Lung Abscess in Children

Journal of Pediatric Infectious Diseases 4 (2009) 27–35 27DOI 10.3233/JPI-2009-0148IOS Press

Review Article

Lung abscess in children

Haya Alsubie and Dominic A. Fitzgerald∗Department of Respiratory Medicine, The Children’s Hospital at Westmead, Sydney, NSW, Australia

Received 25 July 2008

Revised 30 July 2008

Accepted 4 September 2008

Abstract. Lung abscess is an uncommon but challenging condition to manage. Predisposing factors including pulmonaryaspiration and impaired mucociliary defense mechanisms increase the likelihood of developing a secondary lung abscess.Aspirating anaerobic organisms from the mouth leading to pneumonia and a secondary lung abscess is more likely to beseen in children with neuro-cognitive impairment. The more likely anaerobic organisms include Peptostreptococcus species,Fusobacterium nucleatum and Prevotella melaninogenica. These organisms may be difficult to isolate without specific anaerobictransport vials and culture media. The rise of interventional radiology, higher positive culture results, better targeted antibioticregimes and a greater awareness of hospital acquired pathogens have been significant is decreasing the length of hospitalizationfor children with lung abscesses. The morbidity and mortality for lung abscess in children is vastly superior to that in adultpatients because of the lack of co-morbidities in the pediatric population.

Keywords: Lung abscess, pathophysiology, microbiology, anaerobes, interventional radiology, antibiotic therapy

1. Introduction

Lung abscess is an uncommon but important pedi-atric problem. It is believed to be less common in chil-dren than adults, although the literature is accordinglyrelatively sparse. Lung abscesses may be classified asprimary or secondary, depending upon the existenceof predisposing conditions. Similarly, lung abscessesmay be single or multiple. Those that are secondaryare far more likely to be caused by anaerobic bacteria.Typically, in children as in adults, it is the existenceof underlying conditions, which will influence the ap-proach to management, and the prognosis of a patientwho presents with a lung abscess [1–3].

∗Correspondence: Dr. Dominic A. Fitzgerald, Department of Res-piratory Medicine, The Children’s Hospital at Westmead, LockedBag 4001, Westmead, Sydney, NSW, Australia, 2145. Tel.: +61 29845 3397; Fax: +61 2 9845 3396; E-mail: [email protected]

2. Definition

A lung abscess is a thick-walled cavity that containspurulent material resulting from suppuration and necro-sis of the lung parenchyma [1–4]. The lung abscessmay be primary or secondary. A primary lung abscessoccurs in a previously well child with normal lungs,usually as a complication of pneumonia, and will usu-ally reach a full recovery without any sequalae. A sec-ondary lung abscess occurs in a child with an under-lying airway or lung abnormality, which may be con-genital (cystic fibrosis, immunodeficiency or structuralmalformation) or acquired (achalasia or a neurodevel-opmental abnormality) [1–3].

3. Epidemiology

It has been suggested that lung abscesses were morecommon in previous years [1] before the ability of pre-

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28 H. Alsubie and D.A. Fitzgerald / Lung abscess in children

Table 1Factors predisposing to secondary lung abscesses may be seen inchildren at increased risk of pulmonary aspiration such as those withthe following predisposing factors

Immunocompromised host:ChemotherapyImmunosuppressive treatment (corticosteroids)Nutritional deficiencies

Localized structural lung abnormalities:Congenital cystic adenomatoid malformationBronchogenic cystTracheo-esophageal fistula (H-type)

Generalized suppurative lung disease:Cystic fibrosis

Hematogenous spreadNeurodevelopmental abnormalities:

Poorly coordinated swallowingNeuromuscular condition such as myotonic dystrophy andDuchenne muscular dystrophy

Esophageal motility problems:Following tracheo-esophageal atresia repairEsophageal stricturesAchalasia

venting aspiration of infected fluid at the time of ton-sillectomy, the widespread availability of antibioticsto treat chest infections and the more recent evolutionof better lung imaging to enable earlier treatment ofpneumonia before complications, such as lung abscessand pneumonia arose [1]. Figures from Canada in the1980s put the incidence of children hospitalized witha lung abscess at 0.7 per 100,000 [5]. Lung abscessmay occur at any age but is thought to be less commonin the neonatal period [1]. However, this may changewith the increasing shift of neonatal care to support in-fants at the extreme of viability and the resulting inva-sive techniques (e.g. central venous lines for parenteralnutrition) to support these technology dependent chil-dren, often with significant neurocognitive and physicaldisabilities [1,2,6].

