Thorax Inflammatory Surgical Diseases of · Parapneumonic pleural effusions Lung abscess Pneumatocele Pneumothorax Spontaneous Pneumothorax Primary spontaneous pneumothorax Secondary

Inflammatory Surgical Diseases ofThorax

Денис Овечкін

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ЗмістInflammatory Surgical Diseases of Thorax

PLEURAL EFFUSIONParapneumonic pleural effusions

LUNG ABSCESSPNEUMATOCELEPNEUMOTHORAX

Spontaneous PneumothoraxPrimary spontaneous pneumothoraxSecondary spontaneous pneumothorax

MEDIASTINITIS

Inflammatory Surgical Diseases of Thorax 3

Inflammatory Surgical Diseases of ThoraxPleural effusion

Parapneumonic pleural effusionsLung abscessPneumatocelePneumothorax

Spontaneous PneumothoraxPrimary spontaneous pneumothoraxSecondary spontaneous pneumothorax

Mediastinitis

Inflammatory Surgical Diseases ofThorax

Pulmonary infections affect children of all ages. The availability of vaccines and the use of a larger

arsenal of antibiotics have decreased the incidence of severe lung infections and their complications.Nevertheless pneumonia and other lower respiratory tract infections are the leading causes of deathworldwide [43].

Pneumonia may originate in the lung or may be a focal complication of a contiguous or systemicinflammatory process.

One particular form of pneumonia present in the pediatric population, congenital pneumonia, presentswithin the first 24 hours after birth.

Common complications of pneumonia include the following:

Pleural effusion Empyema Pneumatocele Lung abscess Air leak syndrome, including pneumothorax, pneumomediastinum, pneumopericardium, andpulmonary interstitial emphysema Sepsis

Complications are more frequently associated with bacterial pneumonia than with viral pneumonia. Themost common complications include Pleural effusion, Empyema, Pneumatocele, Lung abscess.

PLEURAL EFFUSIONPleural effusion is excess fluid that accumulates in the pleural cavity, the fluid-filled space that surroundsthe lungs. Excessive amounts of such fluid can impair breathing by limiting the expansion of the lungsduring inhalation.

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Four types of fluids can accumulate in the pleural space:

· Serous fluid (hydrothorax)· Blood (hemothorax)· Chyle (chylothorax)· Pus (pyothorax or empyema)

Clinical presentationThe clinical signs of pleural effusion include: decreased movement of the chest on the affected side,

dullness to percussion over the fluid, diminished breath sounds on the affected side, decreased vocalresonance and fremitus (though this is an inconsistent and unreliable sign), pleural friction rub. Abovethe effusion, where the lung is compressed, there may be bronchial breathing and egophony. In largeeffusion there may be tracheal deviation away from the effusion.

DiagnosisPleural effusion is usually diagnosed on the basis of medical history and physical exam, and confirmed


by chest x-ray. ¤ Chest x-ray. The initial imaging of the chest generally consists of a front view (PA - posterior-

anterior) and a side or lateral view (LL - latero-lateral)). Whenever possible the patient should beimaged in an upright position. The upright position is very important in order to visualize possible airand fluid levels.

Chest films acquired in the lateral decubitus position (with the patient lying on his side) are moresensitive, and can pick up as little as 50 ml of fluid, than upright chest films (e.g., blunted costophrenicangles).

¤ Thoracentesis. Once a pleural effusion is diagnosed, the cause must be determined. Pleural fluid is

drawn out of the pleural space in a process called thoracentesis. A needle is inserted through the back ofthe chest wall in the 6th, 7th or 8th intercostal space on the midaxillary line, into the pleural space [14,45].

The fluid may then be evaluated for the following:

Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pHand glucose Gram stain and culture to identify possible bacterial infections Cell count and differential Cytology to identify cancer cells, but may also identify some infective organisms Other tests as suggested by the clinical situation – lipids, fungal culture, viral culture, specificimmunoglobulins

Transudate vs. exudateThe important step in the evaluation of pleural fluid is to determine whether the effusion is a

transudate or an exudate.Causes1. Transudate pleural effusions are formed when fluid leaks from blood vessels into the pleural space.

Examples of transudate pleural effusions include: congestive heart failure, liver failure or cirrhosis, kidneyfailure or nephritic syndrome, and peritoneal dialysis.

2. Exudate pleural effusions are caused by inflammation of the pleura itself and are often due todisease of the lung. The most common causes of exudative pleural effusions are pneumonia(parapneumonic pleural effusions), cancer (with lung cancer, breast cancer, and lymphoma causingapproximately 75% of all malignant pleural effusions), viral infection, and pulmonary embolism. Althoughpulmonary embolism can produce either transudative or exudative pleural effusions, the latter is morecommon.

Transudative and exudative pleural effusions are differentiated by comparing chemistries in the pleuralfluid to those in the blood.

