumonia has historically also been studied as:

Focal non-segmental or lobar pneumonia: involvement of a single lobe of the lung.
Multifocal bronchopneumonia or lobular pneumonia
Focal or diffuse interstitial pneumonia[5]

Etiology

While identifying an etiologic agent for pneumonia is essential for effective treatment as well as epidemiological record keeping, this is seldom seen in clinical practice. Widespread reviews have shown that a single cause of pneumonia has often been identified in less than 10% of patients presenting to the emergency department.[6] Nonetheless, the most common organisms causing pneumonia can be studied under the headings mentioned earlier.

Community-Acquired Pneumonia

Bacterial causes

They have been classically studied under the subheadings “typical” and “atypical” organisms in terms of ease of culture positivity. Common typical organisms include Pneumococcus, Haemophilus influenzae, Moraxella catarrhalis, Group A Streptococcus, and other aerobic and anaerobic gram-negative organisms. Atypical organisms commonly seen in clinical practice include Legionella, Mycoplasma, Chlamydia, among others.[7] In the United States, the most common bacterial causes of CAP include Streptococcus pneumoniae, Staphylococcus aureus, Mycoplasma pneumoniae, and gram-negative enteric bacilli. [8]

Viral causes

It is often observed that viral species colonize nasopharynx of patients with CAP. Whether they are the primary cause or contribute to the pathogenesis by secondary bacterial causes is still being investigated. However, some of the most frequent viral agents implicated in CAP in the United States include influenza virus followed by respiratory syncytial virus, parainfluenza virus, and adenoviruses. [8]

Fungal causes

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 unfavorable outcomes. The 3 commonest ones in North America include Histoplasma, Blastomyces, and Coccidioides. [9]

Hospital-Acquired Pneumonia and Ventilator-Associated Pneumonia

There is considerable overlap in the etiologic agents in non-ventilated hospitalized patients and ventilated patients with pneumonia, and it is, therefore, appropriate to consider them together. These include:

Gram-negative bacilli like Escherichia coli, Pseudomonas Aerugenosa, Acinetobacter, and Enterobacter among others
Gram-positive cocci like Staphylococcus aureus; both Methicillin-sensitive and resistant, although the latter is more prevalent[10][11]
Other viruses and fungi that are more prevalent in immunocompromised and severely ill patients

Epidemiology

Pneumonia is a fairly prevalent disease and carries a heavy burden in all populations. A study carried out by the US Centers for Disease Control and Prevention (CDC) aimed at estimating its burden in North America found that CAP accounted for the eighth leading cause of mortality in the United States and the seventh leading cause of mortality in Canda after adjusting for various gender and age differences.[8] One of the largest studies over a period of 2 years in a Louisville population of 587,499 adults from 2014 to 2016 found that the annual age-adjusted incidence of CAP was 649 patients hospitalized per 100,000 adults (95% confidence interval, 628. 2 to 669.8), corresponding to 1,591,825 annual adult CAP hospitalizations in the United States.[12] Moreover, the study found that the mortality during hospitalization was 6.5%, corresponding to 102,821 annual deaths in the United States. Mortality at 30 days, 6 months, and 1 year was 13.0%, 23.4%, and 30.6%, respectively. These indices were higher in economically weaker sections and in populations that were predominantly Hispanic or African-American.[12] The Community-Acquired Pneumonia Organization (CAPO) database formulated based on incidence in 16 countries clustered in 3 distinct areas, namely the United States/Canada, Europe, and Latin America found that the mortality rates in these regions were 7.3%, 9.1%, and 13.3% respectively.[13]

Data regarding incidence and prevalence of HAP and VAP are not extensive, largely because of the confounding factors related to patient comorbidities. Various estimates have proposed the incidence of VAP is about 2 to 16 episodes per 1000 ventilator days with an attributable mortality of 3% to 17%. [14] The major concern in treating HAP and VAP resides in the high prevalence of multi-drug resistance in the implicated organisms isolated from such patients. The 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.[15]

Pathophysiology

There is an intricate balance between the organisms residing in the lower respiratory tract and the local and systemic defense mechanisms (both innate and acquired) which when disturbed gives rise to inflammation of the lung parenchyma, i.e., pneumonia. Common defense mechanisms that are compromised in the pathogenesis of pneumonia include:

Systemic defense mechanisms like humoral and complement-mediated immunity that is compromised in diseases like common variable immunodeficiency (CVID), X-linked agammaglobulinemia (inherited), and functional asplenia (acquired). Impaired cell-mediated immunity predisposes individuals to infection by intracellular organisms like viruses and organisms of low virulence like Pneumocystis pneumonia (PJP), fungal causes, among others
The mucociliary clearance that is often impaired in cigarette smokers, post-viral state, Kartergerner syndrome, and other related conditions
Impaired cough reflex seen in comatose patients, certain substances of abuse
Accumulation of secretions as seen in cystic fibrosis or bronchial obstruction

The resident macrophages serve to protect the lung from foreign pathogens. Ironically, the inflammatory reaction triggered by these very 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 like neutrophils to the site of infection. They also serve to present these antigens to the T cells that trigger both cellular and humoral defense 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

The histopathology in pneumonia can be broadly studied under 2 main headings: bronchopneumonia/lobular pneumonia or lobar pneumonia.