4. Predisposing factors

A lung abscess may arise from aspiration of infectedfluid, aspiration of non-infected fluid which triggers achemical irritation (e.g. acidic gastric fluids), a primarybacterial lung infection, hematogenous spread of bacte-ria (e.g. bacterial endocarditis of the right sided cham-bers of the heart) or contiguous spread of infection froma neighboring organ [1,3]. Pulmonary aspiration maybe the central factor in the evolution of a lung abscess.Whether this occurs acutely in a previously well childwho has inhaled brackish, infected water or in a debil-itated child with recurrent aspiration of upper airway

secretions and saliva or gastric contents, aspiration is acommon initial step in the progression from pneumoni-tis to pneumonia to lung abscess. Specifically, predis-posing factors in well children in adolescence includeanesthesia, head injury with impaired cognition, exces-sive sedation or alcohol ingestion, poor dental hygienetogether with poor gingival status that may be seen inchildren receiving anticonvulsants [1–3]. The signifi-cance of the introduction of oral flora into the lung isthat the bacteria are predominantly anaerobic and thiswill alter the antibiotic approach [3,6]. It is worth not-ing that lung abscess is rare in neonates and also maybe associated with predisposing factors such as lungcyst, pneumonia, cognitive impairment or the presenceof central venous lines. Again, the early symptoms andsigns may be non-specific [1–3].

In the child with ongoing pulmonary aspiration, it isthe impaired mucociliary defense mechanisms, whichincrease the likelihood of pulmonary morbidity andmortality [6]. These may occur for a variety of reasons,which begin with pooled oral secretions and poorly co-ordinated swallow mechanisms. Contributing to thismay include: gingival infection, neuromuscular weak-ness, structural proximal airway abnormalities (e.g.cleft larynx), vocal cord palsy, tracheo-bronchomalaciaand significant thoracic scoliosis [2,3,6]. Converse-ly, there may be significant gastro-esophageal refluxof acidic stomach contents and pulmonary aspirationof these fluids. Indeed, it is often gastro-esophagealreflux, which is the focus of investigations and inter-ventions such as gastrostomy tube insertion and fun-doplication of the stomach. The role of fundoplicationmay have been over-emphasized previously as there isnow a trend toward inserting gastrostomy tubes with-out fundoplication in the absence of documented evi-dence of reflux [6]. This is a reasonable approach, butit is important to consider the possibility of inducinggastro-esophageal reflux following gastrostomy feedsat higher volumes (e.g. bolus feeds as opposed to lowervolumes given as continuous overnight feeds) [6].

Additional factors to consider in a previously wellchild include the case of a bacterial pneumonia whichoften follows an otherwise unremarkable viral upperrespiratory tract infection [1,2,4]. The presumed bac-terial infection may or may not have been treated alongthe course of progressing to a lung abscess. Alterna-tively, the child may have developed bacterial endo-carditis, more commonly on an abnormal heart valveor in a structurally abnormal heart, which has sent offseptic emboli to the lungs (Table 1) [1,2,5–7].

H. Alsubie and D.A. Fitzgerald / Lung abscess in children 29

Table 2Common pathogens in lung abscesses

Classification Pathogen

Aerobic Gram-positive cocci Streptoococcus pneumoniaeStaphylococccus aureus

Aerobic Gram-negative Pseudomonas aeruginosabacilli Klebsiella pneumoniaeAnaerobic cocci Peptostreptococcus,