According to a meta-analysis, exudative pleural effusions meet at least one of the following

criteria:* Pleural fluid protein >2.9 g/dL (29 g/L)* Pleural fluid cholesterol >45 mg/dL (1.16 mmol/L)* Pleural fluid lactate dehydrogenase (LDH) >60% of upper limit for serum

According to Light's criteria (Light, et al. 1972), a pleural effusion is likely exudative if at least one

of the following exists:o The ratio of pleural fluid protein to serum protein is greater than 0.5o The ratio of pleural fluid LDH and serum LDH is greater than 0.6o Pleural fluid LDH is more than two-thirds normal upper limit for serum


TreatmentTreatment depends on the underlying cause of the pleural effusion. Therapeutic aspiration may be

sufficient; larger effusions may require insertion of an intercostal drain (either pigtail or surgical).Video 1.

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Parapneumonic pleural effusionsParapneumonic pleural effusions (PPE) and pleural empyema (PE) are pleural effusions thatdevelop as a consequence of bacterial pneumonia, lung abscess or bronchiectasis [36, 43].

PPE and PE are clinically challenging conditions, both therapeutically and diagnostically, because oftheir heterogeneity. They range from small, uncomplicated, pleural effusions that do not require specifictreatment to multiloculated effusions and empyema with pleural fibrosis, trapped lung, systemic sepsis,respiratory failure, and metastatic infection.

Table 6.1 shows the biochemical characteristics of a parapneumonic effusion. Table 6.1 Biochemical Characteristics of the Stages of Parapneumonic Pleural Effusions

Parameter Uncomplicated Undetermined ComplicatedpH >7.3 7.3-7.1 60 60-40 500 1000

PathophysiologyThe progression of an uncomplicated PPE to an organized PE represents an inflammatory continuum

from a small, free-flowing, non-infected pleural effusion to a large volume of frank pus, which may bemulti-loculated with thick visceral pleural peels that prevent the underlying lung from expanding to thechest wall after pleural fluid drainage ("trapped lung") [14].

During the early stages of pneumonia, pleural membranes respond to pulmonary pathogens with avigorous inflammatory response that promotes the formation of pleural fluid, which is exudative in naturewith increased concentrations of leukocytes and proteins.

Classification of parapneumonic pleural effusionsVarious classification schemes have been described. In 2003, British Thoracic Society proposed a

simple classification scheme for parapneumonic pleural effusions. It contains 3 stages (Table 6.2). Table 6.2 British Thoracic Society classification scheme for parapneumonic pleural effusions

Stages MacroscopicappearancePleural fluidcharacteristics Comments

Simple(uncomplicated)parapneumonic

Clear fluid

pH >7.2LDH 2.2

mmol/lNo organisms

on culture orGram stain

Will usuallyresolve withantibiotics alone.

Perform chesttube drainagefor symptomrelief if required


Complicatedparapneumonic

Clear fluid orcloudy/

turbid

pH 1000 IU/lGlucose >2.2

mmol/lMay be positive

Gramstain/culture

Requires chesttube drainage

Empyema Frank pusMay be positiveGramstain/culture

Requires chesttube drainage

No additionalbiochemicaltests necessary

on pleuralfluid (do notmeasure pH)

An uncomplicated PPE is usually small in volume, free-flowing without loculations, and inflammatory innature without the presence of detectable pathogens. Most often, uncomplicated PPE resolve withantibiotic therapy of the underlying pneumonia.

A complicated PPE usually results from pleural infection and requires at least catheter drainage ofpleural fluid and possibly surgical intervention.

A PPE progresses to a PE when the concentration of leukocytes becomes sufficient to form pus, as

characterized by viscous, whitish-yellow, and turbid to opaque fluid. Empyema fluid consists of fibrin,cellular debris, and viable or dead bacteria.

Empyemas are defined by results of chemical pleural fluid analysis (e.g., low pH) or the presence of

detectable intrapleural pathogens in the setting of non-purulent pleural fluid.

Loculated PPEUnloculated PPE

A loculated PPE develops from the intrapleural formation of fibrinous and fibrous adhesions that preventthe free-flow of pleural fluid. Loculated effusions may be unilocular or multilocular.

EmpyemaEmpyema is the accumulation of infected matter in the pleural space.In children, empyema most commonly results from infection of a parapneumonic effusion, although

infection of thoracic structures other than lung can also spread to fluid in the pleural space. Other lesscommon causes include trauma, intrathoracic perforation of the esophagus, or infection of theretropharyngeal or mediastinal spaces [14, 36, 43].

The most common organisms identified in childhood cases of empyema are Staphylococcus aureus,

Hemophilis influenzae and Streptococcus pneumoniae [2, 6, 16, 43]. Other streptococci, mixed oral flora,and anaerobes have also been classically associated with the development of empyema. The changes inbacteriology are likely due to changing antibiotic resistance patterns.

