Infecciones pulmonares hraepy

Infecciones PulmonaresDr.Héctor Domínguez Hernández

Médico Residente Imagenología, Diagnóstica y Terapéutica

Introducción

• Mecanismo de defensa.

• Activación de sistemas inmunitario y humoral.

• Neumonía.

Fundamentals of Diagnostic Radiology. Fourth Edition. William E. Brant. Clyde A Helms. 2012

Anatomía

High Resolution Computed Tomography of the Lungs: A Practical Guide14

Figures 1-21A and B Schematic of acini and alveolus

Figure 1-22 Schematic of tracheobronchial tree

A B

SECONDARY PULMONARY LOBULE

The most useful subsegmental unit of the lung in terms of HRCT is the secondary pulmonary lobule (SPL). Defined as the smallest

unit of lung function marginated by connective tissue septae. It is a polyhedral structure that measures approximately 1-2.5 cm on each side, and is supplied by 3-5 terminal bronchioles, and therefore include 5-17 acini within the borders formed by interlobular septa. The secondary pulmonary lobule is divided into core and septal structures, the core structures include the pulmonary arteriole,

High Resolution Computed Tomography of the Lungs: A Practical Guide14

Figures 1-21A and B Schematic of acini and alveolus

Figure 1-22 Schematic of tracheobronchial tree

A B

SECONDARY PULMONARY LOBULE

The most useful subsegmental unit of the lung in terms of HRCT is the secondary pulmonary lobule (SPL). Defined as the smallest

unit of lung function marginated by connective tissue septae. It is a polyhedral structure that measures approximately 1-2.5 cm on each side, and is supplied by 3-5 terminal bronchioles, and therefore include 5-17 acini within the borders formed by interlobular septa. The secondary pulmonary lobule is divided into core and septal structures, the core structures include the pulmonary arteriole,

Computed Tomography Techniques and Anatomy 15

terminal bronchiole–termed as centrilobular artery and bronchus, and accompanying lymphatics. The septal structures include pulmonary veins, lymphatics and the septum itself (Figure 1-23).

Normally they are visible over the upper lobes, the anterior and lateral aspects of right middle lobe, lingula, and along the dia-phragmatic surface of lower lobes, the centrilobular arteries and bronchus branch dichotomously within the secondary pulmonary lobule (SPL) producing interlobular arteries, respiratory bronchi-oles and acinar arteries. Terminating in pulmonary gas exchange unit.

Interlobular SeptaeSecondary lobules are marginated by septae which extend inward from the pleural surface. These septae are well defined in the anterior, lateral and diaphragmatic surface, they measure about 100 mmu (0.1 mm) in the subpleural location. Few normal septae are often visible on routine HRCT. They appear as thin straight lines of uniform thickness and are 1-2 cm long.

In central lung these septae are thinner and less well defined (Figure 1-24).

Lobular CoreThe HRCT appearances and the visibility of structures in the core are determined by the size. Secondary lobule is supplied by arteries and bronchioles that measure approximately 1 mm in diameter, intralobular bronchioles and arteries measure 0.7 mm. Acinar bronchioles and arteries measure 0.5 mm. The visible lobular core structures do not extend to the pleural surface.

Important rule to remember is that on routine HRCT intralobular bronchioles are not normally visible and bronchioles are normally not seen within 2-3 cm of pleural surface.

It is necessary to identify the peripheral pulmonary arteries to define the center of the pulmonary lobule.

The substance of the secondary lobule which surrounds the lobular core and is contained within the interlobular septae consists of functioning lung parenchyma namely the alveoli, alveolar ducts,

Figure 1-23 Schematics of secondary pulmonary lobule and alveoli

UNIDAD FUNCIONAL BÁSICA

Alveolar Pneumonia

Excursus: Alveolar Pattern

Alveolar pneumonias can be subdivided according to their distri-bution pattern as follows:" Lobar pneumonia" Bronchopneumonia" Focal pneumonia

The following section will examine the basic “alveolar” pattern(Fig. 3.5). First, the radiologic term “alveolar shadow” requiressome explanation. “Alveolar” describes changes leading to in-creased attenuation in the region of the alveoli or caused by dis-orders of the alveolar space. Causes include:" Intra-alveolar edema (Fig. 3.6)" Inflammatory alveolar congestion (Fig. 3.8)" Other consolidation of the alveolar space such as proteinosis or

tumor spread (Fig. 3.7)

Other causes of increased radiodensity in the alveolar space in-cluded under the term “alveolar shadow”with somewhat less jus-tification include:" Collapse of the alveoli" Thickening of the alveolar wall in fibrosis

The radiographic signs indicative of increased alveolar radiodensi-ty are rarely defined clearly and comprehensively, and they causeproblems especially for the beginner. Radiographic signs of alveo-lar infiltrate (and of other alveolar processes) include:" The classic acinar pattern" Blurring of anatomic structures" Ground-glass opacification" Homogeneous area consolidation" With or without air bronchogram

The most important CT signs of alveolar processes include:" Ground-glass opacities" Area consolidations

In defining these alveolar shadow signs one should consider, as ina differential diagnosis, findings that simulate alveolar patterns.The same applies to the CT patterns.

Acinar Pattern

Acinar pattern (Fig. 3.9) is the term used to describe the dissemi-nated occurrence of tiny nodular shadows. This does not meanthat individual consolidated lobules are directly visualized on theradiograph. They are too small and would escape detection. Theradiographic sign is a summation effect produced by several su-perimposed lobules similar to the effect of vessel imaged end-on.The acinar pattern is difficult to distinguish from micronodularchanges due to other causes (the most common of these is respi-ratory bronchiolitis-interstitial lung disease in chronic smokerʼsbronchitis).

Alveolar space

Alveolar space

Alveolar space

1

23

4

Fig. 3.5 Interstitial and alveolar compartments. The air-filled alveolar spaceis subdivided by the interstitium, a space filled with collagen connective tissuebetween blood and lymph vessels.1 Surfactant2 Erythrocyte3 Vascular endothelium4 Interstitium

3 Pneumonia

104

de 22

• Tener en cuenta datos clínicos asociados en hemorragia alveolar: tomade anticoagulantes, hematuria (Goodpasteur), afectación nasofaríngea(Wegener), recurrencia (hemosiderosis).

• Patologías que cursan con infiltrados difusos crónicos: proteinosis alveolar,neoplasias (carcinoma bronquioloalveolar y linfoma pulmonar), sarcoidosis.

Images for this section:

Fig. 1

Patrón Alveolar Pulmonar. Un reto diagnóstico para el Radiólogo General. SERAM. 2012

Patrón Alveolar• Aparece cuando el aire del alveolo respiratorio es sustituido por otro

material de mayor densidad.

• Signos radiológicos: Bordes mal definidos/algodonosos.

• Nódulo acinar. 5 a 10mm.

• Tendencia a la coalescencia.

• Broncograma aéreo.

• Alveolograma aéreo.

• Ocultación de vasos.

• Volumen pulmonar conservado.Patrón Alveolar Pulmonar. Un reto diagnóstico para el Radiólogo General. SERAM. 2012

de 22

Fig. 2

Distribución.