Microaerophilic streptococciAnaerobic Gram-negative Bacteroides speciesbacilli Prevotella, Fusobacterium

speciesFungus Candida albicans, Aspergillus

species

5. Pathophysiology

Once the lungs are soiled, an inflammatory cascadeis triggered giving rise to the chemical pneumonitis,which predisposes to infection. Aspiration pneumoni-tis is an acute lung injury, which occurs after the in-halation of regurgitated gastric contents [7]. Aspira-tion pneumonitis, was originally described as Mendel-son’s syndrome from the adult obstetric literature [8],is a chemical injury caused by the inhalation of sterilegastric contents which is seen as distinct from aspira-tion pneumonia which is an infectious process resultingfrom the inhalation of oropharyngeal secretions whichare colonized by pathogenic bacteria [7]. There is con-siderable overlap between these conditions and it maybe difficult to distinguish them in the clinical setting.Nonetheless, both may contribute to the subsequent de-velopment of the relatively uncommon complication oflung abscess (Table 2).

Aspiration pneumonitis is seen in children with amarked disturbance of consciousness which may beseen in conditions including: status epilepticus, hypox-ic and metabolic encephalopathies, catastrophic cere-brovascular events, cerebral trauma as well as patientswith severe neurocognitive impairment of uncertain eti-ology, often referred to as having “cerebral palsy” [4,6,7]. It is a recognized complication of general anesthe-sia for any operative procedure and may occur despiteall appropriate anesthetic precautions [6,7]. Again, inthe adult literature, a correlation between the level ofimpaired consciousness as measured by the GlasgowComa Scale and the risk of aspiration was demonstrat-ed [9]. It has been suggested that a gastric aspirate pHof less than 2.5 and a volume of greater than 0.3 mLper kilogram of body weight are required for the devel-opment of aspiration pneumonitis in adults [7]. Thereis no corresponding data for children. However, thestomach contents contain other irritants besides gas-

tric acid and so it is possible to cause an inflammatoryresponse without highly acidic fluid [7–10].

It is likely that the number of episodes of aspira-tion, the volume of aspirated material and any impair-ment of mucociliary clearance mechanisms contributeto the development of a lung abscess [1,2,6,7]. Thetime course for progression from aspiration to pneu-monia and abscess is not rapid. Indeed, the course issomewhat insidious, especially in children with chroniclow-grade cough related to impaired mucociliary clear-ance. Interestingly, it takes days before the symptomsand signs develop even after a known aspiration eventhas occurred, because the body’s host defense mecha-nisms may decrease perfusion to an area of aspirationand thereby reduce the influx of defense mediators andthe egress of infective material [5–7]. Animal workhas demonstrated that there is a biphasic response afteracid aspiration [10].

A lung abscess may arise from embolic phenomenasuch as right-sided bacterial endocarditis, more likelyin children with right-sided heart valve abnormalitiesand post-surgery or the placement of a central venousline [2,6,7]. Rarely, children with septicemia may havefoci in the lung from hematogenous spread or fromthrombophlebitis with septic emboli. In addition, lo-cal extension from pharyngeal abscesses or abdominalcollections is also seen [7].

In the case of a single small lung abscess, the changesin ventilation and perfusion may be minimal. As theabscess grows there may be more significant changesin ventilation and perfusion, resulting in hypoxemiaand tachypnea. With the evolution of pleuritic painfrom pleural inflammation, there may be a restrictivecomponent to lung function due to the loss of lungvolume and reduced lung compliance [1].

6. Clinical presentation

The presentation of lung abscess may be insidious,typically evolving over two weeks in a child with feverand cough. Other features may include chest pain, dys-pnea, sputum production and hemoptysis (Table 3) [1,2,5]. The physical findings may range from no de-tectable abnormality in the chest to signs of consolida-tion (Table 4). Not infrequently, the diagnosis is madeon a chest radiograph as an investigation in a child witha persisting cough where a well-circumscribed shadowis seen containing an air-fluid level [2]. This is more of-ten the case in children with a primary lung abscess [1,2,11].