The development of empyema is described in three stages:

- The early stage or exudative stage (24 to 72 hours) is characterized by an accumulation ofthin pleural fluid with low cellular content.

- The fibrinopurulent stage (7 to 10 days) - during which the infected pleural fluidconsolidates, fibrinous material accumulates and may cause loculation, all resulting in decreasedlung mobility.

- The organized fibrous stage (2 to 4 weeks) - when the involved lung frequently becomesentrapped by a fibrous pleural peel eventually leading to a fibrous thorax.

The empyema may be diffuse and involve the entire pleural space, or it may be localized and

encapsulated in an interlobar, diaphragmatic, or paramediastinal location. Symptoms and DiagnosisChildren with empyema present with high fever, cough, respiratory distress and chest pain.Physical examination reveals decreased breath sounds, dullness to percussion and tactile fremitus

over the involved hemithorax. Irritation of the pleura results in a friction rub on auscultation. Chest X-ray typically identifies thickened pleura in association with a pleural effusion (Image 6.1).

Decubitus chest radiograms can aid in the diagnosis and help determine the degree of "fluidity" of the


Image 6.1 AP Chest X-ray. A pleural empyema on left.

effusion/empyema [14].The radiographic appearance oftenincludes bilateral pulmonary involvementwith pneumatoceles occasionallyidentified within the lung. Haziness of ahemithorax may represent eitherpulmonary consolidation or pleural fluid.

In the early exudative phase, thepleural fluid flows freely along the lateralchest wall on decubitus views. Inadvanced empyema, the exudate is asolid mass of fibrin and does not movewith changes in position. In theintermediate fibrinopurulent stage,loculations typically develop [14, 16].

Air-fluid levels within the loculationssuggest the presence of anaerobes in thepleural contents [43].

Ultrasound may be used to determine the presence of loculations; however, CT is by far the mostsensitive study to determine the degree of pleural thickness.

Indeed, CT is an excellent means by which to differentiate between consolidated, infected lungparenchyma and extrapulmonary pleural disease. However, for patients referred relatively early in theircourse, the most surgeons prefer to use ultrasound, which is rapidly obtained and avoids unnecessaryradiation exposure [36, 43, 45].

Thoracentesis with fluid analysis can occasionally confirm the diagnosis.It is expected that the gross appearance of the fluid would be turbid and thick. Laboratory data

characteristic of empyema include pH 200 U/Land WBC >15,000/mm3. Gram stain and culture of the pleural fluid is important to help guide antibiotictherapy [16].

Treatment and OutcomePrimary therapy for empyema is the administration of high-dose intravenous antibiotics. NB: Effective drainage of the pleural space speeds the resolution of the empyema. Fluid that layers in the decubitus position may be amenable to chest tube drainage. Loculated fluid

collections may not be sufficiently drained in such a manner, and the optimal management of thesepatients is still debated [36, 43, 45].

Failure of antibiotics and thoracostomy tube drainage is frequently seen and is the result of

inadequate drainage of loculated fluid or lung entrapment in the fibrinous peel.The treatment options for these patients are either video-assisted thoracoscopic surgery

(VATS) or catheter-directed fibrinolytic therapy [14, 16, 43, 45]. VATS is an excellent alternative to thoracotomy for this purpose and has been advocated by many as

a primary intervention in pediatric patients. Given that patients with nonloculated effusions (stage 1) tendto recover with appropriate antibiotic therapy and chest tube drainage, VATS may play more of a role inlate-stage empyema. Advantages include the ability to visualize and operate in all regions of the pleuralspace and to remove the fibrinous peel from the entire surface of the pleura, which often allowsimmediate reexpansion [43].

In most patients, VATS employs three incisions (two 5 mm and one 12 mm) for the thoracoscope andworking ports.

A number of recent studies have shown that fibrinolytics provide the same clinical benefits. Most

loculations can be lysed using urokinase or streptokinase (20,000 IU of diluted urokinase, 3instillations per day) [14, 43].

The recent studies have seen promising early results with tissue plasminogen activator (tPA).Using 4 mg in 30 mL of normal saline (2 mg in 15 mL for children less than 1 year old), a total of sixdoses are instilled through the chest tube every 12 h. So far, overall success rates, duration of illness,and hospital course have been similar to the experience with VATS [43].


The major reported complications with fibrinolytic therapy, including anaphylactic/allergic reactions

(with streptokinase), chest pain, hemorrhage, and bronchopleural fistula occurred rarely in these reports[16, 43].

Pulmonary function after recovery is usually normal although mild restrictive or obstructive disease on

follow-up spirometry has been reported.

LUNG ABSCESSA pulmonary abscess develops when a localized infection in the lung parenchyma leads to necrosis andcavitation [43].