• Focal (lobar o segmentaria) en : Neumonías bacterianase

• Multifocal. Bronconeumonías y Hongos.

• Difusa. Neumonías atípicas (pneumocystis jirovecci, legionella, vírica).

Patrón Alveolar Pulmonar. Un reto diagnóstico para el Radiólogo General. SERAM. 2012

FIEBRE, DOLOR TORÁCICO Y TOSBacterias Gram +

Ancianos y Alcohólicos Esplenectomía

Lóbulos inferiores (LI) Segmentos Posteriores (LS) Distribución no segmentaria.

Empiema o Derrame 50% de los casos.


J.Manuel Cardoso. Pulmón, Pleura y Mediastino. 1999.

Representa el 80% de las NAC. 10% de las Hospitalarias.

Neumococo

Fig. 3.17 Homogeneous shadowing of the left lower lung field. The patient is a35-year-old woman with sudden severe malaise, cough, and fever. The posteroante-rior radiograph shows a homogeneous area consolidation in the left lower lung fieldthat obliterates the silhouette of the diaphragm.

Fig. 3.16 Air bronchogram in lobar pneumonia inthe right upper lobe. Homogeneous area consolida-tion of the right upper lobe with an air bronchogram.The patient is a 30-year-old man with normal heart sizeand no signs of chronic pulmonary damage.

Fig. 3.18 Infiltrate is present in the lower lobe with a significant increase involume. The lateral radiograph confirms the tentative diagnosis of lower lobe in-volvement. Marked protrusion of the oblique fissure indicative of increased volume.The findings respect the anatomic boundaries.

109

Alveolar Pneumonia

Chest Radiology: A residents Manual. 2011

Fig. 3.20 Lobar pneumonia in both lower lobes. The silhouette of the diaphragmis obliterated bilaterally in this 28-year-old woman with normal heart function. Thepatient has been intubated for respiratory failure.

Fig. 3.19 Infiltrate in the middle lobe. The posteroanterior radiograph shows arather homogeneous consolidation in the right lower lung field with a sharp hori-zontal cranial demarcation (this in itself defines middle lobe involvement). The rightcardiomediastinal silhouette is obliterated. The silhouette of the diaphragm is pre-served.

Fig. 3.21a,b Pectus excavatum simulating infiltrate in the middle lobe.

a Posteroanterior view. Right cardiac border is obliterated and a right paramedias-tinal opacity is present.

b Lateral view. Severe pectus excavatum with no sign of increased attenuation.

111

Alveolar Pneumonia


Neumonía Lobular

1 Semana

5 Semanas

Bacterias Gram +

EstafilococoNiños y Ancianos. Hospitalizados.

Endocarditis o Catéteres. Drogas IV.

Opacidades Parcheadas. Bilateral.

Abscesos 25-75%. Derrame y Empiema 50% Fístulas broncopleurales


Representa el 10% de las NAC.


Neumonía Lobulillar

436 C. Beigelman-Aubry et al.

Figure 7. Septic emboli in a patient with septicaemia caused by Staphylococcus aureus secreting Panton-Valentine leukodicin whichstarted out as a case of scrotal cellulitis with testicular abscess. Axial views with lung window: a: subpleural nodules in the right inferiorlobe; b: subpleural wedge-shaped density in the left inferior lobe centred on a feeding vessel representing a septic infarct.

Pulmonary abscess

Pulmonary abscesses, possibly with bronchopulmonary fis-tula, are seen above all in infections caused by anaerobicbacteria. CT findings show single or multiple masses,between 2 and 6 cm in diameter, with central hypoattenua-tion or cavitation representing purulent liquefying necrosis,and peripheral enhancement after intravenous contrastmedium injection. The internal wall of the abscess is usu-ally smooth, with numerous air-fluid levels and consolidationin the adjacent parenchyma in half of all cases. The mainlocalisations are those of aspiration pneumonia, which iscommonly involved in these complications, namely the pos-terior segments of the right superior and left inferior lobeand the superior segments of the inferior lobes [4].

Necrotising pneumonia or pulmonary gangrene

Necrotising pneumonia or pulmonary gangrene can besecondary to acute community-acquired pneumonia orpulmonary tuberculosis. Abscesses caused by S. aureus,K. pneumoniae and P. aeroginosa are associated with highermortality [27]. Anaerobic bacterial or even fungal infec-tions can also be the cause. It should be noted thatpleural and pulmonary complications in acute community-acquired pneumonia caused by S. aureus that secretesPanton-Valentine leukodicin, both in cases of methicillin-sensitive and resistant types, can be severe and rapid inonset (Fig. 8). On imaging, pulmonary gangrene usuallystarts with bilateral consolidation of the superior lobe, fol-lowed by the development of coalescent lucencies. The aircrescent sign may also be present.

Pneumatoceles

Pneumatoceles manifest as single or multiple thin-walledair-filled lucencies located in areas of consolidation or

Figure 8. Lung infection with Staphylococcus secreting Panton-Valentine leukodicin. Axial view with lung window. Bilateral alveolarconsolidation predominating on the right side with multiple cavities.

ground glass opacity. These lucencies are associated witha recent infection, progressively increasing in size over thefollowing days and weeks, and then resolving after weeks ormonths. They are most likely due to drainage of a necroticsite in the pulmonary parenchyma, followed by obstructionof an airway due to the check-valve mechanism. They usu-ally occur in S. aureus or P. jirovecii infections (Fig. 3), butthey can be seen in other infections including E. coli andS. pneumoniae.

Associated abnormalities

Mediastinal abnormalities

The most commonly found mediastinal abnormality is lym-phadenopathy. Where there is necrosis, tuberculosis will be

Lung infections: The radiologist´s perspective. ELSEVIER. 2012.

50% DE LAS NEUMONIAS HOSPITALARIAS.

Nódulos pequeños. Opacidades Parcheadas. Bilateral y Multifocal. Lóbulos Inferiores.

Abscesos y Cavitaciones. Derrame y Empiema.

Bacterias Gram -

Enterobacterias (Klebsiella E. Coli.

Proteus)

Haemophilus Influenzae

Alcohólicos y Ancianos

Ventilación MecánicaPseudomona Aeruginosa

EPOC. Alcoholismo.

Esplenectomía.

AncianosLegionella Pneumophila Opacificación periférica sublobular. Progresión Rápida Bilateral.

Derrame en el 30%. No se ve cavitación.

Fundamentals of Diagnostic Radiology. Fourth Edition. William E. Brant. Clyde A Helms. 2012J.Manuel Cardoso. Pulmón, Pleura y Mediastino. 1999.