Lobar Pneumonia

Lobar pneumonia is diffuse consolidation involving the entire lobe of the lung. Its evolvement can be broken down into 4 stages as follows:

Congestion: This stage is characterized by grossly heavy and boggy appearing lung tissue, diffuse congestion, vascular engorgement, and the accumulation of alveolar fluid rich in infective organisms. There are few red blood cells (RBC) and neutrophils at this stage.
Red hepatization: Marked infiltration of red blood cells, neutrophils, and fibrin into the alveolar fluid is seen. Grossly, the lungs appear red and firm akin to a liver, hence the term hepatization.
Gray hepatization: The RBC break down and is associated with fibrinopurulent exudates causing a red to gray color transformation.
Resolution: Characterized by clearing of the exudates by resident macrophages with or without residual scar tissue formation.

Bronchopneumonia

Bronchopneumonia is characterized by suppurative inflammation localized in patches around bronchi which may or may not be localized to a single lobe of the lung.

Very rarely, severe forms of pneumonia may result in the formation of lung abscess, a complete breakdown of tissue and formation of pus-filled pockets in focal areas of the lung. Also, the infection may spread to the pleural space forming a fibrinopurulent exudate filling this space- known as empyema.

History and Physical

Historically, the chief complaints in case of pneumonia include systemic signs like fever with chills, malaise, loss of appetite, and myalgias. These findings are more common in viral pneumonia as compared to bacterial pneumonia. A small fraction of patients may have an altered mental status, abdominal pain, chest pain, and other systemic findings. Pulmonary findings 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. Dyspnea and a diffuse heaviness of the chest are also seen occasionally.

Common findings on physical examination include:

Tachypnea
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
Dullness on percussion

Evaluation

Evaluation of CAP and HAP involves:

Clinical Evaluation

Involves performing a thorough history and physical examination as summarized in the section above.

Radiological Evaluation

According to the Infectious Diseases Society of America (IDSA) and American Thoracic Society (ATS) guidelines, a demonstratable infiltrate by chest x-ray is necessary and is considered the best method (with supportive clinical findings) for the diagnosis of pneumonia.[2] Findings may vary from lobar to interstitial infiltrate, to occasionally cavitary lesions with air-fluid levels suggestive of a more severe disease process.

Laboratory Evaluation

These include a series of tests like blood culture, sputum culture and microscopy, routine blood counts, and lymphocyte count. Special tests such as urinary antigen testing, bronchial aspirate, or induced sputum may be used for certain pathogens. Two tests, procalcitonin and C-reactive protein help differentiate viral from bacterial causes when clinical and radiological findings may not be obvious. It is also noteworthy that empiric antibiotic treatment may be initiated in all typical cases of pneumonia, and the entire battery of tests is seldom needed. [2]

Evaluation of VAP, on the other hand, is a bit different from that of CAP. It requires radiological and microbiological evidence prior to initiation of antimicrobial therapy. VAP should be suspected in ventilated patients who have new onset dyspnea, fall in oxygen saturation on the same ventilator settings, fevers with chills or new onset lung infiltrates. All suspected patients require a chest x-ray (or a CT scan if x-ray findings are inconclusive). This must be followed by invasive sampling techniques like mini broncho-alveolar lavage (BAL) or bronchoscopic BAL or even protected specimen brush (PSB) to identify causal organisms. Once the diagnosis is confirmed, the appropriate antimicrobial therapy can be initiated.[16]

Treatment / Management

Management of CAP involves initial risk stratification of the patient and to decide whether to manage the patient on an outpatient basis, in a general medicine ward, or in an intensive care unit (ICU) setting. The “CURB-65” scale has been used extensively for this purpose. The components of this scale include confusion, uremia (BUN greater than 20 mg/dl), a respiratory rate greater than 30 per minute, blood pressure less than 90 mm Hg systolic or less than 60 mm Hg diastolic, and age greater than 65. One point is awarded for every positive criterion that the patient meets. Patient disposition is decided as follows.

A score of 0 to 1: Outpatient management. These patients are treated empirically using Fluoroquinolones or Beta-lactams+ Macrolides if adverse comorbidities are present and with Macrolides or Doxycycline if no comorbidities are present.
A score of 2 to 3 indicates admission and management in a general medicine ward. The first line of treatment is a choice between fluoroquinolones or macrolides plus beta-lactams.
A score of 4 or more warrants management in an ICU. The empiric regimen, in this case, is a choice between a combination of a beta-lactam plus fluoroquinolones or beta-lactams plus macrolides. [17][2]

Management of VAP and HaP is in accordance with the ATS/IDSA guidelines. It is much more prolonged, complicated, and involves the use of broad-spectrum antibiotics as compared to the management of CAP. It involves early identification of signs of pneumonia and thorough evaluation as discussed above, before starting empiric therapy. Empiric therapy is guided by resistance patterns prevalent in that region as well as patient risk factors for multi-drug resistant organisms. Generally, regimes coving S. aureus, Pseudomonas, and gram-negative bacilli are designed for patients of HAP and VAP. For patients without MDR risk factors, the regimen generally followed is piperacillin/tazobactam plus cefepime plus levofloxacin. For patients with MDR risk factors, the preferred regime involves a combination of an Aminoglycoside along with one of imipenem, meropenem, aztreonam, piperacillin/tazobactam, ceftazidime, or cefepime.[3]

Differential Diagnosis

Differential diagnosis of pneumonia includes asthma, chronic obstructive pulmonary disease (COPD), pulmonary edema, malignancies, non-infective consolidative processes of the lung, pleuritis, pulmonary embolism, aspiration of a foreign body, bronchiectasis, bronchiolitis, and others just to name a few. In case a differentiation becomes difficult, parameters like C-reactive protein, erythrocyte sedimentation rate, procalcitonin levels, leucocyte count, and temperature may be used to establish a diagnosis.[18]

Complications

Complications of untreated or under-treated pneumonia include respiratory failure, sepsis, metastatic infections, empyema, lung abscess, and multi-organ dysfunction.[7]