It is a type of coagulation necrosis of the pulmonary tissue and formation of cavities containingnecrotic debris or fluid caused by microbial infection.

Lung abscess is much less frequent in the pediatric population than in adults. It occurs much lessfrequently than pneumonia or empyema [43].

When a lung abscess occurs in infants, an underlying congenital anomaly, such as a bronchogenic cyst

or congenital cystic adenomatoid malformation, should be suspected. These lesions require resectionbut initial treatment with antibiotics with or without drainage is usually indicated [3, 14, 36].

ClassificationClassically, pulmonary abscesses were classified into primary (occurring in healthy children) or

secondary (occurring in otherwise compromised children) [43]. PathogenesisSome of the relevant deficiencies that can contribute to the development of lung abscesses in

children are provided in Table 6.3 [45]. Table 6.3

Deficiencies That Can Contribute to the Development ofLung Abscesses in Children

InadequateMechanicalClearanceMechanisms

Structural abnormalities

Retained endobronchial foreign body Tracheostomy Underlying cystic disease of the lung

Cystic fibrosisAlpha 1-antitrypsin deficiencyAny cause of partial bronchial obstructionIneffective cough (neurologically impairedpatients)Immotile cilia (Kartagener syndrome)

InadequateCellular HostDefenses

Transplantation, oncology, or other patientswho are iatrogenically immunosuppressed bychemotherapy or antirejection regimensSevere combined immunodeficiencysyndromeChronic granulomatous diseaseOther hereditary granulocyte deficiencies

InadequateHumoral HostDeficiencies

Hereditary complement deficienciesAgammaglobulinemiaImmunoglobulin A deficiencyIatrogenic manipulation of humoral defenses(monoclonal antibodies, receptor antagonists,and other strategies to alter the humoralcomponent of the inflammatory response arecurrently in preclinical trials)

Children with cellular or humoral immune deficiencies, either congenital or acquired, are occasionallyunable to eradicate a pulmonary infection despite appropriate antibiotics, leading to inflammation, thebreakdown of pulmonary parenchyma, and eventual abscess formation.

Both cellular lung elements and the extracellular lung matrix are destroyed; tissue necrosis andcavitation within the lung parenchyma follow. The involved area is surrounded by atelectasis and


pneumonia [14, 43].A chronic lung abscess develops with varying degrees of circumferential fibrosis and may involve

substantial destruction of parenchyma, usually in a lobar distribution.Typically, the abscess cavity communicates with the normal tracheobronchial tree, and this relation

has important diagnostic and treatment implications. EtiologyAs elsewhere, the abscess results from tissue necrosis related to pyogenic, toxin-producing bacterial

organisms and to phagocytic cells that generate cytotoxic oxidants and proteases.Lung abscesses are typically polymicrobial, with both anaerobic and aerobic bacteria [45].The most common causative organisms are anaerobes, followed by S. aureus, Pseudomonas,

streptococcal species, pneumococci, and occasionally H. influenzae Other bacteria implicated in lungabscess include Klebsiella, Escherichia coli, Peptostreptococcus, and Peptococcus [6, 8, 14, 16].

Nonbacterial and atypical bacterial pathogens may also cause lung abscesses, usually in theimmunocompromised host. These microorganisms include parasites (Paragonimus and Entamoebaspecies), fungi (Aspergillus, Cryptococcus, Histoplasma, Blastomyces, and Coccidioides species), andMycobacterium species.

Clinical presentationPhysical findings may be secondary to associated conditions such as underlying pneumonia or pleural

effusion.The physical examination findings may also vary depending on the organisms involved, the severity

and extent of the disease, and the patient's health status and comorbidities.The most common symptoms caused by lung abscess include fever, cough, chest pain, anorexia,

productive sputum, weight loss, malaise, hemoptysis, and chills [2, 3, 8].Purulent sputum may be easily obtained from older children to help with a bacteriologie diagnosis;

younger patients usually swallow their secretions.Putrid sputum is characteristic of an anaerobic abscess. The affected area of the chest may be dull to

percussion and have decreased breath sounds. Patients may also present with restrictive lung diseasepatterns from the enlarging abscess or secondary to pleuritic chest pain.

DiagnosisLaboratory Studies

A complete white blood cell count with differential may reveal leukocytosis and a left shift.Obtain sputum for Gram stain, culture, and sensitivity.If tuberculosis is suspected, acid-fast bacilli stain and mycobacterial culture is requested.Blood culture may be helpful in establishing the etiology.

Examination of sputum is important in any pulmonary infections and here often reveals mixed flora.Transtracheal or transbronchial (via bronchoscopy) aspirates can also be cultured. Imaging Studies

Chest X-ray (Image 6.2 & 6.3). The typical chest radiographic appearance of a lung abscess is anirregularly shaped cavity without or with an air-fluid level inside. Presence of air-fluid levels impliesrupture into the bronchial tree or rarely growth of gas forming organism.CT (Image 6.4).Ultrasonography


Image 6.2 Chest X-ray. Lung abscess without ofair-fluid level (a complication of necrotizingpneumonia).