Table 3Symptoms reported in several series for children with a lung abscess

Parameters Ho et al. [2] Tan et al. [18] Chan et al. [24] Yen et al. [25](n = 23) (n = 23) (n = 27) (n = 23)

Fever 83% 84% 100% 91%Cough 65% 53% 67% 87%Dyspnea 36% 35% 19% 35%

Table 4Clinical signs elicited in children with primary and secondary lung abscess from the Children’sHospital at Westmead (1985–2001) [2]

Parameters Primary lung abscess Secondary lung abscess(n = 29) (n = 14)

Tachypnea 100% 71%Dull percussion note or reduced air entry 44% 79%Fever 44% 50%Localized crepitations 33% 36%

In contrast, a child with a secondary lung abscess ismore likely to have underlying medical problems. Suchproblems may include recurrent pulmonary aspirationof saliva and upper airway secretions, debilitation, sig-nificant neuron-cognitive disability, dysphagia, naso-gastric tube feeding, seizure disorders, altered levelsof consciousness, congenital or acquired immunodefi-ciency states and congenital abnormalities of proximalairway structures [11]. In vulnerable individuals, thepresence of poor oral hygiene predisposes to aspirationpneumonia, lung abscess and empyema with anaerobicorganisms [7].

7. Microbiology

The pathogens causing a lung abscess may be classi-fied as being aerobic, anaerobic or fungal. More com-monly isolated pathogens are listed in Table 1. In addi-tion to Staphylococcus aureus,one should also considergroup B Streptococcus, Escherichia coli and Klebsiellapneumoniae in young infants [1]. However, with age,the likelihood of predisposing factors to lung abscessincreases and therefore the likelihood of an anaerobicpathogen increases. From the work in the 1970s, us-ing trans-tracheal aspiration, studies demonstrated thatanaerobic bacteria accounted for 60–80% of lung ab-scess, with Peptostreptococcus species, Fusobacteriumnucleatum and Prevotella melaninogenica predominat-ing [12–15]. These bacteria matched known oral flora,which had been implicated by Dr David Smith at DukeUniversity in the pre-antibiotic era of the 1920s [15].

In children with aspiration pneumonia, the likelihoodof yielding an anaerobic organism was reported to beas high as 90% in trans-tracheal aspirates evaluated in

a cohort of 74 children with aspiration pneumonia: 52with pneumonitis, 12 with necrotizing pneumonia and10 with a lung abscess [12]. Interestingly, an averageof 4.9 organisms per aspirate was isolated (2.7 anaer-obes and 2.2 aerobes) in that study. It is not uncommonto isolate multiple organisms from lung abscesses andmore commonly in secondary lung abscesses [12–17].This is not only related to how the specimen is col-lected, percutaneous or trans-tracheal versus purulentsputum or unprotected bronchial brushings where con-tamination with oral flora may occur [12–14]. Anaer-obes are more common in patients who are predisposedto aspiration, such as with dental caries, seizure dis-orders and impaired co-ordination of swallowing [13–16]. In a cohort of adults presenting with acute lungabscess in South Africa in the early 1990s, 29 of 34patients had predisposing factors for lung abscess (i.e.secondary lung abscess). In these subjects, anaerobesaccounted for 74% of the bacterial yield, and apart fromthose subjects with tuberculosis, the bacterial culturesobtained consisted of anaerobes alone in 52% and ofaerobes alone in only 22% [17]. In a pediatric sampleof patients presenting with an acute lung abscess fromZimbabwe in 1992, more aerobic organisms were cul-tured, especially S. aureus, reflecting different risk fac-tors for lung abscess (e.g. post-viral lower respiratorytract infection) and the higher proportion of primarylung abscesses seen [17].

Importantly, the key issues are to consider the likeli-hood of anaerobic pathogens, to attempt to obtain un-contaminated purulent material from the abscess cavity,culture the pus in appropriate anaerobic media and treataccordingly. The sensitivity of some obligate anaer-obes to die when exposed to air will undermine attemptsto isolate causal anaerobic bacteria and so a liquid spec-


imen of pus is best injected directly after aspiration intoan oxygen-free (anaerobic) transport vial [11].