Enhancing Healthcare Team Outcomes

Pneumonia is a common cause of mortality and morbidity. It can have a myriad of clinical presentations and can pose a diagnostic dilemma especially in the setting of severely ill patients with several comorbidities and underlying lung pathologies. It is vital to have a strong interplay among physicians, the ICU team, nursing staff, pharmacists, and radiologists, functioning as an interprofessional team, to improve patient outcomes. The nursing staff plays a pivotal role in recording temperature variations and other vitals that the physician needs before arriving at a diagnosis. The nursing staff has an important role to play especially in the ICU setting by maintaining clean and hygienic ventilator settings and preventing aspiration among the patients. The pharmacist has to provide the right dose and the right drugs as prescribed by the clinician. Also, the pharmacy has a special role to play in the dosing of special antibiotics like vancomycin; the clinician may want to consult with a board-certified infectious disease pharmacist and review the latest antibiogram data to decide on which antimicrobial to use. The radiologists also take center stage because of the radiological findings in the different types of pneumonia vary considerably and require expert interpretation. The current guidelines for the management of CAP, VAP, and HAP are laid down by the American Thoracic Society in conjunction with the Infectious Diseases Society of America and are reviewed periodically.[2][3] [Level 1] With an interprofessional paradigm pneumonia outcomes for patients will be optimized, leading to a quicker recovery. [Level 5]

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Figure

Ventilator associated pneumonia
Aspiration Pneumonia. Contributed by Melvil (CC By S.A. 4.0 https://creativecommons.org/licenses/by-sa/4.0/deed.en)

Figure

Aspiration pneumonia. Image courtesy O.Chaigasame

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Lung pneumonia with fibrosis. Contributed by Fabiola Farci, MD

References

1.: Mackenzie G. The definition and classification of pneumonia. Pneumonia (Nathan). 2016;8:14. [PMC free article: PMC5471962] [PubMed: 28702293]
2.: Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, Dowell SF, File TM, Musher DM, Niederman MS, Torres A, Whitney CG., Infectious Diseases Society of America. American Thoracic Society. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis. 2007 Mar 01;44 Suppl 2(Suppl 2):S27-72. [PMC free article: PMC7107997] [PubMed: 17278083]
3.: Kalil AC, Metersky ML, Klompas M, Muscedere J, Sweeney DA, Palmer LB, Napolitano LM, O’Grady NP, Bartlett JG, Carratalà J, El Solh AA, Ewig S, Fey PD, File TM, Restrepo MI, Roberts JA, Waterer GW, Cruse P, Knight SL, Brozek JL. Executive Summary: Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016 Sep 01;63(5):575-82. [PMC free article: PMC4981763] [PubMed: 27521441]
4.: Canadian Critical Care Trials Group. A randomized trial of diagnostic techniques for ventilator-associated pneumonia. N Engl J Med. 2006 Dec 21;355(25):2619-30. [PubMed: 17182987]
5.: Gharib AM, Stern EJ. Radiology of pneumonia. Med Clin North Am. 2001 Nov;85(6):1461-91, x. [PubMed: 11680112]
6.: Bartlett JG. Diagnostic tests for agents of community-acquired pneumonia. Clin Infect Dis. 2011 May;52 Suppl 4:S296-304. [PubMed: 21460288]
7.: Sattar SBA, Sharma S. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 24, 2022. Bacterial Pneumonia. [PubMed: 30020693]
8.: Jain S, Self WH, Wunderink RG, Fakhran S, Balk R, Bramley AM, Reed C, Grijalva CG, Anderson EJ, Courtney DM, Chappell JD, Qi C, Hart EM, Carroll F, Trabue C, Donnelly HK, Williams DJ, Zhu Y, Arnold SR, Ampofo K, Waterer GW, Levine M, Lindstrom S, Winchell JM, Katz JM, Erdman D, Schneider E, Hicks LA, McCullers JA, Pavia AT, Edwards KM, Finelli L., CDC EPIC Study Team. Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults. N Engl J Med. 2015 Jul 30;373(5):415-27. [PMC free article: PMC4728150] [PubMed: 26172429]
9.: Hage CA, Knox KS, Wheat LJ. Endemic mycoses: overlooked causes of community acquired pneumonia. Respir Med. 2012 Jun;106(6):769-76. [PubMed: 22386326]
10.: Weiner LM, Webb AK, Limbago B, Dudeck MA, Patel J, Kallen AJ, Edwards JR, Sievert DM. Antimicrobial-Resistant Pathogens Associated With Healthcare-Associated Infections: Summary of Data Reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2011-2014. Infect Control Hosp Epidemiol. 2016 Nov;37(11):1288-1301. [PMC free article: PMC6857725] [PubMed: 27573805]
11.: Jones RN. Microbial etiologies of hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia. Clin Infect Dis. 2010 Aug 01;51 Suppl 1:S81-7. [PubMed: 20597676]
12.: Ramirez JA, Wiemken TL, Peyrani P, Arnold FW, Kelley R, Mattingly WA, Nakamatsu R, Pena S, Guinn BE, Furmanek SP, Persaud AK, Raghuram A, Fernandez F, Beavin L, Bosson R, Fernandez-Botran R, Cavallazzi R, Bordon J, Valdivieso C, Schulte J, Carrico RM., University of Louisville Pneumonia Study Group. Adults Hospitalized With Pneumonia in the United States: Incidence, Epidemiology, and Mortality. Clin Infect Dis. 2017 Nov 13;65(11):1806-1812. [PubMed: 29020164]
13.: Arnold FW, Wiemken TL, Peyrani P, Ramirez JA, Brock GN., CAPO authors. Mortality differences among hospitalized patients with community-acquired pneumonia in three world regions: results from the Community-Acquired Pneumonia Organization (CAPO) International Cohort Study. Respir Med. 2013 Jul;107(7):1101-11. [PubMed: 23660396]
14.: Barbier F, Andremont A, Wolff M, Bouadma L. Hospital-acquired pneumonia and ventilator-associated pneumonia: recent advances in epidemiology and management. Curr Opin Pulm Med. 2013 May;19(3):216-28. [PubMed: 23524477]
15.: Shorr AF, Zilberberg MD, Reichley R, Kan J, Hoban A, Hoffman J, Micek ST, Kollef MH. Validation of a clinical score for assessing the risk of resistant pathogens in patients with pneumonia presenting to the emergency department. Clin Infect Dis. 2012 Jan 15;54(2):193-8. [PubMed: 22109951]
16.: Torres A, Niederman MS, Chastre J, Ewig S, Fernandez-Vandellos P, Hanberger H, Kollef M, Li Bassi G, Luna CM, Martin-Loeches I, Paiva JA, Read RC, Rigau D, Timsit JF, Welte T, Wunderink R. International ERS/ESICM/ESCMID/ALAT guidelines for the management of hospital-acquired pneumonia and ventilator-associated pneumonia: Guidelines for the management of hospital-acquired pneumonia (HAP)/ventilator-associated pneumonia (VAP) of the European Respiratory Society (ERS), European Society of Intensive Care Medicine (ESICM), European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and Asociación Latinoamericana del Tórax (ALAT). Eur Respir J. 2017 Sep;50(3) [PubMed: 28890434]
17.: Mbata GC, Chukwuka CJ, Onyedum CC, Onwubere BJ. The CURB-65 scoring system in severity assessment of Eastern Nigerian patients with community-acquired pneumonia: a prospective observational study. Prim Care Respir J. 2013 Jun;22(2):175-80. [PMC free article: PMC6443104] [PubMed: 23633130]
18.: Castro-Guardiola A, Armengou-Arxé A, Viejo-Rodríguez A, Peñarroja-Matutano G, Garcia-Bragado F. Differential diagnosis between community-acquired pneumonia and non-pneumonia diseases of the chest in the emergency ward. Eur J Intern Med. 2000 Dec 20;11(6):334-339. [PubMed: 11113658]