Klebsiella

Chapter 16: Pulmonary Infec:tion 437

l

FIGURE 16.2. A. Frontal radiograph of an HIV-positive man with fever and progressive respiratory symptoms shows multifoc:al airspace opacities with de.o.se apical opacification with cavi-tation (m"TOWs). B. A CI' scan through the apices shows airspace opacification with left apical cavitatio.D. C. A sc:an at the level of the tracheal cariJ1a shows airspace disease in the anterior segments of right and left upper lobes with sparing of the dependent portions of lung. Bronchoscopy revealed PseudomottaS.

pyogena. Acute streptococcal pneumonia is rarely seen today, though it can occasionally complicate viral infection or streptococcal pharyngitis. Its radiographic appear-ance is similar to that of staphylococcal pneumonia, with lob-ular or segmental lower lobe opacities. The process may be complicated by abscess formation and cavitation; empyema is relatively common.

Bacilllu antlwaeis. Anthrax is caused by a sporulating gram-positive bacillus that is distributed worldwide. Naturally occurring inhalational anthrax is rare; however, anthrax has been used as an agent of bioterrorism in the United States. The primary radiographic manifestations of inhalational anthrax

are related to the underlying pathology of hemorrhagic lymphadenitis and mediastinitis accompanied by hemorrhagic pleural effusions. Conventional radiographs demonstrate mediastinal widening, hilar enlargement, and often pleural effusion. Frank areas of consolidation are not usually present but peribronchial opacities may be seen. CT scans of recent bioterrorism victims, performed in 2001 without intravenous conttast, demonsttated high-attenuation lymphadenopathy and pleural effusions secondary to hemorrhage. cr scans may show extensive adenopathy in the setting of normal radio-graphs and should be obtained if the suspicion of anthrax is high (2).

FlGURE 16.3. tUWeiiS Pneumonia. cr scans at the top of the aortic arch (A) and central pulmonary arteries (B) show a combina-tion of abscess and cavity formation (llrrowhuds) and lobular coll!lolicbtion (MrOW$). Sputum cultures showed S aurt!US pneumonia.


l







l






Opacidades Parcheadas.

Sin broncograma aéreo.Bilaterales.

Predominantemente Lóbulos Inferiores.


PSEUDOMONA

Lung infections: The radiologist’s perspective 433

pneumonia, which is usually caused by a S. pneumoniaeinfection, occurs most often in children [8].

Differential diagnosisInvolvement of the parenchyma must be distinguished frominvolvement of the pleura which may be a loculated pleuraleffusion, with or without empyema. Atelectasis without theair bronchogram sign suggests a mucoid impaction. Aspira-tion pneumonia must be considered when the lower lungis affected, either on the right or bilaterally. Lobar orsegmental consolidation may be secondary to an obstruc-tion, a pulmonary oedema, or a haemorrhage. Alveolarconsolidation can in addition be seen in organising pneu-monia, radiation pneumonia, bronchioloalveolar carcinoma[9], lymphoma, pulmonary alveolar proteinosis, and acuteinterstitial pneumonia.

Bronchopneumonia

General pointsBronchopneumonia is an infectious process that initiallycentres on the epithelium of the small airways, definedon histopathology by acute bronchial inflammation withepithelial ulceration and the formation of an endoluminaland peribronchiolar fibrinopurulent exudate. These bron-chiolar lesions are combined with peribronchiolar foci ofinflammation with a patchy distribution. The inflamma-tion can spread to the adjacent alveoli and go on toaffect the lobules, segments, or lobes. The predominantlybronchiolar and peribronchiolar localisation of inflamma-tion could be due to the presence of more virulentorganisms, resulting in more significant tissue destructionand less abundant oedema formation, with the infectionspreading more slowly to the lung [10]. The bacteriamost often involved are S. aureus, Haemophilus influen-zae, P. aeruginosa, anaerobes, and some species of fungus,especially Aspergillus. Bronchopneumonia is most commonly

encountered in nosocomial infection and these cases areusually caused by a GNB, especially P. aeruginosa or E. coli.

CT signsThickening of the bronchial walls, centrilobular nodules, andthe tree-in-bud sign are the expression of infectious bron-chiolitis. The inflammation spreads to the peribronchiolaralveoli in the form of centrilobular nodules with blurredmargins that are generally smaller than 1 cm in size, withareas of ground glass opacity or peribronchiolar consolida-tion with an acinar pattern [11] that can progress to lobular,segmental, or lobar consolidation (Fig. 2). Involvement maybe multifocal, multilobar, or diffuse. When the lobes areaffected, the findings are similar to those seen in lobar pneu-monia. There are no specific findings for different causativebacteria. Aspergillosis or atypical mycobacteriosis will beconsidered where the clinical setting supports it.

Differential diagnosisOrganising pneumonia appears in the form of alveolar conso-lidation and/or peribronchial and/or subpleural ground glassopacities. It can have a number of causes. Bronchioloalve-olar carcinoma and lymphoma can present as multifocalalveolar consolidation. This finding is seen in 30% of casesof bronchioloalveolar carcinoma and corresponds to a muci-nous histologic sub-type [9,12]. Depending on the context,multifocal alveolar consolidation may also be found in radi-ation pneumonia or acute hypereosinophilic syndrome. Incase of chronic disease, the differential diagnoses alsoinclude pulmonary alveolar proteinosis, inflammation, gran-uloma, or lipoid pneumonia [13].

Diffuse alveolar consolidation

General pointsDiffuse alveolar consolidation is suggestive of diffuse alveo-lar damage [14]. An air bronchogram sign and small pleural

Figure 2. Haemophilus influenzae bronchopneumonia and herpes virus in a nosocomial infection: a: native axial view; b: the sameanatomical area on an MIP view 5 mm thick. There are centrilobular micronodules with branching opacities and acinar pattern with lobularconsolidation, both of which are better visualised on MIP (b).

Lung infections: The radiologist’s perspective 433

pneumonia, which is usually caused by a S. pneumoniaeinfection, occurs most often in children [8].

Differential diagnosisInvolvement of the parenchyma must be distinguished frominvolvement of the pleura which may be a loculated pleuraleffusion, with or without empyema. Atelectasis without theair bronchogram sign suggests a mucoid impaction. Aspira-tion pneumonia must be considered when the lower lungis affected, either on the right or bilaterally. Lobar orsegmental consolidation may be secondary to an obstruc-tion, a pulmonary oedema, or a haemorrhage. Alveolarconsolidation can in addition be seen in organising pneu-monia, radiation pneumonia, bronchioloalveolar carcinoma[9], lymphoma, pulmonary alveolar proteinosis, and acuteinterstitial pneumonia.

Bronchopneumonia

General pointsBronchopneumonia is an infectious process that initiallycentres on the epithelium of the small airways, definedon histopathology by acute bronchial inflammation withepithelial ulceration and the formation of an endoluminaland peribronchiolar fibrinopurulent exudate. These bron-chiolar lesions are combined with peribronchiolar foci ofinflammation with a patchy distribution. The inflamma-tion can spread to the adjacent alveoli and go on toaffect the lobules, segments, or lobes. The predominantlybronchiolar and peribronchiolar localisation of inflamma-tion could be due to the presence of more virulentorganisms, resulting in more significant tissue destructionand less abundant oedema formation, with the infectionspreading more slowly to the lung [10]. The bacteriamost often involved are S. aureus, Haemophilus influen-zae, P. aeruginosa, anaerobes, and some species of fungus,especially Aspergillus. Bronchopneumonia is most commonly

encountered in nosocomial infection and these cases areusually caused by a GNB, especially P. aeruginosa or E. coli.

