Pleural infection

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

A parapneumonic effusion progresses from a free-flowing sterile exudate to fibrin deposition, septation, bacterial invasion and an organised pleural peel. Antibiotics penetrate and sterilise early fluid more readily than an acidic loculated empyema. Source control therefore becomes increasingly important as pH falls, glucose is consumed and fibrin partitions the cavity.

The drainage decision combines appearance, microbiology, pH and anatomy. Frank pus or positive Gram stain or culture mandates drainage. For non-purulent fluid, BTS uses immediate pH as the primary discriminator, with LDH, glucose, volume, pleural enhancement and septation refining intermediate results. A small residual effusion in a clinically improving patient is not managed like a large loculated collection with ongoing sepsis.

Treatment is multidisciplinary: respiratory or pleural clinicians provide ultrasound and drainage; microbiology guides antimicrobials; radiology helps access difficult locules; surgeons provide VATS debridement or decortication when medical treatment fails. Exact pH handling, fibrinolytic regimen and drain-care steps should follow the current BTS document and the local pleural procedure protocol.

Key points

Pleural infection includes complicated parapneumonic effusion and empyema; pus or organisms in pleural fluid establishes the need for drainage regardless of pH.
Persistent fever, pleuritic pain or sepsis despite pneumonia treatment should prompt thoracic ultrasound, even when the chest radiograph shows only basal shadowing.
Use ultrasound guidance for aspiration and drain placement. Septations and echogenic fluid support complexity but do not replace fluid analysis.
Measure pleural pH immediately in a heparin-free blood-gas syringe without local-anaesthetic contamination. Air, delay and lidocaine can materially distort the result.
In non-purulent fluid, pH at or below 7.20 indicates high risk and usually warrants a drain if safely accessible. Intermediate pH requires LDH, glucose, imaging and clinical context under the BTS pathway.
Send pleural fluid in both sterile containers and inoculated blood-culture bottles to improve microbiological yield, alongside cytology when malignancy remains possible.
Start antibiotics covering likely community- or hospital-acquired organisms and anaerobes, then narrow to cultures and clinical response. Duration is individualised and usually extends beyond initial intravenous therapy.
A small-bore chest tube is usually adequate initially when positioned in the collection and flushed according to protocol.
If drainage has stopped with residual collection, combined intrapleural tPA and DNase can improve drainage; do not use either agent alone as a substitute.
Failure of sepsis and collection to improve requires early thoracic-surgical review. Do not wait for prolonged organ failure before discussing VATS.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Parapneumonic spread

Bacterial pneumonia extends inflammation and organisms into an adjacent pleural effusion, the most frequent pathway to complicated infection.

Aspiration-associated infection

Poor dentition, swallowing dysfunction and impaired consciousness increase polymicrobial lower-airway infection and pleural extension, with the final risk shaped by exposure and individual susceptibility.

Direct inoculation

Thoracic surgery, trauma, pleural procedures and oesophageal rupture can introduce organisms directly into pleural space, with the final risk shaped by exposure and individual susceptibility.

Host vulnerability

Frailty, diabetes, alcohol dependence and immune suppression increase infection severity and may produce less obvious systemic signs.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Reactive exudate
Adjacent pneumonia increases pleural permeability, initially producing free-flowing inflammatory fluid, and the downstream physiological effect determines clinical severity.
2
Microbial invasion
Bacteria enter the collection; neutrophil and microbial metabolism acidifies fluid and consumes glucose, and the downstream physiological effect determines clinical severity.
3
Loculation
Fibrin deposition creates septations that isolate infected pockets and prevent effective passive drainage, which links the underlying lesion to the observed respiratory dysfunction.
4
Organised rind
Fibroblast ingrowth thickens visceral pleura, traps the lung and sustains restriction after the acute infection, which helps produce the characteristic physiological impairment.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Complicated parapneumonic effusionRed flag

Pneumonia with persistent fever, pleuritic pain, systemic inflammation and a pleural collection whose low pH, low glucose, high LDH or septation predicts failure of antibiotics alone.

EmpyemaRed flag

Frank pus, a positive pleural culture or a thick infected collection establishes pleural infection and requires drainage plus antibiotics.

Occult or delayed infection

Older, frail or immunosuppressed people may have little fever; anorexia, delirium, weight loss or failure to recover after pneumonia should prompt ultrasound.