: Disclosure: Vardhmaan Jain declares no relevant financial relationships with ineligible companies.
: Disclosure: Rishik Vashisht declares no relevant financial relationships with ineligible companies.
: Disclosure: Gizem Yilmaz declares no relevant financial relationships with ineligible companies.
: Disclosure: Abhishek Bhardwaj declares no relevant financial relationships with ineligible companies.

Pneumonia Pathology – StatPearls – NCBI Bookshelf

Continuing Education Activity

Objectives:

Identify the types of pneumonia.
Describe the typical exam findings in a patient with pneumonia.
Outline considerations that influence the management of pneumonia.
Summarize interprofessional team strategies for improving care coordination and communication to enhance outcomes for patients affected by pneumonia.

Access free multiple choice questions on this topic.

Introduction

Community-Acquired Pneumonia (CAP)

Any pneumonia acquired outside of a hospital in a community setting.[2]

Hospital-Acquired Pneumonia (HAP)

Ventilator Associated Pneumonia (VAP)

Any pneumonia acquired 48 hours after endotracheal intubation is considered as VAP.[4]

Depending on the pattern of involvement, pneumonia has historically also been studied as:

Focal non-segmental or lobar pneumonia: involvement of a single lobe of the lung.
Multifocal bronchopneumonia or lobular pneumonia
Focal or diffuse interstitial pneumonia[5]

Etiology

While identifying an etiologic agent for pneumonia is essential for effective treatment as well as epidemiological record keeping, this is seldom seen in clinical practice. Widespread reviews have shown that a single cause of pneumonia has often been identified in less than 10% of patients presenting to the emergency department. [6] Nonetheless, the most common organisms causing pneumonia can be studied under the headings mentioned earlier.

Community-Acquired Pneumonia

Bacterial causes

Viral causes

Fungal causes

Hospital-Acquired Pneumonia and Ventilator-Associated Pneumonia

Gram-negative bacilli like Escherichia coli, Pseudomonas Aerugenosa, Acinetobacter, and Enterobacter among others
Gram-positive cocci like Staphylococcus aureus; both Methicillin-sensitive and resistant, although the latter is more prevalent[10][11]
Other viruses and fungi that are more prevalent in immunocompromised and severely ill patients

Epidemiology

Pneumonia is a fairly prevalent disease and carries a heavy burden in all populations. A study carried out by the US Centers for Disease Control and Prevention (CDC) aimed at estimating its burden in North America found that CAP accounted for the eighth leading cause of mortality in the United States and the seventh leading cause of mortality in Canda after adjusting for various gender and age differences.[8] One of the largest studies over a period of 2 years in a Louisville population of 587,499 adults from 2014 to 2016 found that the annual age-adjusted incidence of CAP was 649 patients hospitalized per 100,000 adults (95% confidence interval, 628.2 to 669.8), corresponding to 1,591,825 annual adult CAP hospitalizations in the United States.[12] Moreover, the study found that the mortality during hospitalization was 6.5%, corresponding to 102,821 annual deaths in the United States. Mortality at 30 days, 6 months, and 1 year was 13.0%, 23.4%, and 30.6%, respectively. These indices were higher in economically weaker sections and in populations that were predominantly Hispanic or African-American. [12] The Community-Acquired Pneumonia Organization (CAPO) database formulated based on incidence in 16 countries clustered in 3 distinct areas, namely the United States/Canada, Europe, and Latin America found that the mortality rates in these regions were 7.3%, 9.1%, and 13.3% respectively.[13]