Image 6.3 Chest X-ray. Lung abscess with an air-fluid levelinside (a complication of necrotizing pneumonia).


Image 6.4 Chest CT scan reveals a lung abscess with an air-fluid level(a complication of necrotizing pneumonia of the right middle lobe in an adolescent).Note several small pneumatoceles throughout the consolidated lung parenchyma. TreatmentThe preferred treatment of lung abscess is appropriate intravenous antibiotic therapy and drainage [2,

4, 14, 43]. A specific bacteriologie diagnosis should be established before treatment whenever possible. Intravenous antibiotics are recommended for 2 to 4 weeks, followed by oral antibiotics for a total

treatment period of 6 to 8 weeks. Antibiotics are discontinued when the child is symptom free and thechest radiographs are clear. This may take from 1 to 6 months [16, 43, 45].

Medical therapy for lung abscesses is frequently unsuccessful in neonates and immunocompromisedchildren, in whom the mortality approaches 20% [14].

Lung abscesses often occur at the periphery of a segment or lobe, making them amenable to external

drainage procedures. The needle aspiration of a peripheral abscess cavity under imaging guidance toisolate bacterial species and drain collections has been used with moderate success [43, 45].

Isolation of the causative organism is possible with this technique even if patients are concurrentlyreceiving antibiotic therapy.

The complications related to percutaneous techniques of drainage occur occasionally and includepneumothorax, hemothorax, incomplete drainage, and bronchopleural fistulas.

Satisfactory drainage can usually be accomplished by chest physiotherapy with postural drainage and

percussion and by occasional bronchoscopic aspiration.For children who are unable to cough adequately, therapeutic bronchoscopy with direct aspiration of

purulent fluid or transbronchial drainage may be necessary [14, 16, 43, 45]. Surgery is very rarely required for patients with uncomplicated lung abscesses.Surgical resection of the lung abscess by segmental resection or lobectomy is recommended for the

chronic, large, and thick-walled abscesses or for those few patients who do not respond to intensiveantibiotic therapy or percutaneous drainage Other indications for resection include chronic abscesseslasting longer than 3 months, persistent significant hemoptysis, bronchial stenosis, significantbronchiectasis, and massive pulmonary necrosis [14, 43, 45].

Complications of Lung abscesses:

Rupture into pleural space causing empyema.Pleural fibrosis.Trapped lung.Respiratory failure.Bronchopleural fistula.Pleural cutaneous fistula.


PNEUMATOCELEPulmonary pneumatoceles are thin-walled, air-filled cysts that develop within the lung parenchyma.Pneumatoceles are secondary to alveolar and bronchiolar necrosis.

Pneumothorax and pyopneumothorax are complications resulting from the rupture of infectedpneumatoceles. These lesions can be difficult to distinguish from congenital cysts of the lung. However,pneumatoceles are prone to spontaneous resolution whereas congenital abnormalities should notinvolute [3, 43, 45].

AgeInfants younger than 1 year account for three fourths of the cases of staphylococcal pneumonia.

Because pneumatoceles commonly develop as a complication of staphylococcal pneumonia,pneumatoceles are found more frequently in infants and young children. 70% of pneumatoceles occurredin children younger than 3 years [43].

ClassificationThey can be single emphysematous lesions but are more often multiple, thin-walled, air-filled cyst

like cavities. EtiologyMost often (up to 80% of patients), pneumatoceles occur as a sequela to acute pneumonia,

commonly caused by Staphylococcus aureus [14, 16, 45].However, pneumatocele formation also occurs with other agents, including Streptococcus

pneumoniae, Haemophilus influenzae, Escherichia coli, group A streptococci, Serratia marcescens,Klebsiella pneumoniae, adenovirus, and tuberculosis.

Non infectious etiologies include hydrocarbon ingestion, trauma, and positive pressure ventilation. Clinical presentationChildren present with typical features of pneumonia, including cough, fever, and respiratory distress. NB: No clinical findings differentiate pneumonia with or without pneumatocele formation. Mild, moderate, or severe respiratory distress may be present, with tachypnea, retractions, grunting,

and nasal flaring. Fever is almost always present and may be as high as 40-41°C.Lung examination findings vary depending on the stage of the pneumonia. Auscultation of the

chest reveals focal or bilateral decreased breath sounds. Inspiratory crackles are frequently heard. As thepneumonia resolves and the pneumatocele persists, the lung examination findings can be normal orfocal decreases in breath sounds can be present, depending on the size of the pneumatocele [2, 8].