CT signsThickening of the bronchial walls, centrilobular nodules, andthe tree-in-bud sign are the expression of infectious bron-chiolitis. The inflammation spreads to the peribronchiolaralveoli in the form of centrilobular nodules with blurredmargins that are generally smaller than 1 cm in size, withareas of ground glass opacity or peribronchiolar consolida-tion with an acinar pattern [11] that can progress to lobular,segmental, or lobar consolidation (Fig. 2). Involvement maybe multifocal, multilobar, or diffuse. When the lobes areaffected, the findings are similar to those seen in lobar pneu-monia. There are no specific findings for different causativebacteria. Aspergillosis or atypical mycobacteriosis will beconsidered where the clinical setting supports it.

Differential diagnosisOrganising pneumonia appears in the form of alveolar conso-lidation and/or peribronchial and/or subpleural ground glassopacities. It can have a number of causes. Bronchioloalve-olar carcinoma and lymphoma can present as multifocalalveolar consolidation. This finding is seen in 30% of casesof bronchioloalveolar carcinoma and corresponds to a muci-nous histologic sub-type [9,12]. Depending on the context,multifocal alveolar consolidation may also be found in radi-ation pneumonia or acute hypereosinophilic syndrome. Incase of chronic disease, the differential diagnoses alsoinclude pulmonary alveolar proteinosis, inflammation, gran-uloma, or lipoid pneumonia [13].

Diffuse alveolar consolidation

General pointsDiffuse alveolar consolidation is suggestive of diffuse alveo-lar damage [14]. An air bronchogram sign and small pleural

Figure 2. Haemophilus influenzae bronchopneumonia and herpes virus in a nosocomial infection: a: native axial view; b: the sameanatomical area on an MIP view 5 mm thick. There are centrilobular micronodules with branching opacities and acinar pattern with lobularconsolidation, both of which are better visualised on MIP (b).

Haemophilus Influenzae

Legionella Pneumophila

Fig. 3.30 Lower-lobe infiltrate on the lateral radiograph. The patient is a43-year-old man with confirmed Haemophilus influenzae pneumonia. Findingsinclude peribronchial shadowing and nodular-to-patchy opacities in the postero-basal lower lobes. The middle thoracic vertebrae are more distinct than the lowerthoracic vertebrae because of the infiltrate.

Fig. 3.29 Bronchopneumonia in an 89-year-oldwoman with known COPD and heart failure. Thepatient presented with severe dyspnea, fever, and pro-ductive cough. Findings include left heart enlargementwith significant decompensation, redistribution ofperfusion, and Kerley lines (black arrows). Circum-scribed densities are seen in both lower lung fields.The patient was diagnosed with hypostatic pneumo-nia; the causative pathogen was Enterobacter cloacae.

117

Alveolar Pneumonia

Legionella Pneumophila

INFECCIONES MICOBACTERIANAS

Aumento asimétrico del tamaño ganglios linfáticos.

Reacción granulomatosa. Complejo de Ranke.

Mycobacterium tuberculosis

Primaria

Reactivación segmentos apicales y posteriores de los lóbulos

superiores.

Areas de consolidación de focos múltiples.

Cavitación.

Posprimaria

Fibrosis, Bronquiectasias y Pérdida de Volumen.

Hipertensión Arterial Pulmonar.

Hemoptisis. Micetoma.

Miliar


El signo radiológico más común es la consolidación homogénea y

unilateral

Aneurisma de Rasmussen

Micetoma

FISTULA BRONCOPLEURAL

Bronchopleural fistula and the role of contemporary imaging. Puja Gaur, MD, Ruth Dunne, MD, Yolonda L. Colson, MD, and Ritu R. Gill, MD. The Journal of Thoracic and Cardiovascular Surgery Volume 148, Number 1:341-7.

Neumonía Vírica

Hallazgos inespecíficosDx Exclusión

Influenza

Varicela Zóster

Embarazadas y Ancianos

NiñosVirus Sincital Respiratorio

Inmunodeprimidos

Adenovirus

Opacificación parchada. en los lóbulos inferiores que suele ser

bilateral.**

**Consolidación lobar Derrame

Cavitación

Opacidades nodulares mal definidas bilaterales y difusas de 5 a 10 mm de

diámetro.


INICIO MÁS GRADUAL, TOS NO PRODUCTIVA Y SÍNTOMAS EXTRAPULMONARES.


Engrosamiento de la pared bronquial.

Neumonía Intersticial

Common Radiologic FindingsTracheobronchitis seldom results in any radio-logic abnormalities in the acute stage; however,mucosal injury may manifest many years later asbronchiectasis. With bronchiolitis, the airway ob-struction is usually partial and results in hyperin-flation and poorly defined nodular opacities ra-diologically.

Viral pneumonia manifests radiologically aspoorly defined nodules (air-space nodules of4–10 mm in diameter) and patchy areas of peri-bronchial ground-glass opacity and air-space con-solidation. Because of the associated bronchioli-tis, hyperinflation is commonly present (4,5). Theprogressive form of pneumonia shows the rapidconfluence of consolidation leading to diffuse al-veolar damage, consisting of homogeneous orpatchy unilateral or bilateral air-space consolida-tion and ground-glass opacity or poorly definedcentrilobular nodules (9) (Fig 2).

VirusesThe respiratory viruses can be divided into twolarge groups according to the type of nucleic acidthey contain: (a) the RNA group, which includesmyxoviruses (influenza viruses and measles virus)and Hantaviruses; and (b) the DNA group, whichincludes adenoviruses and herpesviruses (herpessimplex type 1, varicella-zoster virus, cytomegalo-viruses, Epstein-Barr virus).

Various Viral Pneumonias

Influenza Virus PneumoniaInfluenza virus infection usually involves the up-per respiratory tract including the trachea andmajor bronchi in children and young adults.However, elderly and immunocompromised per-sons are at increased risk for development of ful-minant pneumonia. Influenza viruses are dividedinto three groups (A, B, and C) according to in-ternal membrane and nucleoprotein antigens. Ofthese three groups, type A and occasionally type

Figure 2. Pneumonia due to influenza virus (type C)in a 46-year-old man with dyspnea. (a) Initial chest ra-diograph shows diffuse reticulonodular areas of in-creased opacity in both lungs. (b) Follow-up chest ra-diograph obtained 15 days after a shows progression ofthe extent of disease with diffuse consolidation through-out both lungs. (c) Thin-section (1-mm collimation)computed tomographic (CT) scan obtained 16 days af-ter a at the level of the aortic arch shows diffuse ground-glass attenuation with some irregular linear areas of in-creased attenuation in both lungs. (Case courtesy of DrJung Hwa Hwang, Soonchunhyang University SeoulHospital, Korea.)

