Lung Abscess: Cavitation, Foul Sputum and the Cause Behind It

Introduction

A lung abscess is a localised collection of pus within a cavity formed by necrosis of lung parenchyma. By convention the term is applied to a single cavity greater than 2 cm; multiple smaller cavities are described as necrotising pneumonia, and the two lie on the same pathological spectrum.

Abscesses are conventionally divided into:

• Primary - arising in otherwise normal lung, almost always following aspiration. This accounts for the large majority.
• Secondary - arising because of an underlying problem: bronchial obstruction by tumour or foreign body, septic emboli from right-sided endocarditis, bronchiectasis, an infected bulla, immunosuppression, or direct spread from a subphrenic or hepatic abscess

The incidence has fallen substantially since the introduction of antibiotics, and it is now most often seen in people with alcohol dependence, poor dentition, neurological swallowing impairment, diabetes or immunosuppression. Because it is uncommon and the presentation is subacute, it is frequently misdiagnosed for weeks as unresolving pneumonia, tuberculosis or malignancy.

Aetiology

Why aspiration explains the anatomy

Aspirated material travels down the path of least resistance and then settles under gravity, which is why abscesses occur in predictable places. The right lung is affected more often because the right main bronchus is wider, shorter and more vertical than the left.

Risk factors

• Reduced conscious level - alcohol intoxication, drug misuse, seizures, general anaesthesia, head injury, sedation
• Impaired swallow - stroke, bulbar and pseudobulbar palsy, motor neurone disease, Parkinson's disease, dementia
• Poor dental hygiene and periodontal disease - the reservoir of anaerobic organisms, and the reason abscesses are rare in edentulous patients unless there is an obstructing tumour
• Oesophageal disease - achalasia, strictures, reflux, pharyngeal pouch, tracheo-oesophageal fistula
• Bronchial obstruction - carcinoma, an inhaled foreign body, or extrinsic compression by nodes
• Immunosuppression - HIV, chemotherapy, corticosteroids, transplantation, poorly controlled diabetes
• Intravenous drug use - through right-sided infective endocarditis producing septic pulmonary emboli, which characteristically cause multiple peripheral cavitating nodules
• Pre-existing lung disease - bronchiectasis, cystic fibrosis, emphysematous bullae

Organisms

• Anaerobes - Peptostreptococcus, Prevotella, Bacteroides and Fusobacterium. The classic cause of the primary aspiration abscess and the source of the putrid sputum.
• Streptococcus anginosus (milleri) group - strongly associated with abscess and empyema formation
• Staphylococcus aureus - including Panton-Valentine leukocidin-producing strains, which cause a fulminant necrotising cavitating pneumonia in young previously healthy people, often after influenza, and carry a very high mortality
• Klebsiella pneumoniae - upper lobe cavitation with redcurrant jelly sputum, classically in alcohol dependence and diabetes
• Pseudomonas aeruginosa and other Gram-negatives in hospital-acquired disease
• Mycobacterium tuberculosis - always in the differential of any cavity
• Nocardia and Actinomyces - subacute, in the immunosuppressed and after dental disease respectively; actinomycosis classically crosses tissue planes and produces sulphur granules
• Fungi - Aspergillus and, in the profoundly immunosuppressed, others
• Infection is often polymicrobial, particularly after aspiration

Clinical features

The presentation is characteristically subacute, evolving over one to several weeks, in contrast to the abrupt onset of pneumococcal pneumonia. This indolent course is itself a diagnostic clue, and is why patients often present having already had one or more unsuccessful courses of antibiotics.

Symptoms

• Fever, rigors and night sweats
• Cough productive of large volumes of sputum. Once the abscess ruptures into a bronchus, the patient may expectorate a large quantity of pus at once (vomica), which is dramatic and clinically important because it establishes bronchial communication.
• Foul-smelling or putrid sputum - strongly suggests anaerobic infection, and is one of the few genuinely specific clinical signs in respiratory medicine
• Weight loss, anorexia and profound malaise over weeks
• Pleuritic chest pain if the pleura is involved
• Haemoptysis - usually mild, but occasionally massive if the cavity erodes a vessel

Signs

• Fever and tachycardia
• Signs of consolidation over the affected area - dull percussion, bronchial breathing, coarse crackles
• Amphoric or cavernous breath sounds over a large superficial cavity - hollow and blowing, like air across the mouth of a bottle. Uncommon but classic.
• Finger clubbing - developing over weeks in a chronic abscess
• Poor dentition and gingival disease - examine the mouth, as it is both diagnostic and a treatment target
• Cachexia and anaemia in chronic disease
• Signs of the underlying cause - a swallowing abnormality, needle marks and a murmur suggesting endocarditis, or lymphadenopathy and cachexia suggesting malignancy

Investigations

Imaging

• Chest radiograph - a thick-walled cavity with an air-fluid level, usually surrounded by consolidation. The air-fluid level only appears once the abscess has ruptured into a bronchus, and is best seen on an erect film.
• CT thorax with contrast - more sensitive and the key investigation. It confirms the cavity, defines its size and site, identifies multiple lesions, and above all distinguishes an abscess from an empyema and reveals an underlying obstructing lesion.