Diagnosis¤ Initial chest radiography often reveals pneumonia without evidence of a pneumatocele.

Parapneumonic effusion or empyema can be present. Radiographic evidence of a pneumatocele mostoften occurs on day 5-7 of hospitalization [14]. Rarely, it may be visible on the initial chest radiograph(Image 6.5).

¤ Usually, chest CT scanning with contrast is notnecessary to diagnose a pneumatocele, but CTscanning occasionally helps to differentiate anabscess from a pneumatocele (Image 6.6).


Image 6.5 Pneumonia with multiplepneumatoceles on the right.

Image 6.6 Chest CT scan of pneumonia withpneumatocele.

TreatmentIn most circumstances, pneumatoceles are asymptomatic and do not require surgical

intervention. Treatment of the underlying pneumonia with antibiotics is the first-line therapy [16, 43,45].

Close observation in the early stages of the infection and periodic follow-up care until resolution of thepneumatocele is usually adequate treatment. The natural course of a pneumatocele is slow resolutionwith no further clinical sequelae.

Invasive approaches should only be reserved rare for patients who develop complications.Percutaneous catheter drainage should only be considered for a significant tension pneumatocele or asecondarily infected pneumatocele [43].

PNEUMOTHORAXPneumothorax is a collection of air in the pleural space.

Pneumothorax can occur spontaneously. It can also occur as the result of disease (e.g., complicated

pneumonia, chronic obstructive pulmonary disease (COPD)) or injury to the lung, or due to a puncture tothe chest wall. Pneumothorax can be created therapeutically to collapse a lung [14, 16, 45].

Classification of pneumothoraxPneumothorax is classified according to:A. Etiology.B. Extent.C. Mechanism.D. Duration. A. Classification by ‘Etiology’:Basically:

Primary pneumothoraxSecondary pneumothorax

More fully

i. Spontaneous pneumothorax – It is the most common form of pneumothorax in clinicalpractice.

Primary spontaneous pneumothorax – occurs in apparently healthy persons due to leak ofair through a weak area of the pleura.Secondary spontaneous pneumothorax – is seen in cases with any underlying lungconditions, e.g., COPD usually.


i. Traumatic pneumothorax (non-iatrogenic) – due to blunt or penetrating thoracic traumaii. Iatrogenic or artificial pneumothorax – occurs as a result of any diagnostic or therapeutic

procedure (postoperative; mechanical ventilation; thoracocentesis; central venous cannulation)

B. Classification by ‘Extent’:§ Simple pneumothorax – without shif of the mediastinum§ Tension pneumothorax – leads to shift of the mediastinum to opposite side and to significant

impairment of respiration and/or blood circulation (inferior vena cava “kinks” on diaphragm ® decreasedvenous return ® cardiovascular collapse ® death)

Asymptomatic – small pneumothorax (

Image 6.7. Chest X-ray. A large right-sidedspontaneous pneumothorax (left in theimage). An arrow indicates the edge of thecollapsed lung.

Image 6.8.

patient has a lung infection or a collapsed lung.The test is simple to perform and requires only two coins and a stethoscope. A coin held against the

chest is tapped by another coin on the side where the problem is suspected. A stethoscope is placed onthe back to listen to breath sounds and the sound of the coins. If a tinkling sound is heard, it is likely thatair or fluid has found its way into the pleural cavity. In healthy patients, this sound will not be audible.

If the signs and symptoms are doubtful, a chest X-ray can be performed, but in severe hypoxia, or

evidence of tension pneumothorax emergency treatment has to be administered first. NB: On a roentgenogram of the chest, a pneumothorax is classically seen as an area of “absent”

lung markings between the bony thoracic cage and the edge of the lung (Image 6.7).In a supine chest X-ray the deep sulcus sign isdiagnostic, which is characterized by a low lateralcostophrenic angle on the affected side.

In neonates the use of a transilluminator tosuspected area will help visualize the air as radiatingrings from light source out [43].

The assessment of the size of pneumothoraxThe estimated size of a pneumothorax is a key factor

in determining the initial management.

For clinical

practice, size isassessed on PAchest X-ray mainlyby the Light index.There is an excellentcorrelation (r = 0.84)between the Lightindex and theamount of air thatcan be aspiratedfrom apneumothorax.

The lungdehiscence over thewhole length oflateral chest wall is

defined as a large pneumothorax, in which case the Light index can be used with a cut-off point of20% guiding therapeutic strategy.

The Light index is calculated as follows: size of pneumothorax (in %) = [1 – (DL/DH)3] x 100 where DL isthe diameter of the lung measured at the hilar level and DH is the internal diameter of the hemithoraxmeasured at the hilar level (Image 6.8). In general, a partial pneumothorax is defined as small.

Differential diagnosis1. The sudden onset of chest pain and dyspnoea may simulate:

Myocardial infarction.Pulmonary embolism.Pulmonary infarction.Perforated peptic ulcer.