8. Imaging

The basic diagnostic test for lung abscess is the chestradiography, which typically demonstrates an air-fluidlevel within a spherical area of consolidation (Fig. 1).The possibility of lung abscess is greater in the de-pendent areas of lung, which are more prone to reflectpulmonary aspiration, specifically the posterior upperlobe or the superior lower lobe [11]. In one series of45 lung abscesses in subjects aged from 1 month to 28years, the distribution was as follows: right upper lobe(36%), right lower lobe (33%), right middle lobe (24%)and left upper lobe (9%). Eleven of the 45 subjects hadinvolvement of more than one lobe and in 16% of allcases; a pleural effusion was demonstrated [18]. Thisimportant data was gathered from one large US centreover nearly 14 years (1982–1993). The data present-ed, when contrasted with current practice, highlightshow the role of interventional radiology has come tothe fore in the role of management of lung abscess, therole of computerized tomography (CT) guided imaginghas improved and the duration of inpatient stay has re-duced. Today, not withstanding concerns about the useof ionizing radiation, low dose, contrast-enhanced CTscans are usually considered to be the investigation ofchoice to distinguish lung abscess from an empyema,necrotizing pneumonia with a pneumatocele, seques-tration or underlying congenital abnormality such asbronchogenic cyst [2–4]. This is particularly relevantif image guided drainage is considered to distinguishbetween necrotizing pneumonia and lung abscess [4].

The characteristic appearance of a lung abscess ona CT image is shown in Figs 2a and 2b. In particular,the thick-walled cavity contains mobile, central fluidoccurring in the midst of an area of consolidated lung.An air-fluid level is often apparent on the CT scan,even when it may not be evident on the plain chestradiograph [19]. Magnetic resonance imaging scansoffer no diagnostic advantage over CT scans and arenot routinely used in most centers for investigation andtreatment of lung abscess as the resolution provided is,at present in clinical practice, not as helpful as the CTimaging [19].

Fig. 1. Chest radiograph of a lung abscess in the right upper lobe.

8.1. The role and type of interventional approach

The traditional mode of therapy has involved intra-venous antibiotic treatment with a lengthy hospital stayfollowed by several weeks of enteral antibiotics [1,3,20]. The alternative was surgery, usually with a lobec-tomy or segmentectomy where possible [1,5]. Howev-er, this was not a simple procedure and came with sig-nificant morbidity and some mortality, particularly inpatients with predisposing conditions for a secondarylung abscess [1]. Consequently, the involvement ofinterventional procedures in the management of lungabscess became established [4].

The aspiration of lung abscesses with or without anexternal drain under CT guidance for large, peripheral-ly located abscesses has been used in the pediatric pop-ulation since the 1980s, with reports of improved suc-cess rates, reduced morbidity and mortality [2]. Nee-dle aspiration under image guidance has been used formany years with success for diagnostic and therapeuticpurposes, but lacks the utility of a small percutaneousdrain (pigtail catheter) which may drain the collectionfor several days if required. Originally, the conceptof CT-guided drainage and the insertion of a pigtailcatheter for lung abscess and empyema were consid-ered when medical therapy had failed or for rapid di-agnostic and therapeutic benefit in patients consideredtoo unwell for surgery [21–23]. With experience, thepractice has broadened to the point where intervention-al radiology is considered the standard of care wheresuch expertise is available [2]. This has been suggest-ed to result in more rapid defervescence of fever andsymptoms, shorter periods of intravenous antibiotics


(a)

(b)

Fig. 2. (a) Computerized tomography scan image of a lung abscess,(b) Computerized tomography scan imaging assisting in the place-ment of a pigtail catheter drain.

and a decreased length of inpatient care [2]. However,there does remain a role for surgery in selected cases.In a recent series of 27 cases (eight primary and 19secondary lung abscesses occurring between 1987 and2003) from Taiwan, lobectomy was needed in five of27 patients (18.5%) [24]. In this series, surgical in-terventions were required in eight (42%) of 19 of pa-tients with secondary lung abscess. In the cohort, 10/27had ultrasound-guided aspiration of their abscesses andonly one had CT guided aspiration [24].