Microbiology and blood tests

• Sputum culture - including anaerobic culture, though yield is limited because sputum is contaminated by oral flora, which are the same organisms
• Blood cultures - and repeat sets if endocarditis is suspected
• Sputum for AFB smear and culture - in every cavitating lesion, since tuberculosis is the most important infective mimic
• Bronchoscopy with washings or protected specimen brush - for microbiology where the diagnosis is unclear, and essential where bronchial obstruction is suspected or the abscess is not responding
• Percutaneous or transbronchial aspiration - occasionally used in specialist centres to obtain uncontaminated material
• FBC, CRP, U&Es, LFTs and albumin - a neutrophilia with anaemia of chronic disease and a low albumin is typical
• HIV test, and consider immunodeficiency or diabetes screening
• Echocardiogram if septic emboli or endocarditis are suspected

Differential diagnosis of a lung cavity

• Cavitating bronchial carcinoma - especially squamous cell carcinoma, which cavitates most readily. A thick, irregular, nodular wall in an older smoker with fewer infective features.
• Tuberculosis - upper lobe, with fibrosis, calcification and volume loss, and a longer history of weight loss and night sweats
• Granulomatosis with polyangiitis - multiple cavitating nodules with upper airway and renal involvement, and positive c-ANCA
• Septic pulmonary emboli - multiple peripheral cavitating nodules, in intravenous drug use or with an infected line
• Pulmonary infarction - which may cavitate
• Rheumatoid nodules
• Infected emphysematous bulla - a thin wall with little surrounding consolidation
• Fungal infection - including an aspergilloma, in which a fungal ball sits within a pre-existing cavity

Management

Antibiotics

• Prolonged antibiotic treatment is the mainstay, and around 80 to 90% of abscesses resolve on antibiotics alone
• Anaerobic cover is essential. First line is usually co-amoxiclav, or clindamycin in penicillin allergy; a combination such as a cephalosporin with metronidazole is an alternative. Follow local microbiology guidance.
• Start intravenously until the patient is afebrile and improving, then switch to oral
• Continue for 4 to 6 weeks, and often longer - the endpoint is radiological resolution or a stable residual scar, not simply clinical improvement. Stopping early is the commonest cause of relapse.
• Note that metronidazole alone is inadequate - it does not cover the microaerophilic streptococci that are frequently co-pathogens

Drainage and clearance

• Postural drainage and chest physiotherapy - to help the abscess empty through the bronchus
• Percutaneous catheter drainage under image guidance - considered for large abscesses (typically above 6 to 8 cm), or where there is no response after 5 to 7 days of appropriate antibiotics
• Bronchoscopic drainage - occasionally used, and also allows the exclusion of an obstructing lesion
• Surgical resection (lobectomy or segmentectomy) - required in fewer than 10%. Indications are failure of medical treatment, massive haemoptysis, a very large abscess, suspected underlying malignancy, or a bronchopleural fistula.
• Nutritional support, correction of anaemia, and VTE prophylaxis

Treating the cause

Follow-up

• Serial chest radiographs to confirm resolution - typically at 4 to 6 weeks and then until stable. A residual thin-walled cavity or scar may persist and is acceptable if the patient is clinically well.
• Any cavity that fails to resolve requires further investigation for malignancy or tuberculosis
• Monitor CRP and clinical progress to guide the duration of treatment

Complications

• Rupture into the pleural space - producing an empyema or a pyopneumothorax, and requiring chest drainage
• Bronchopleural fistula
• Massive haemoptysis - from erosion of a bronchial artery within the cavity wall; a life-threatening emergency treated with airway protection, tranexamic acid and bronchial artery embolisation
• Metastatic infection - especially brain abscess, and also osteomyelitis and septic arthritis. New neurological symptoms in a patient with a lung abscess warrant urgent brain imaging.
• Sepsis and septic shock
• Chronic abscess with persistent cavitation, recurrent infection and clubbing
• Bronchiectasis in the surrounding lung
• Secondary AA amyloidosis - rare, from prolonged chronic suppuration
• Respiratory failure, particularly in necrotising pneumonia

Red flags

Prognosis

With appropriate prolonged antibiotic treatment, the outlook for a primary aspiration abscess in an otherwise reasonably well patient is good: 80 to 90% resolve on medical treatment alone, and overall mortality is around 5 to 10%.

The picture is considerably worse in secondary abscess, where mortality rises above 20% or more. The factors that predict a poor outcome are an underlying bronchial carcinoma, immunosuppression, large abscesses over 6 cm, multiple abscesses, hospital-acquired and Gram-negative organisms, low serum albumin and advanced age.

Radiological resolution is slow, taking weeks to months, and a residual thin-walled cavity or area of scarring is common and not in itself concerning if the patient is well. What always matters is whether the underlying cause was found and treated - a patient whose teeth are fixed and whose swallow is assessed is unlikely to return with a second abscess, while one who is simply given antibiotics frequently does.