Data regarding incidence and prevalence of HAP and VAP are not extensive, largely because of the confounding factors related to patient comorbidities. Various estimates have proposed the incidence of VAP is about 2 to 16 episodes per 1000 ventilator days with an attributable mortality of 3% to 17%.[14] The major concern in treating HAP and VAP resides in the high prevalence of multi-drug resistance in the implicated organisms isolated from such patients. The 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.[15]

Pathophysiology

There is an intricate balance between the organisms residing in the lower respiratory tract and the local and systemic defense mechanisms (both innate and acquired) which when disturbed gives rise to inflammation of the lung parenchyma, i. e., pneumonia. Common defense mechanisms that are compromised in the pathogenesis of pneumonia include:

Systemic defense mechanisms like humoral and complement-mediated immunity that is compromised in diseases like common variable immunodeficiency (CVID), X-linked agammaglobulinemia (inherited), and functional asplenia (acquired). Impaired cell-mediated immunity predisposes individuals to infection by intracellular organisms like viruses and organisms of low virulence like Pneumocystis pneumonia (PJP), fungal causes, among others
The mucociliary clearance that is often impaired in cigarette smokers, post-viral state, Kartergerner syndrome, and other related conditions
Impaired cough reflex seen in comatose patients, certain substances of abuse
Accumulation of secretions as seen in cystic fibrosis or bronchial obstruction

Histopathology

The histopathology in pneumonia can be broadly studied under 2 main headings: bronchopneumonia/lobular pneumonia or lobar pneumonia.

Lobar Pneumonia

Lobar pneumonia is diffuse consolidation involving the entire lobe of the lung. Its evolvement can be broken down into 4 stages as follows:

Congestion: This stage is characterized by grossly heavy and boggy appearing lung tissue, diffuse congestion, vascular engorgement, and the accumulation of alveolar fluid rich in infective organisms. There are few red blood cells (RBC) and neutrophils at this stage.
Red hepatization: Marked infiltration of red blood cells, neutrophils, and fibrin into the alveolar fluid is seen. Grossly, the lungs appear red and firm akin to a liver, hence the term hepatization.
Gray hepatization: The RBC break down and is associated with fibrinopurulent exudates causing a red to gray color transformation.
Resolution: Characterized by clearing of the exudates by resident macrophages with or without residual scar tissue formation.

Bronchopneumonia

Bronchopneumonia is characterized by suppurative inflammation localized in patches around bronchi which may or may not be localized to a single lobe of the lung.

History and Physical

Common findings on physical examination include:

Tachypnea
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
Dullness on percussion

Evaluation

Evaluation of CAP and HAP involves:

Clinical Evaluation

Involves performing a thorough history and physical examination as summarized in the section above.

Radiological Evaluation

Laboratory Evaluation

Treatment / Management

A score of 0 to 1: Outpatient management. These patients are treated empirically using Fluoroquinolones or Beta-lactams+ Macrolides if adverse comorbidities are present and with Macrolides or Doxycycline if no comorbidities are present.
A score of 2 to 3 indicates admission and management in a general medicine ward. The first line of treatment is a choice between fluoroquinolones or macrolides plus beta-lactams.
A score of 4 or more warrants management in an ICU. The empiric regimen, in this case, is a choice between a combination of a beta-lactam plus fluoroquinolones or beta-lactams plus macrolides. [17][2]

Differential Diagnosis

Complications

Complications of untreated or under-treated pneumonia include respiratory failure, sepsis, metastatic infections, empyema, lung abscess, and multi-organ dysfunction.[7]

Enhancing Healthcare Team Outcomes

Review Questions

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Figure

Ventilator associated pneumonia
Aspiration Pneumonia. Contributed by Melvil (CC By S.A. 4.0 https://creativecommons.org/licenses/by-sa/4.0/deed.en)