2. Extensive bullous emphysema (“vanishing lung”).3. Pneumomediastinum.4. Pneumopericardium.


TreatmentSmall pneumothoraces are often managed conservatively as they will resolve on their own. Repeat

observation via chest X-rays and oxygen administered.Larger pneumothoraces may require a needle aspiration or chest tube placement (tube

thoracostomy). Treatment options1. A small or shallow pneumothorax – less than 20% collapse – can usually be left to absorb

spontaneously; this takes about a month. A few days of rest or limitation of activity is all that is required,and it will absorb progressively.

2. Any type of large pneumothorax – more than 20% collapse and accompanied by dyspnoea

needs to be aspirated using a suitable gauge needle, a large syringe, and a two-way tap.NB: The puncture site is commonly in the second or third intercostal space in the midclavicular line or

in the 4th or 5th intercostal space over the superior rib margin in the anterior axillary line 3. In the presence of a continual leak. A plastic or rubber catheter is inserted on the same site.

The catheter is to be connected to an underwater-seal bottle. This helps evacuate the air.

The intercostal tube is usually left in situ for 24 hours after full re-expansion of the lung has beenachieved, i.e., a total period of 3 – 4 days in most cases. A tube in the chest is quite painful andanalgesics are necessary – if there are no contraindications like asthma, severe bronchitis, oremphysema – to make the patient comfortable.

4. In a case of tension pneumothorax – it is a life-threatening emergency that requires instant

action. Severe symptoms and signs of respiratory distress suggest the presence of tensionpneumothorax.

Treatment is with oxygen and emergency needle decompression [1, 3, 34].Insert a large-bore needle into the pleural space through the second or third anterior intercostal

space. A gush of air confirms the diagnosis. Typical clinical situations where tension pneumothorax arises include:

· Ventilated patients· Trauma patients· Resuscitation patients (CPR)· Lung disease, especially acute presentations of asthma and COPD· Blocked, clamped or displaced chest drains· Patients receiving non-invasive ventilation· Patients undergoing hyperbaric oxygen treatment

If the valvular mechanism continues to function, the tension element will recur and the needle must

then be replaced with either an indwelling needle of the Foster-Carter type, or by an intercostal catheter(Malecot type), connected to a water-sealed suction until the lung re-expands and seals off the leak [14,34, 43].

5. When there is a large air leak and aspiration proves inadequate – a thoracoscopy (or

thoracotomy) with suturing of the damaged lung / bronchus is necessary. NB: In all cases where a chest tube has been inserted, the rule of thumb is that the tube should not

be removed till bubbling in the underwater-seal bottle is absent on coughing, and the lung has re-expanded. Also, the tube should not be left in one position for more than seven days. But if the tube is


Image 6.9. A schematic drawing of a bulla and a bleb, two lungabnormalities that may rupture and lead to pneumothorax [45].

still required, it should be replaced through a new puncture 2 cm away [43, 34].

Spontaneous PneumothoraxSpontaneous pneumothorax can be classified as primary and secondary. In primary spontaneouspneumothorax, it is usually characterized by a rupture of a bleb in the lung while secondary spontaneouspneumothorax mostly occurs due to COPD [14, 16].

Primary spontaneous pneumothoraxA primary spontaneous pneumothorax may occur without either trauma to the chest or any kind of blastinjury. This type of pneumothorax is caused when a bleb (an imperfection in the lining of the lung) burstscausing the lung to deflate (Image 6.9) [14, 45].

Primary spontaneous

pneumothorax is most commonin tall, thin men between 17 and40 years of age, without anyhistory of lung disease. Thoughless common, it also occurs inwomen, usually of the same ageand body type.

The tendency for primary

spontaneous pneumothoraxsufferers to be tall and thin isnot due to weight, diet orlifestyle, but because thegenetic predisposition towardthose traits often coincides witha genetic predisposition towardhigh volume lungs with large,burstable blebs. A small portionof primary spontaneouspneumothoraxes occur inpersons outside the typicalrange of age and body type.

DiagnosticCT is more sensitive at detecting blebs and bullae than normal chest X-rays, but it is unclear if its

routine use for spontaneous pneumothorax ultimately changes management [14, 16]. TreatmentThe lung is reinflated by the surgical insertion of a chest tube. A minority of patients will suffer a

second instance. In this case, thoracic surgeons often recommend thorascopic pleurodesis to improvethe contact between the lung and the pleura [14, 43, 45].

NB: Pleurodesis (or sclerotherapy) – this is the medical procedure in which the pleural space isartificially obliterated.

If multiple and/or bilateral occurrences continue, surgeons may opt for a far more invasive bullectomy

and pleurectomy to permanently adhere the lung to the interior of the rib cage with scar tissue, makingcollapse of that lung physically impossible [3, 8, 14].