RG f Volume 22 ● Special Issue Kim et al S139

Radio

Gra

phic

s

Virus Influenza CViral Pneumonias in Adults. Radiographics. 2002

B organisms cause influenza virus pneumonia(10). Although the pneumonia is usually mild, itcan be overwhelming and fatal within 24 hours.Predisposing conditions for the infection includemitral stenosis, pregnancy, diabetes, old age, andimmunosuppression (6,11).

Histologically, airway walls are congested andlumina contain mononuclear cell infiltrates. De-generation and desquamation of the epithelialcells are seen. Parenchymal change shows typicalfeatures of diffuse alveolar damage (7,12).

Serial radiographs show poorly defined, patchyareas of air-space consolidation, 1–2 cm in diam-eter, that rapidly become confluent (Fig 2). Dif-fuse or patchy areas of ground-glass attenuationmixed with consolidation are frequently seen atCT (Fig 2). Small centrilobular nodules repre-senting alveolar hemorrhage may be associated(Fig 3). Pleural effusion is rare. The radiologicabnormalities usually resolve in approximately 3weeks (9). In one study, influenza virus pneumo-nia showed air-space consolidation or ground-glass attenuation with a lobular distribution athigh-resolution CT. Hyaline membrane forma-tion in the alveolar parenchyma around the bron-

chiole probably accounts for the predominant CTfindings of air-space consolidation or ground-glass attenuation with a lobular distribution (13).

Measles Virus PneumoniaMeasles virus infection is a disease of small chil-dren. Even with active immunization, a signifi-cant number of older individuals develop the dis-ease, probably due to combined causes of nonim-munization, vaccine failure, and exposure to theorganism in later adulthood (14). Pulmonary dis-ease from measles virus infection occurs mainly intwo forms: one is primary measles virus pneumo-nia and secondary bacterial pneumonia and theother is atypical measles virus pneumonia. Al-though measles virus can cause pneumonia in3%–4% of infected patients, the majority of af-fected patients with this organism have secondarybacterial infection. Haemophilus influenzae andNeisseria meningitidis are the most common organ-isms of the secondary bacterial infection (15).

Figure 3. Pneumonia due to influenza virus in a21-year-old man with a cough. (a) Initial chest ra-diograph shows poorly defined nodules (arrows) andreticular areas of increased opacity in both lungs.(b, c) Thin-section (1-mm collimation) CT scansobtained at the levels of the aortic arch (b) and su-prahepatic inferior vena cava (c) show multifocalperibronchovascular or subpleural consolidationand ground-glass attenuation in both lungs. Somelesions have a lobular distribution (arrows). Notethe acinar nodules (arrowheads). (Case courtesy ofJin Mo Goo, MD, PhD, Seoul National UniversityHospital, Korea.)

S140 October 2002 RG f Volume 22 ● Special IssueRadio

Gra

phic

s

B organisms cause influenza virus pneumonia(10). Although the pneumonia is usually mild, itcan be overwhelming and fatal within 24 hours.Predisposing conditions for the infection includemitral stenosis, pregnancy, diabetes, old age, andimmunosuppression (6,11).

Histologically, airway walls are congested andlumina contain mononuclear cell infiltrates. De-generation and desquamation of the epithelialcells are seen. Parenchymal change shows typicalfeatures of diffuse alveolar damage (7,12).

Serial radiographs show poorly defined, patchyareas of air-space consolidation, 1–2 cm in diam-eter, that rapidly become confluent (Fig 2). Dif-fuse or patchy areas of ground-glass attenuationmixed with consolidation are frequently seen atCT (Fig 2). Small centrilobular nodules repre-senting alveolar hemorrhage may be associated(Fig 3). Pleural effusion is rare. The radiologicabnormalities usually resolve in approximately 3weeks (9). In one study, influenza virus pneumo-nia showed air-space consolidation or ground-glass attenuation with a lobular distribution athigh-resolution CT. Hyaline membrane forma-tion in the alveolar parenchyma around the bron-

chiole probably accounts for the predominant CTfindings of air-space consolidation or ground-glass attenuation with a lobular distribution (13).

Measles Virus PneumoniaMeasles virus infection is a disease of small chil-dren. Even with active immunization, a signifi-cant number of older individuals develop the dis-ease, probably due to combined causes of nonim-munization, vaccine failure, and exposure to theorganism in later adulthood (14). Pulmonary dis-ease from measles virus infection occurs mainly intwo forms: one is primary measles virus pneumo-nia and secondary bacterial pneumonia and theother is atypical measles virus pneumonia. Al-though measles virus can cause pneumonia in3%–4% of infected patients, the majority of af-fected patients with this organism have secondarybacterial infection. Haemophilus influenzae andNeisseria meningitidis are the most common organ-isms of the secondary bacterial infection (15).

Figure 3. Pneumonia due to influenza virus in a21-year-old man with a cough. (a) Initial chest ra-diograph shows poorly defined nodules (arrows) andreticular areas of increased opacity in both lungs.(b, c) Thin-section (1-mm collimation) CT scansobtained at the levels of the aortic arch (b) and su-prahepatic inferior vena cava (c) show multifocalperibronchovascular or subpleural consolidationand ground-glass attenuation in both lungs. Somelesions have a lobular distribution (arrows). Notethe acinar nodules (arrowheads). (Case courtesy ofJin Mo Goo, MD, PhD, Seoul National UniversityHospital, Korea.)

S140 October 2002 RG f Volume 22 ● Special Issue

Radio

Gra

phic

s

Virus Influenza CViral Pneumonias in Adults. Radiographics. 2002

Varicela Zoster

Varicella-Zoster Virus PneumoniaVaricella-zoster virus pneumonia is the most seri-ous complication of disseminated varicella-zostervirus infection with mortality rates of 9%–50%(37). Reported prevalences of varicella-zoster vi-rus pneumonia have varied from less than 5% toup to 50% of all varicella infections in adults (38).Varicella-zoster virus most commonly causes self-limited benign disease (chickenpox) in children.However, in adults it tends to cause significantcomplications such as varicella-zoster virus pneu-monia. More than 90% of cases of varicella-zostervirus pneumonia in adults occur in patients withlymphoma and immunocompromised patients(39).

Histologic features of varicella-zoster viruspneumonia are those of diffuse alveolar damage.With recovery from the initial disease, sphericalnodules are seen, scattered randomly throughoutthe lung parenchyma. Histologically, the nodulesare composed of an outer, often lamellated fi-brous capsule frequently enclosing areas of hya-linized collagen or necrotic tissue. Calcificationvaries in intensity (40).

Chest radiographic findings of varicella-zostervirus pneumonia consist of multiple 5–10-mmill-defined nodules that may be confluent andfleeting. Hilar lymphadenopathy and pleural effu-sion are unusual. The small, round nodules usu-ally resolve within a week after the disappearanceof the skin lesions but may persist for months.Usually resolving in 3–5 days in milder disease,the small nodules may persist for several weeks inwidespread disease. The lesions calcify and can

persist as numerous, well-defined, randomly scat-tered, 2–3-mm dense calcifications (40,41).