Figure

Aspiration pneumonia. Image courtesy O.Chaigasame

Figure

MAI pneumonia. Image courtesy S Bhimji MD

Figure

Lung pneumonia with fibrosis. Contributed by Fabiola Farci, MD

References

1.: Mackenzie G. The definition and classification of pneumonia. Pneumonia (Nathan). 2016;8:14. [PMC free article: PMC5471962] [PubMed: 28702293]
2.: Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, Dowell SF, File TM, Musher DM, Niederman MS, Torres A, Whitney CG., Infectious Diseases Society of America. American Thoracic Society. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis. 2007 Mar 01;44 Suppl 2(Suppl 2):S27-72. [PMC free article: PMC7107997] [PubMed: 17278083]
3.: Kalil AC, Metersky ML, Klompas M, Muscedere J, Sweeney DA, Palmer LB, Napolitano LM, O’Grady NP, Bartlett JG, Carratalà J, El Solh AA, Ewig S, Fey PD, File TM, Restrepo MI, Roberts JA, Waterer GW, Cruse P, Knight SL, Brozek JL. Executive Summary: Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016 Sep 01;63(5):575-82. [PMC free article: PMC4981763] [PubMed: 27521441]
4.: Canadian Critical Care Trials Group. A randomized trial of diagnostic techniques for ventilator-associated pneumonia. N Engl J Med. 2006 Dec 21;355(25):2619-30. [PubMed: 17182987]
5.: Gharib AM, Stern EJ. Radiology of pneumonia. Med Clin North Am. 2001 Nov;85(6):1461-91, x. [PubMed: 11680112]
6.: Bartlett JG. Diagnostic tests for agents of community-acquired pneumonia. Clin Infect Dis. 2011 May;52 Suppl 4:S296-304. [PubMed: 21460288]
7.: Sattar SBA, Sharma S. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 24, 2022. Bacterial Pneumonia. [PubMed: 30020693]
8.: Jain S, Self WH, Wunderink RG, Fakhran S, Balk R, Bramley AM, Reed C, Grijalva CG, Anderson EJ, Courtney DM, Chappell JD, Qi C, Hart EM, Carroll F, Trabue C, Donnelly HK, Williams DJ, Zhu Y, Arnold SR, Ampofo K, Waterer GW, Levine M, Lindstrom S, Winchell JM, Katz JM, Erdman D, Schneider E, Hicks LA, McCullers JA, Pavia AT, Edwards KM, Finelli L., CDC EPIC Study Team. Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults. N Engl J Med. 2015 Jul 30;373(5):415-27. [PMC free article: PMC4728150] [PubMed: 26172429]
9.: Hage CA, Knox KS, Wheat LJ. Endemic mycoses: overlooked causes of community acquired pneumonia. Respir Med. 2012 Jun;106(6):769-76. [PubMed: 22386326]
10.: Weiner LM, Webb AK, Limbago B, Dudeck MA, Patel J, Kallen AJ, Edwards JR, Sievert DM. Antimicrobial-Resistant Pathogens Associated With Healthcare-Associated Infections: Summary of Data Reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2011-2014. Infect Control Hosp Epidemiol. 2016 Nov;37(11):1288-1301. [PMC free article: PMC6857725] [PubMed: 27573805]
11.: Jones RN. Microbial etiologies of hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia. Clin Infect Dis. 2010 Aug 01;51 Suppl 1:S81-7. [PubMed: 20597676]
12.: Ramirez JA, Wiemken TL, Peyrani P, Arnold FW, Kelley R, Mattingly WA, Nakamatsu R, Pena S, Guinn BE, Furmanek SP, Persaud AK, Raghuram A, Fernandez F, Beavin L, Bosson R, Fernandez-Botran R, Cavallazzi R, Bordon J, Valdivieso C, Schulte J, Carrico RM., University of Louisville Pneumonia Study Group. Adults Hospitalized With Pneumonia in the United States: Incidence, Epidemiology, and Mortality. Clin Infect Dis. 2017 Nov 13;65(11):1806-1812. [PubMed: 29020164]
13.: Arnold FW, Wiemken TL, Peyrani P, Ramirez JA, Brock GN., CAPO authors. Mortality differences among hospitalized patients with community-acquired pneumonia in three world regions: results from the Community-Acquired Pneumonia Organization (CAPO) International Cohort Study. Respir Med. 2013 Jul;107(7):1101-11. [PubMed: 23660396]
14.: Barbier F, Andremont A, Wolff M, Bouadma L. Hospital-acquired pneumonia and ventilator-associated pneumonia: recent advances in epidemiology and management. Curr Opin Pulm Med. 2013 May;19(3):216-28. [PubMed: 23524477]
15.: Shorr AF, Zilberberg MD, Reichley R, Kan J, Hoban A, Hoffman J, Micek ST, Kollef MH. Validation of a clinical score for assessing the risk of resistant pathogens in patients with pneumonia presenting to the emergency department. Clin Infect Dis. 2012 Jan 15;54(2):193-8. [PubMed: 22109951]
16.: Torres A, Niederman MS, Chastre J, Ewig S, Fernandez-Vandellos P, Hanberger H, Kollef M, Li Bassi G, Luna CM, Martin-Loeches I, Paiva JA, Read RC, Rigau D, Timsit JF, Welte T, Wunderink R. International ERS/ESICM/ESCMID/ALAT guidelines for the management of hospital-acquired pneumonia and ventilator-associated pneumonia: Guidelines for the management of hospital-acquired pneumonia (HAP)/ventilator-associated pneumonia (VAP) of the European Respiratory Society (ERS), European Society of Intensive Care Medicine (ESICM), European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and Asociación Latinoamericana del Tórax (ALAT). Eur Respir J. 2017 Sep;50(3) [PubMed: 28890434]
17.: Mbata GC, Chukwuka CJ, Onyedum CC, Onwubere BJ. The CURB-65 scoring system in severity assessment of Eastern Nigerian patients with community-acquired pneumonia: a prospective observational study. Prim Care Respir J. 2013 Jun;22(2):175-80. [PMC free article: PMC6443104] [PubMed: 23633130]
18.: Castro-Guardiola A, Armengou-Arxé A, Viejo-Rodríguez A, Peñarroja-Matutano G, Garcia-Bragado F. Differential diagnosis between community-acquired pneumonia and non-pneumonia diseases of the chest in the emergency ward. Eur J Intern Med. 2000 Dec 20;11(6):334-339. [PubMed: 11113658]

: Disclosure: Vardhmaan Jain declares no relevant financial relationships with ineligible companies.
: Disclosure: Rishik Vashisht declares no relevant financial relationships with ineligible companies.
: Disclosure: Gizem Yilmaz declares no relevant financial relationships with ineligible companies.
: Disclosure: Abhishek Bhardwaj declares no relevant financial relationships with ineligible companies.

Degrees of lung injury: CT1, CT2, CT3, CT4

Computed tomography (CT) of the lungs is considered the “gold standard” for diagnosing pneumonia, in particular pneumonia associated with COVID-19. On tomograms – multiple scans of the respiratory organ in three planes – non-functional areas of compaction or infiltration of the lung tissue are visualized.

When talking about lung damage in pneumonia, they mean that the alveoli – small bubble-shaped cavities of the lungs, which are responsible for storing air and gas exchange, are filled with liquid, mucus, fibrous tissue and “fail”.