By way of contrast, at the Children’s Hospital atWestmead in Sydney, the rise in interventional radiolo-gy over the past 20 years has resulted in routine use ofCT-guided aspiration for abscesses and, in more recentyears, in the use of CT-guided pigtail drainage cathetersat the time of presentation. This has translated into ahigher proportion of positive cultures overall, with a

Table 5Antibiotic treatment doses∗

Intravenous antibiotics Dose [26]

Benzylpenicillin (30 mg/kg up to) 1.2 g 4 to 6 hourlyDi/Flucloxacillin (50 mg/kg up to) 2 g 6 hourlyCefotaxime 50 mg/kg 8 hourlyCeftriaxone 50 mg/kg once dailyClindamicin (10 mg/kg up to) 450 mg 8 hourlyVancomycin (10 mg/kg up to) 500 mg 6 hourlyMetronidazole (12.5 mg/kg up to) 500 mg 8 to 12 hourlyMeropenem (20 mg/kg up to) 1 g 8 hourly∗Derived from the Children’s Hospital at Westmead Handbook [26].

higher prevalence anaerobes, a reduced proportion ofS. aureus and Haemophilus influenzae type b (since theintroduction of routine immunization in 1992) and ashorter length of hospital stay than reported in previ-ous series [2]. Most interestingly, for the 19 patientsmanaged exclusively in our institution (mean age 8.3years; range 20 days to 19.5 years) between 1985 and2000 with a primary lung abscess (n = 9), the averagelength of stay in our institution was 12.4 days [95%confidence interval (CI) 8.4, 16.5] and for those withsecondary lung abscess (n = 10) it was 25.1 days (95%CI 14.6, 35.6), giving an overall average of 19.1 days(95% CI 13.0, 25.2) [2]. Subsequently, over the past 5years, the length of hospital stay has decreased in ourinstitution. Current practice at the Children’s Hospitalat Westmead in Sydney sees children presenting withprimary lung abscess managed routinely undergoingplacement of a CT-guided pigtail catheter at presenta-tion, with 2–3 days of drainage, intravenous antibioticsand discharge within 7 days on a course of oral (enteralfor those managed with gastrostomy feeds and medi-cations) antibiotic therapy to complete a month of totalantimicrobial therapy guided by culture results [1,2,6,13,20].

9. Antibiotics

The choice of antibiotics (Table 5) varies somewhatbetween institutions and is guided by a number of fac-tors, including the ability to isolate organisms throughaspiration and drainage of the abscess, whether the ab-scess is believed to be a primary or secondary phe-nomenon, the likelihood of penicillin resistance, costand local practices [1,2,6,13,20,25,26]. At our in-stitution, we initially prefer to use a third-generationcephalosporin and flucloxacillin (or clindamicin) un-til the aspirated lung abscess fluid culture results areavailable to rationalize therapy.


For primary lung abscess, antibiotic choice shouldcover likely organisms including S. aureus, Streptococ-cus pneumoniae and other streptococcal species andgram-negative bacilli that are normally found in the up-per respiratory tract. Therefore, the use of flucloxacillinand cefotaxime/ceftriaxone would be appropriate start-ing points. With the increasing threat of multiply resis-tant S. aureus (MRSA), the role of vancomycin is likelyto increase. For patients at risk of a hospital acquired in-fection with Klebsiella spp. or Enterobacter spp., theseare resistant to penicillin and there is an increasing riskof antibiotic resistance to third and fourth generationcephalosporins owing to the production of plasmid-mediated extended-spectrum beta-lactamases. Conse-quently, most isolates are sensitive to fluoroquinolones,trimethoprim/ sulfamethoxazole, aminoglycosides andcarbapenems (e.g. meropenem) and a combination ofa carbapemem (or fluoroquinolone) with an aminogly-coside may be appropriate [20].

For patients at risk of secondary lung abscess throughaspiration, it is important to cover anaerobes normallyfound in the upper airway, with clindamicin provid-ing coverage against these organisms as well as S. au-reus. Alternatives could include benzylpenicillin andmetronidazole. For an immunocompromised host, an-tibiotic coverage is broader and likely to include con-sideration of fungal pathogen. Once the child has de-fervesced, an oral antibiotic would replace the intra-venous therapy and the child would be discharged onan oral antibiotic to complete a four-week course oftreatment [1,2,13,20,25,26].