High-resolution CT usually shows 1–10-mmwell-defined and ill-defined nodules diffuselythroughout both lungs (Fig 8). Nodules with asurrounding halo of ground-glass opacity, patchyground-glass opacity, and coalescence of nodulesare also seen. These findings disappear concur-rently with healing of skin lesions after antiviralchemotherapy (40).

Cytomegalovirus PneumoniaCytomegalovirus is considered a member of theherpesviruses family and can cause severe symp-tomatic pulmonary disease in immunocompro-mised patients.

It has been suggested that cytomegaloviruspneumonitis in allogenic transplant recipients iscaused by immune mechanisms mediated by a Tcell response to virally induced antigens expressedin the lungs. Severe necrotizing pneumonitis mayoccur despite suppression of virus replication dur-ing ganciclovir therapy. AIDS patients, with moreprofound immune deficiency than transplant re-cipients, may be unable to begin the immune re-sponse necessary to cause cytomegalovirus pneu-monitis by this mechanism. In AIDS patients, thelung damage may be due directly to cytopatho-genic effects of cytomegalovirus, related to theextent of active virus replication. These differ-ences in pathogenic mechanisms of pulmonarycytomegalovirus infection result in different his-topathologic features between AIDS patients andtransplant recipients. In transplant recipients withcytomegalovirus pneumonia, necrotizing inflam-mation is predominant with relatively few cyto-megalovirus-infected cells at histopathologic ex-amination. In AIDS patients with cytomegalovi-rus pneumonia, a high density of cytomegalovirusinclusion bodies is present and they are respon-sible for severe, symptomatic pneumonitis. Thecytopathogenic effect of cytomegalovirus prob-ably causes diffuse alveolar damage more fre-quently in AIDS patients than in patients withoutAIDS.

The CT findings of cytomegalovirus pneumo-nia are diverse and have been described withoutdistinction between AIDS patients and patientswithout AIDS. Common findings are mixed al-veolar-interstitial infiltrates such as ground-glassattenuation, consolidation, nodules, poorly de-fined small centrilobular nodules, bronchial dila-tation, and thickened interlobular septa (42–45)

Figure 8. Pneumonia due to varicella-zoster virus ina 30-year-old man with a fever and skin rash. Thin-section (1-mm collimation) CT scan obtained at thelevel of the bronchus intermedius shows multiple 1–2-mm-diameter nodules scattered throughout both lungs.(Courtesy of Dong Wook Sung, MD, Kyung Hee Uni-versity Hospital, Seoul, Korea.)

RG f Volume 22 ● Special Issue Kim et al S145Radio

Gra

phic

s

Viral Pneumonias in Adults. Radiographics. 2002

Sx de Swyer-James

infiltrates is very rare (48). Splenomegaly is com-mon and may be seen in up to 47% of chest ra-diographic examinations (49).

A rapidly progressive respiratory illness in in-fectious mononucleosis has rarely been reported(50).

ConclusionsThe radiologic findings of adult viral pneumoniasare variable and overlapping (Table 2). Specific-organism diagnosis of a viral pneumonia cannotbe made on the basis of imaging features alone.Clinical features such as patient age; immune sta-tus; time of year; illness in other family members;community outbreaks; onset, severity, and dura-tion of symptoms; and the presence of a rash re-main important aids in diagnosing viral causes ofboth atypical pneumonia and pneumonia in im-munocompromised patients.

Therefore, recognition of the radiologic find-ings will help narrow the differential diagnosisand the combination of clinical features can sig-nificantly improve the accuracy of diagnosis inviral pneumonias.

References1. Greenberg SB. Viral pneumonia. Infect Dis Clin

North Am 1991; 5:603–621.2. Sullivan CJ, Jordan MC. Diagnosis of viral pneu-

monia. Semin Respir Infect 1988; 3:148–161.3. Retails P, Strange C, Harley R. The spectrum of

adult adenovirus pneumonia. Chest 1996; 109:1656–1657.

4. Han BK, Son JA, Yoon HK, Lee SI. Epidemicadenoviral lower respiratory tract infection in pedi-atric patients: radiographic and clinical character-istics. AJR Am J Roentgenol 1998; 170:1077–1080.

5. Palmer SM Jr, Henshaw NG, Howell DN, MillerSE, Davis RD, Tapson VF. Community respira-tory viral infection in adult lung transplant recipi-ents. Chest 1998; 113:944–950.

6. Tillett HE, Smith JW, Clifford RE. Excess mor-bidity and mortality associated with influenza inEngland and Wales. Lancet 1980; 1:793–795.

7. Feldman PS, Cohan MA, Hierholzer WJ Jr. FatalHong Kong influenza: a clinical microbiologicaland pathological analysis of nine cases. Yale J BiolMed 1972; 45:49–63.

8. Yeldandi AV, Colby TV. Pathologic features oflung biopsy specimens from influenza pneumoniacases. Hum Pathol 1994; 25:47–53.

9. Galloway RW, Miller RS. Lung changes in therecent influenza epidemic. Br J Radiol 1959; 32:28–32.

10. Nolan TF Jr, Goodman RA, Hinman AR, et al.Morbidity and mortality associated with influenzaB in the United States, 1979–1980: a report fromthe Centers for Disease Control. J Infect Dis 1980;142:360–362.

11. Mullooly JP, Barker WH, Nolan TF. Risk of acuterespiratory disease among pregnant women duringinfluenza A epidemics. Public Health Rep 1986;101:205–211.

12. Soto PJ, Broun GO, Wyatt JP. Asian influenzalpneumonitis: a structural and virologic analysis.Am J Med 1959; 27:18–21.

13. Tanaka N, Matsumoto T, Kuramitsu T, et al.High resolution CT findings in community-ac-quired pneumonia. J Comput Assist Tomogr1996; 20:600–608.

14. Hinman AR, Orenstein WA, Block AB, et al. Im-pact of measles in the United States. Rev InfectDis 1983; 5:439–444.

15. Gremillion DH, Crawford GE. Measles pneumo-nia in young adults: an analysis of 106 cases. Am JMed 1981; 71:539–542.

16. Margolin FR, Gandy TK. Pneumonia of atypicalmeasles. Radiology 1979; 131:653–655.

17. Atmar RL, Englund JA, Hammill H. Complica-tions of measles during pregnancy. Clin Infect Dis1992; 14:217–226.

Table 2Summary of CT Findings in Viral Pneumonias

Cause of PneumoniaCentrilobular

Nodules

Ground-GlassAttenuationwith LobularDistribution

SegmentalConsolidation

ThickenedInterlobular

Septa

DiffuseGround-GlassAttenuation

Influenza virus !!! !!! ! . . . !Measles virus !! ! ! . . . !Hantavirus . . . . . . !! ! !!!Adenovirus !! ! !!! . . . . . .Herpes simplex virus ! !!! !!! . . . !Varicella-zoster virus !!! ! . . . . . . . . .Cytomegalovirus !! !! ! ! !!Epstein-Barr virus ! ! ! . . . !

Note.—Plus signs indicate the relative frequency of the findings from lowest (!) to highest (!!!).