In the early stages, pneumonia can be almost asymptomatic or cause minor discomfort: cough, shortness of breath, fever. However, it quickly becomes more severe and the person begins to feel short of breath, chest spasm caused by pulmonary edema, or acute respiratory distress syndrome – an extensive inflammatory process that causes heart complications and in some cases leads to death.

In this regard, it is very important to recognize pneumonia in time and start treatment. CT of the lungs is the only diagnostic method that allows you to identify foci of infiltration and assess the degree of their severity, even if less than 5% of the lungs are affected.

After computed tomography of the lungs, especially if there is a suspicion of viral pneumonia, patients are primarily interested in the results and interpretation of examinations. In this article we will talk about what CT1, CT2, CT3, CT4 means in conclusion, and what you should pay attention to if pneumonia was nevertheless detected.

What does CT1, CT2, CT3, CT4 mean for COVID-19 viral pneumonia?

To enable clinicians to objectively assess the extent of lung involvement, weigh risks, and respond to challenges, a single standard for classifying viral pneumonias by severity has been adopted, where:

CT-0 — no signs of viral pneumonia;

CT-1 — mild form of pneumonia with ground glass areas, severity of pathological changes less than 25%;

CT-2 – moderate pneumonia, 25-50% of the lungs are affected;

CT-3 — moderate pneumonia, 50-75% of lungs are affected;

CT-4 — severe pneumonia, >75% of lungs affected.

The percentage of lung tissue destruction is determined by tomograms. The radiologist evaluates each of the five lobes of the lungs on a five-point scale. * If no signs of pneumonia are detected, then the value corresponds to 0; 1 point indicates 5% lung damage, and so on.

* According to the “Temporary Guidelines” of the Ministry of Health of the Russian Federation of October 2020, the scoring system for assessing lung segments and lobes adopted and described above has been abolished. The objectivity of the assessment is supported by software and medical expertise.

In other words, the abbreviation CT1, CT2, CT3 or CT4, which the radiologist writes in the conclusion, indicates the volume of non-functional lung tissue in combination with other signs characteristic of a particular stage. It is an empirical visual scale adopted by radiologists.

This computed tomography (or MSCT) lung imaging scale was only developed during the novel coronavirus pandemic. It was introduced by specialists from the Center for Diagnostics and Telemedicine of the United States, having studied CT examinations of 13,003 people who made up the main sample.

It is noteworthy that the rate of transition of pneumonia to the next, more complicated degree depends not only on the age of the patient (the older, the faster), but also on the current stage of the disease. Namely, if SARS-CoV-2 viral pneumonia was detected in a patient at the first stage (CT1), then it will be easier to prevent the transition to the next one (CT2), at least because a relatively small number of virions take more time to spread through the lungs and provoke a more extensive inflammatory process. While the transition from CT3 to CT4 is very fast, and then the life of the patient is at risk. Analyzing the already mentioned group of patients, scientists from the USA came to the conclusion that when moving to the next group, the risk of death from coronavirus increased by about 38%.

The percentage of involvement of the parenchyma (actual lesion) of the lungs in the conclusions is usually indicated approximately, so the range of values \u200b\u200bcan be quite wide, but this is not the main indicator. When determining the severity of pneumonia, other signs of pneumonia are taken into account:

1) The presence of “ground glasses” on CT scans, their localization, consolidation. “Ground glasses” are light areas of the lungs on tomograms, which indicate foci of infiltration. Dense fabric does not transmit x-rays. Ground glass is the main sign of lung damage on CT. Their prevalence and consolidation corresponds to the severe stages of pneumonia CT3 and CT4.

2) Thickening of the interlobular space of the lungs or “cobblestone symptom” – lung tissue on CT scans has an external visual resemblance to paving stones. Corresponds to the severe stage of pneumonia CT4.

3) Symptom of “reverse halo” or “rim” – looks like bright rings on tomograms. These are areas of compaction around the focus of infection. Considered a sign of organizing pneumonia.

4) Reticular changes — thin lines of pathologically altered pulmonary interstitium forming a network.

If the conclusion indicates “polysegmental pneumonia”, this means that signs of an inflammatory process were found in both lungs, in several segments.

Lung injury CT1

Lung CT scans showed less than three ground glasses. The diameter of the focus of infiltration does not exceed 3 cm, no other pathological changes in the lungs were found. The patient may have a high fever, shortness of breath, cough, sometimes there are no obvious symptoms. You can be treated for community-acquired pneumonia CT1 on an outpatient basis and at home after consulting a doctor.

Lung injury CT2

CT2 means that more than three areas of ground-glass inflammation of the lungs with a diameter of no more than 5 cm were found. As in the case of CT1, this is community-acquired pneumonia, which does not require hospitalization. The patient is treated at home, following the recommendations of the doctor. CT of the lungs will help answer the question – is there an active inflammatory process and a tendency to consolidate “frosted glasses”. If the treatment does not help, and it gets worse, it is recommended to do a second CT scan of the lungs to assess the dynamics and adjust the treatment. Since up to 50% of the lungs can be affected in a patient with moderate CT2 pneumonia, rehabilitation is necessary after the main treatment.

Lung injury CT3

Found multiple ground glass areas with a tendency to consolidation. This is the main symptom, but others are also possible: reticular changes, “tree in the kidneys” or centrilobular foci. With CT3 pneumonia, more than 50% of the lungs are affected, urgent hospitalization and intensive care are needed. Multiple infectious foci and suppressed body defenses contribute to the fact that the transition from CT3 to CT4 is faster and easier than from CT1 to CT2.