10. Clinical course

If intravenous antibiotics alone are used, the fevermay resolve in seven to ten days and the illness resolveswithin a further two weeks [1,5]. It is our experiencethat the use of interventional radiology has since ap-proximately halved the length of hospitalization fromour figures from 1985 to 2000 of 12.4 days for a pri-mary lung abscess and 25 days for a secondary lungabscess [2]. The use of percutaneous aspiration or pig-tail catheter drainage (Fig. 3) shortens the course ofthe illness considerably and probably has an associatedcost saving allowing for the costs of anesthesia and in-terventional procedures given the costs of intravenoustherapies and hospital bed days [2]. More importantly,a shorter hospital stay is better for the children and theirfamilies [1,2].

Fig. 3. Transcutaneous drain in situ in treatment of a lung abscess(Photo courtesy of Dr David Lord).

The rate of resolution of the abscess cavity lags be-hind the clinical resolution of the abscess. In fact,whilst children would routinely receive another 3 weeksof oral antibiotics after discharge, the abscess cavityon the chest radiograph may persist for months to evenyears after appropriate therapy [1]. Pulmonary functiontypically returns to baseline [5].

10.1. Complications

In the pre-antibiotic era, a lung abscess was fatal in30% to 40% of cases [1]. In contrast, whilst deathsdue to lung abscess still occur in children, they are be-lieved to be infrequent for primary lung abscess butmore common in secondary lung abscess. Deaths aremore commonly reported in cases of secondary lungabscess where host factors (e.g. malnutrition in patientsin the developing world; immunodeficiencies or malig-nancies) are more likely to determine the outcome incases [1]. In our experience, there have been no deathsfrom lung abscess in the last 20 years [2], yet in a sim-ilar time period from Taiwan there were 5/27 (18.5%)of patients who died due to the severity of their under-lying conditions [21]. The series from Taiwan reported


Table 6Complications of lung abscess

Spontaneously rupture into adjacent compartmentEmpyema, pyothorax or pneumothorax

The connection between the abscess cavity and the pleural spaceBronchopleural fistula

Hematogenous spread leading to multiple abscessesAnesthesia complication:

Aspiration, reaction, post-op nausea and feverRadiation exposure:

Computerized tomography scans, chest radiographsReaction to antibiotics:

Fever, rash or anaphylaxisSite scar

a complication rate of 41%, which included respiratoryfailure (6/27), pneumothorax (3/27), shock (1/27), os-teomyelitis (1/27) and colon perforation (1/27). In ad-dition, four surviving patients had sequelae (2/27 withbronchiectasis and 2/27 with lung fibrosis) [24].

Spontaneous complications described include over-expansion of the abscess with lung compression andmediastinal shift, tension pneumothorax after abscesswall rupture into the pleural space and spontaneousrupture of the abscess with seeding to other parts of thelung [1].

Complications leading to significant morbidity mayalso occur and are more likely to result from interven-tions than to the underlying disease process [1]. Thesemay include abscess rupture and intrabronchial spreadof pus at the time of evaluation with bronchoscopy,bleeding and subcutaneous emphysema from transtra-cheal needle aspiration. Transcutaneous drainage maybe associated with pneumothorax or the developmentof a broncho-pleural fistula will require insertion of apleural drain for a number of days with the likely resultof spontaneous closure without surgical intervention [3,4]. Lobectomy has been associated with empyema andpleural effusion (Table 6) [1]. In western centers, thestandard management of empyema includes the use ofimaging and removal of pus from the pleural space withinterventional radiology or surgical intervention withvideo-associated thoracoscopic surgery [22]. There isno fixed length of antibiotic therapy, but most clini-cians would provide for a total of four to six weeks ofantibiotic treatment, with the initial 5–10 days beingdelivered intravenously to coincide with drainage, andthe balance orally as an outpatient [23].

10.2. Long term outcome

The prognosis for children with primary lung abscessis overwhelmingly favorable. In adults, the morbiditywith lung abscess is reported as being 15–20% [24],

whereas in children the mortality is significantly lower,probably of the order of less than 5% and occurs pre-dominantly in those with a secondary lung abscess [21].It is the co-morbidity of the predisposing conditions inboth adults and children that contributes to the worseprognosis and higher mortality rate. Consequently, al-most all immunologically competent children with aprimary lung abscess would be expected to recover,whereas those with predisposing conditions, predom-inantly immunocompromised states, would expect tofare significantly worse [1,2,18,21,24,25].

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Lung Abscess in Children