S148 October 2002 RG f Volume 22 ● Special Issue

Radio

Gra

phic

s

Viral Pneumonias in Adults. Radiographics. 2002

Neumonía Fúngica

Hallazgos inespecíficos

Histoplasma Coccidiodes Blastomyces

Inmunocompetentes Inmunodeprimidos

Aspergillus Candida

Cryptococcus

Reacción granulomatosa necrotizante.


Neumonía Fúngica

Histoplasmosis

Campesinos

RX. Consolidaciones de focos múltiples. Afecta los lóbulos superiores. Nódulos calcificados <1cm.

Ganglios calcificados. Histoplasmoma LI.

Fundamentals of Diagnostic Radiology. Fourth Edition. William E. Brant. Clyde A Helms. 2012J.Manuel Cardoso. Pulmón, Pleura y Mediastino. 1999.

Primaria

Crónica

Pulmonar Diseminada.

FIEBRE, TOS , PERDIDA DE PESO, ESPLENOMEGALIA Y ADENOPATÍAS.

Neumonía Fúngica

Aspergillus

Inmunocomprometidos

Aspergiloma o Micetoma. Aspergilosis broncopulmonar alérgica. Crónica necrotizante o semi-invasiva.

Invasiva.



Bronquiectasias centrales y taponamiento bronquial.

Bronconeumonía necrotizante de focos múltiples y áreas infectadas hemorrágicas o infartos con

nódulos simples o múltiples.

Fig. 3.56 Secondary aspergilloma (fungus ball in a preexisting cavity). Thepatient is a 76-year-old man with a history of many years of COPD. Status post pul-monary tuberculosis in the postwar years. Preoperative chest image in the presenceof rectal carcinoma. A solid lobulated mass measuring 3 cm in diameter and largelysurrounded by air is seen within a thin-walled cavity in the severely scarred rightupper lobe.

Fig. 3.55 “Foolʼs cap bell” in aspergilloma (detail). The patient is a 79-year-oldman with severe COPD and emphysema, now presenting with dyspnea, fever, andproductive cough. In addition to extensive bronchopneumonia of the right upperlobe, the radiograph also demonstrates a mass 4 cm in diameter with an apical aircrescent (white arrows).

Fig. 3.57a–c Development of a primary aspergilloma from invasive pulmo-nary aspergillosis. Initially there are minimal marginal air inclusions (a) within a le-sion in the posterior segment of the upper lobe. Later the lesion is interspersed withcrescentic air inclusions (b). In the final stages, there is significant marginal air accu-mulation as the central masses retract from the surrounding tissue (c).

131

Opportunistic Lung Infections

Aspergilloma

Clinical terminology identifies two types of aspergilloma. To alesser extent, this distinction also applies to radiologic findings,namely where imaging studies demonstrate the course of the dis-order. These are (Fig. 3.53):" Primary aspergilloma (terminal stage of invasive pulmonary

aspergillosis)" Secondary aspergilloma (colonization of a preexisting cavity by

Aspergillus)

The characteristic radiographic sign of aspergilloma, detectable ona conventional radiograph, is a round shadow (fungus ball) withina radiolucency (preexisting cavity) with an air crescent above it

(Fig. 3.55). This air crescent occasionally has the appearance of abell on a foolʼs cap (Fig. 3.54). As the fungus ball is not adherentto the wall of the cavity, it shows postural movement.

On CT the immediate vicinity of the aspergilloma occasionallyprovides indirect signs of whether it is a primary or secondary le-sion. Significant scarring around a preexisting tapered cavity sug-gests that a fungus ball found there represents secondary coloni-zation (Fig. 3.56).

Occasionally a follow-up study of invasive pulmonary aspergil-losis can directly visualize the development of a primary aspergil-loma (Fig. 3.57).

Fig. 3.54 “Foolʼs cap bell” as a sign of aspergilloma.

Fig. 3.53 Pathophysiologic differentiation of primary and secondary aspergil-loma. In a primary aspergilloma (right diagrams), invasion of the pulmonary arteryby hyphae leads to local infarction and cavitation. Here, hyphae later grow to thefungus ball. In a secondary aspergilloma (left diagrams), a preexisting cavity is colo-nized by hyphae.

3

3 Pneumonia

130

Signo del menisco.


Fig. 3.56 Secondary aspergilloma (fungus ball in a preexisting cavity). Thepatient is a 76-year-old man with a history of many years of COPD. Status post pul-monary tuberculosis in the postwar years. Preoperative chest image in the presenceof rectal carcinoma. A solid lobulated mass measuring 3 cm in diameter and largelysurrounded by air is seen within a thin-walled cavity in the severely scarred rightupper lobe.

Fig. 3.55 “Foolʼs cap bell” in aspergilloma (detail). The patient is a 79-year-oldman with severe COPD and emphysema, now presenting with dyspnea, fever, andproductive cough. In addition to extensive bronchopneumonia of the right upperlobe, the radiograph also demonstrates a mass 4 cm in diameter with an apical aircrescent (white arrows).

Fig. 3.57a–c Development of a primary aspergilloma from invasive pulmo-nary aspergillosis. Initially there are minimal marginal air inclusions (a) within a le-sion in the posterior segment of the upper lobe. Later the lesion is interspersed withcrescentic air inclusions (b). In the final stages, there is significant marginal air accu-mulation as the central masses retract from the surrounding tissue (c).

131


Aspergiloma secundario


Aspergilosis Alérgica

Fig. 3.51 Open bronchus in an Aspergillus lesion. Subsegmental bronchi cours-ing through the center of a lesion 3 cm in diameter located in the posterior segmentof the right upper lobe (same patient as in Fig. 3.49).

Fig. 3.52 Air inclusions in an Aspergillus lesion. The patient is a 42-year-old manwith acute myeloid leukemia; nadir of induction therapy with antibiotic-resistantfever. In the posterior segment of the right upper lobe there is a lesion 3 cm indiameter showing a halo and central air inclusions.

Fig. 3.50 Broad pleural contact and perifocal hemorrhage in aspergillosis.The patient is a 20-year-old man with AIDS, presenting with persistent fever and lossof strength. Opacities surrounded by ground-glass halo are seen in the middle lobesand lingula, here with broad pleural contact (black arrows). Note the severe pericar-dial effusion (black arrowhead).

Fig. 3.49 Wedge-shaped infiltrate in invasive aspergillosis. The patient is a57-year-old man with Wegener granulomatosis receiving immunosuppression ther-apy. He has an antibiotic-resistant fever. The radiograph shows focal infiltrates (blackarrows) with broad pleural contact in the left upper lung field (black arrowheads).

129


Aspergilosis Angioinvasiva

Aspergilosis Angioinvasiva Recuperación

SIGNO DEL HALO

2 semanas

Neumonía Parasitaria

Pneumocystis carinni

SIDA

Patrón reticular lineal perihiliar que progresa a una consolidación

homogénea.


Fig. 3.43a–c Pneumocystis carinii pneumonia in AIDS. The patient is a 38-year-old African woman presenting with massive dyspnea.a Diffuse reticulonodular shadowing is seen with blurring of vascular structures.