Lung injury CT4

The critical stage of lung damage, when more than 75% of the lungs do not participate in gas exchange. On tomograms, it is visualized as a diffuse lesion of the lung tissue with reticular changes and a symptom of “cobblestone pavement”, hydrothorax. The patient may need resuscitation with artificial lung ventilation (ALV).

symptoms, treatment, prevention and complications

Pneumonia or pneumonia is an acute, predominantly infectious disease in which the alveoli and lung tissue of varying severity are affected.

Causes

The most common causative agents of pneumonia are bacteria and viruses. In some cases, the trigger for the development of pneumonia are fungi and parasites.

Infectious pneumonia is mainly provoked by pneumococci, staphylococci and streptococci.

Viral inflammation of the lungs is often the result of infection with influenza or herpes viruses, rhinovirus, adenovirus, etc.

Pneumonia of fungal origin occurs against the background of damage to the lung tissue by fungi of the genus Candida and Aspergillus.

In some cases, pneumonia occurs due to the presence of two or more pathogens in the human body.

Types of pneumonia

Depending on the trigger, severity and location, pneumonia is divided into several types.

According to the nature of distribution, they are distinguished:

focal pneumonia, in which a small area of the lungs is affected;
segmental – extends to one or more sections of the lungs;
lobar, affecting only one lobe of the lung;
confluent, characterized by the fusion of the affected areas of the lung tissue;
total pneumonia, in which the entire lung is affected.

Depending on the localization, inflammation of the lungs is divided into unilateral (one of the lungs is affected) and bilateral (pathological changes are observed in both lungs).

Primary pneumonia occurs as an independent disease, triggered by the above viruses or bacteria.

Secondary pneumonia occurs as a complication against the background of a disease already present in the patient’s body (bronchitis, influenza, etc. ).

Post-traumatic pneumonia is a consequence of past chest injuries, which result in a pathological failure in lung ventilation, which leads to a complication in the form of pneumonia.

X-ray exposure used to treat cancer can lead to radiation pneumonia .

Depending on the severity of the course, pneumonia is divided into:

acute, lasting 3 weeks to 2 months;
is subacute, which usually takes 3 to 6 weeks to heal.

Also isolated in medicine is hospital-acquired pneumonia that occurs 48–72 hours after the patient’s admission to the hospital; community-acquired – developed outside the hospital or in the first 48 hours after the patient’s admission to the hospital.

Typical causative agents of pneumonia, such as pneumococci, streptococci and viruses, provoke the development of typical pneumonia. Non-standard pathogens – fungi, chlamydia, mycoplasmas – are a trigger for the development of SARS.

How is pneumonia transmitted?

Inflammation of the lungs is transmitted by airborne droplets (when sneezing, coughing) from a sick person. In some cases, pneumonia may be the result of infection migration from the upper respiratory tract (if the patient has chronic tonsillitis, sinusitis, adenoiditis).

At increased risk of developing pneumonia are:

infants who have experienced intrauterine hypoxia or asphyxia, birth trauma, with congenital immunodeficiency and lung pathologies;
children of primary and school age with chronic infectious diseases of the nasopharynx or acquired immunodeficiency;
adults with chronic lung disease, endocrine disorders, heart failure.

In addition, people who abuse alcohol and smoke tobacco have a higher chance of contracting pneumonia.

Symptoms of pneumonia

Depending on the type of pathogen, the general health of the person, and the presence of chronic diseases and / or immunodeficiency, pneumonia can occur in different ways.

The most common signs of typical pneumonia:

a sharp increase in body temperature up to 38–40 degrees;
severe cough more often with profuse purulent sputum, less often – dry and unproductive;
chest pain, shortness of breath;
General weakness, fatigue.

SARS is characterized by: dry, unproductive cough, headache, fatigue, concomitant symptoms of colds (rhinitis, sinusitis, sore throat).

Viral pneumonia at the beginning of its course is disguised as a respiratory disease – there is a slight increase in body temperature, signs of a cold. Cough, shortness of breath and pleural pain may appear on the second or third day of illness.

Diagnosis of pneumonia

Diagnosis is made on the basis of examination and examination of the patient. Initial examination may reveal weakening of breathing and the presence of characteristic wheezing.

Further laboratory and instrumental examinations are needed to determine the severity and extent of inflammation, as well as the nature of the pathogen.

As a rule, laboratory diagnostic methods are used:

general and biochemical blood tests;
general sputum analysis;
bacterial culture of sputum – to diagnose the causative agent of the disease and determine its sensitivity to antibiotics.

For hardware diagnostics:

radiographic examination;
computed or magnetic resonance imaging;
pulse oximetry (a non-invasive method of checking blood oxygen saturation, performed using a special device).

Treatment of pneumonia

Antibiotics have been and remain the main treatment for pneumonia.

The antibiotic is selected individually, depending on the severity of the course of the disease and the nature of the pathogen.

Sputum-thinning and bronchial dilating drugs are often given as maintenance treatment, either in the form of syrups or inhaled with a nebulizer.

A speedy recovery is also facilitated by the passage of physiotherapy procedures – electrophoresis, ultraviolet radiation, vibration massage.

Mild forms of pneumonia do not require hospitalization – the patient is treated on an outpatient basis, antibiotics are taken orally.

Moderate to severe inflammation should be treated in a hospital with intravenous drugs.

The course of taking antibiotics for mild pneumonia is 7-10 days. SARS is treated within 14–21 days.

After the end of therapy and complete recovery, the patient is subject to dispensary observation for one year.

Complications of pneumonia

In the event of delayed treatment of such a serious disease as pneumonia, serious complications may occur:

lung abscess;
pleurisy;
acute respiratory failure;
pulmonary edema;
sepsis;
meningitis etc.

Pneumonia Prevention

Vaccination is considered the main means of preventing pneumonia.