Overall outcome is excellent after surgical treatment for pneumothorax.

Secondary spontaneous pneumothoraxIn secondary spontaneous pneumothorax, a known lung disease is the cause of the collapse. The mostcommon cause is COPD with emphysematous bullae (See Image 6.9) [14, 45]. However, there areseveral other diseases that may also lead to spontaneous pneumothorax: tuberculosis; pneumonia;asthma; cystic fibrosis; lung cancer; interstitial lung disease; Marfan syndrome;lymphangioleiomyomatosis (LAM).

Treatment and OutcomeSpontaneous unilateral pneumothorax of 15-20% in size may be monitored by serial chest x-rays if

the patient is asymptomatic. Pleural air can be reabsorbed at a rate of 1,25% per day, and there arerecurring reports, poorly documented or explained, that this rate may be increased by administration of100% oxygen [14, 43].

If the patient is symptomatic or the size of the pneumothorax increases, a thoracostomy tube mustbe inserted. In tension pneumothorax, a 14-gauge angiocatheter can be placed in the second intercostalspace anteriorly to immediately relieve hemodynamic compromise. Continuous suction on the chesttube is maintained until the air leak ceases.

Persistence of air leak may be seen in patients with a chronic underlying condition such as cysticfibrosis, bronchopulmonary dysplasia, lung cysts, or blebs. Treatment of these patients then requiresresection of the diseased lung along with pleurodesis.

Pleurodesis is usually performed by the administration of chemical irritants (talc, tetracycline) or

mechanical rub through the thoracostomy tube, thoracoscope, or at thoracotomy. Talc is the agent ofchoice since it incites less pain and is more effective in treating pneumothorax in patients with cysticfibrosis [43]. Pleurodesis is considered in any teenager after two episodes of spontaneous pneumothoraxbecause of the high recurrence rate [14, 16].

The indications for surgical management include recurrence, persistent air leak (greater than 5 days

duration), bilateral disease, and possibly the presence of large bullae [43].One objective of the operation is the excision of apical lung tissue in an attempt to remove the bullae

responsible for the inciting air leak. The other goal is a thorough mechanical pleurodesis to obliterate thepleural space and minimize the chances for future lung collapse. The operation is effectively performedwith video-assisted thoracic surgery (VATS).

Tube thoracostomyNearly every patient with a secondary spontaneous pneumothorax should initially be managed by tube

thoracostomy. Arterial blood gases (ABG) usually improve within 24 hours of instituting tubethoracostomy.

If the patient has respiratory failure necessitating mechanical ventilation, a chest tube should definitelybe placed because the pneumothorax is likely to enlarge during mechanical ventilation.

Tube thoracostomy is less efficacious in secondary than in primary pneumothorax. On the average,in primary spontaneous pneumothorax, the lung usually expands, and the air leak ceases within 3 days;in secondary spontaneous pneumothorax due to chronic obstructive lung disease, the mean time for thelung to re-expand is 5 days [14].


RecurrenceRecurrences are frequent and the onset of pneumothorax is unpredictable. About 20% of cases of

spontaneous pneumothorax recur, most of them within a year [14, 16]. A few cases become chronic, i.e.,persisting for 3 months or longer, because of the development of a broncho-pleural fistula (BPF).

MEDIASTINITISAcute mediastinitis occurs as a result of contamination and/or soilage of the mediastinal spacesecondary to the trauma or perforation of either the trachea or esophagus [14].

Rarely, mediastinitis can develop from a descending retropharyngeal or cervical abscesses or therupture of suppurative mediastinal lymph nodes.

Infection within the mediastinum can disseminate quickly because this space contains no anatomicbarriers to the spread of infection. Clinically, acute mediastinitis is heralded by high fever, chest pain,dyspnea, cyanosis, and marked tachycardia as well as a significant leukocytosis [3, 8, 14, 45].

In neonates, the signs and symptoms may be subtle, including lethargy, fever, apnea, temperatureinstability, and leukopenia.

The management of mediastinitis includes hemodynamic support, the prompt administration ofintravenous antibiotics, and mediastinal drainage. Cervical, transthoracic, retropleural, or anteriorapproaches may be utilized to facilitate drainage, depending on the location of abscess or leakage [14,43].


ЗмістInflammatory Surgical Diseases of ThoraxPLEURAL EFFUSIONParapneumonic pleural effusions

LUNG ABSCESSPNEUMATOCELEPNEUMOTHORAXSpontaneous PneumothoraxPrimary spontaneous pneumothoraxSecondary spontaneous pneumothorax

MEDIASTINITIS

Thorax Inflammatory Surgical Diseases of · Parapneumonic pleural effusions Lung abscess Pneumatocele Pneumothorax Spontaneous Pneumothorax Primary spontaneous pneumothorax Secondary

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