Marked thickening of the hila suggests a mediastinal lymphoma. Right atrialenlargement.

b Follow-up examination of a. Findings have continued to worsen; the patient nowrequires oxygen. Massively increasing areas of increased attenuation; depth ofinspiration is markedly decreased.

c Ground-glass and finely nodular pattern sparing the periphery. The detail imageof the right lower lung field shows sparing of the periphery with significantblurring of vascular structures and finely nodular opacities.

Fig. 3.44 Terminal stage of Pneumocystis carinii pneumonia with tensionpneumothorax. The patient is a 23-year-old HIV‑positive man with a repeat episodeof Pneumocystis carinii pneumonia. Status post intubation and bilateral placementof pleural drains in pneumothorax from assisted ventilation. “White lung” with per-sistent left pneumothorax and a massive pulmonary fistula. The image partially in-cludes an inflated bulla in the left basal region (black arrows). The patient died a fewhours later.

125


Fig. 3.43a–c Pneumocystis carinii pneumonia in AIDS. The patient is a 38-year-old African woman presenting with massive dyspnea.a Diffuse reticulonodular shadowing is seen with blurring of vascular structures.

Marked thickening of the hila suggests a mediastinal lymphoma. Right atrialenlargement.

b Follow-up examination of a. Findings have continued to worsen; the patient nowrequires oxygen. Massively increasing areas of increased attenuation; depth ofinspiration is markedly decreased.

c Ground-glass and finely nodular pattern sparing the periphery. The detail imageof the right lower lung field shows sparing of the periphery with significantblurring of vascular structures and finely nodular opacities.

Fig. 3.44 Terminal stage of Pneumocystis carinii pneumonia with tensionpneumothorax. The patient is a 23-year-old HIV‑positive man with a repeat episodeof Pneumocystis carinii pneumonia. Status post intubation and bilateral placementof pleural drains in pneumothorax from assisted ventilation. “White lung” with per-sistent left pneumothorax and a massive pulmonary fistula. The image partially in-cludes an inflated bulla in the left basal region (black arrows). The patient died a fewhours later.

125



Fig. 3.7 Pattern of ground-glass opacities in alveolar proteinosis. The filmshows extensive, partially confluent area densities, appearing as ground-glass opac-ities in the peripheral areas. Left heart enlargement without any significant effusion.Radiograph obtained after intubation.

Fig. 3.6 Alveolar pulmonary edema in myocardial infarction and kidney fail-ure. The patient is an 84-year-old man with an acute myocardial infarction and kid-ney failure. Both lungs show diffuse, faint opacification that is most pronounced inthe central region of each lung.

Fig. 3.8 Alveolar opacities in infection. Ground-glass opacities sparing the pe-riphery of the lung and the bronchovascular spaces in Pneumocystis carinii pneumo-nia. The densities correlate with the increasing filling of the alveoli with foamyexudate and pathogens as the disease progresses.

Fig. 3.9 Acinar pattern (detail). Alveolar edema in acute kidney failure. Theedema is composed of myriad confluent small nodular shadows (acinar nodules).

105

Alveolar Pneumonia

Fig. 3.46 Classic picture of Pneumocystis carinii pneumonia. CT clearly demon-strates the position of the ground-glass opacities in the central lung, sparing theperiphery. There is also some sparing of the peribronchovascular region.

Fig. 3.45 Pneumocystis carinii pneumonia with sparing of individual subseg-ments. Findings show a predilection for the central region of the lung while certainsubsegments and individual lobules remain unaffected.

Fig. 3.47 Involvement is primarily limited to the upper lungs fields with inha-lational prophylaxis. This patient receiving inhaled pentamidine shows extensivebilateral ground-glass opacities in the upper lung fields.

Fig. 3.48 Atypical course of Pneumocystis carinii pneumonia. The image showsmultiple bullae, bronchiectasis, and traction bronchiectasis. Other findings includestrands of fibrosis and distraction of the pulmonary architecture. Pneumothorax isseen on the left.

127



Aspiración

Localizadas por efecto de gravedad.

Cavitación y Abscesos. (50%).

Empiema.

Anaerobias

Bacteroides y Fusobacterium

Mycoplasma

Extracción dentaria.Actinomyces Israelí (Actinomicosis)

Niños y Adolescentes.10-30% de las Neumonías

Extrahopitalarias. Miringitis ampollosa y

exantema.

AtípicasOpacidades no segmentarias.

Periferia de Lóbulos inferiores.

Patrón reticular fino. Opacidades parcheadas. Consolidación lobular.

Arbol en gemación.


NEUMONÍAS NECROTIZANTES

FIEBRE DE BAJO GRADO TOS PRODUCTIVA

HEMOPTISIS

de 23

Fig. 5: TC de paciente de 2 años: Neumonia necrotizante con cavidad en LII.

Fig. 6: Masa cavitada con nivel hidroaéreo en paciente con antecedente de flemóndental: Absceso pulmonar

Absceso PulmonarLesiones cavidades pulmonares.. Una aproximación al diagnóstico. 2012. SERAM

Chest Radiology: A residents Manual. 2011Fig. 3.26 Abscesses in lobar pneumonia. Area consolidation is seen in the rightupper lobe, which already shows hypoventilation. Other findings include centralhypodense areas (black arrow) and air inclusions.

Fig. 3.25 Resolving lobar infiltrate in the upper lobe. An area consolidation inthe left upper lobe is still visible but has already thinned out considerably. Loss ofvolume is already detectable while the air bronchogram is still visible. The pneumo-nia remains sharply demarcated from the unaffected lower lobe.

Fig. 3.27 Secondary pneumonic empyema. The infiltrate in the lower lobe haslargely resolved. After repeated aspiration and drainage of an empyema, thickeningof the visceral pleura (black arrows) and parietal pleura (black arrowheads) is stilldetectable.

Fig. 3.28 Carnification of the middle lobe following lobar pneumonia. Severeshrinking of the middle lobe has occurred after lobar pneumonia. The bronchi (blackarrow) in the consolidated area are dilated in response to the retraction processes.

115

Alveolar Pneumonia

441

Necrotizing Pneumonia: v/s Lung Abscess

Very controversial topic because for many authors

is considered as one entity

Lozano, J. Complicaciones Asociadas a Neumonia Bacteriana. Neumologia Pediatrica. 2010; 5(Sup1): 70-75.

Claudio Karsulovic, VIIGillian Lieberman, MD

44

Necrotizing Pneumonia Lung AbscessSevere complication causing necrosis

of lung parenchymaSupurative process with a well‐

defined fibrous wall

Low contrast enhancing wall in Chest

CTContrast enhancing wall in Chest CT

Thick wall > 2 cm with or without air‐

fluid levelThick wall > 2cm, with air‐fluid level

Loss of normal lung parenchyma Normal pulmonary parenchyma

architecture

Lozano,J.ComplicacionesAsociadasaNeumoniaBacteriana.NeumologiaPediatrica.2010;5(Sup1):70-75.

Infecciones pulmonares hraepy

Health & Medicine

Transcript of Infecciones pulmonares hraepy