Hospital-acquired pleural infectionRed flag

Recent surgery, aspiration, hospital pneumonia or pleural instrumentation increases resistant Gram-negative and staphylococcal risk and changes empirical antibiotics.

Ongoing source-control failureRed flag

Persistent sepsis, inflammatory markers or residual loculated fluid despite a patent drain suggests malposition, obstruction, separate locules, bronchopleural fistula or organised disease.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Chest radiograph and thoracic ultrasoundFirst step
Why
Confirm pleural fluid, estimate volume and complexity, and identify a safe sampling or drain site.
Interpretation and limitations
Ultrasound septation and echogenicity increase concern but a simple appearance does not exclude biochemical complexity. A lateral or subpulmonary collection can be missed on radiography.
02
Pleural-fluid appearance, Gram stain and culture
Why
Identify empyema and causative organisms.
Interpretation and limitations
Pus or positive microbiology warrants drainage. Send sterile fluid and inoculate aerobic and anaerobic blood-culture bottles at the bedside when possible.
03
Immediate pleural-fluid pH
Why
Stratify non-purulent parapneumonic fluid for drainage.
Interpretation and limitations
Use a blood-gas analyser promptly and avoid air, delay, heparin excess or lidocaine contamination. Under BTS guidance, pH at or below 7.20 is high risk; intermediate results require supporting evidence.
04
Pleural glucose, LDH and paired serum tests
Why
Support risk assessment when pH is unavailable or intermediate and identify alternative exudative causes.
Interpretation and limitations
Low glucose and high LDH support advanced infection but also occur in rheumatoid, malignant or tuberculous effusions. Interpret alongside imaging and trajectory.
05
Contrast-enhanced CT thorax
Why
Define pleural enhancement, locules, lung abscess, tumour, foreign body and surgical anatomy when disease is complex or not improving.
Interpretation and limitations
CT helps explain drainage failure but should not delay initial ultrasound-guided source control in an unstable patient.
06
Blood cultures, respiratory microbiology and sepsis bloods
Why
Identify systemic infection, organ dysfunction and antimicrobial targets.
Interpretation and limitations
Take cultures before antibiotics only when this creates no harmful delay. Track renal and liver function for antibiotic selection and sepsis-associated injury.
07
Drain imaging and patency assessment
Why
Determine why infection is not resolving after tube placement.
Interpretation and limitations
A well-sited but blocked drain needs flushing or specialist intervention; a drain outside the dominant locule cannot provide source control and should not be managed by suction alone.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Uncomplicated parapneumonic effusion

Small free-flowing fluid without adverse biochemistry, purulence or microbial evidence may settle as the pneumonia resolves.

Malignant pleural effusion

Pleural nodularity, recurrent fluid and malignant cytology suggest cancer, though tumour-related obstruction can become secondarily infected.

Tuberculous pleuritis

A subacute lymphocytic exudate with relevant epidemiology requires pleural tissue and culture because routine fluid microbiology is insensitive.

Rheumatoid pleuritis

Very low glucose and pleural inflammation can mimic infection; systemic phenotype, cultures and cytology guide distinction.

Lung abscess

An intrapulmonary cavity may resemble a pleural locule, but CT shows its parenchymal location and avoids inappropriate drain placement.

Additional chapter-specific clues

Alternative infected cavityRed flag

Lung abscess, infected bulla, subphrenic collection, oesophageal leak or malignant effusion can mimic empyema and make blind drainage hazardous.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Initial assessmentFind complicated fluid earlyFirst stepPneumonia has pleural fluid, persistent sepsis or pleuritic pain.

1Assess sepsis severity, oxygenation and organ function, start appropriate antibiotics promptly and request respiratory or pleural review.
2Use thoracic ultrasound to confirm fluid and perform image-guided aspiration when the result will change drainage.
3Send immediate pH, microbiology, glucose, LDH and other tests required by the differential.
4Drain frank pus, positive microbiology or high-risk biochemical fluid when safely accessible.

02DrainageAchieve reliable source controlPleural infection meets criteria for intervention.

1Insert an appropriately sized image-guided drain into the dominant collection using the BTS pleural-procedure safety process.
2Connect securely to an appropriate one-way drainage system, document depth and position, and prescribe flushing if the local pathway uses it.
3Monitor output, bubbling, pain, observations and imaging; never clamp a bubbling drain unless directed for a specific controlled reason.
4Re-image and correct blockage, malposition or an undrained locule promptly when sepsis fails to improve.

03Residual loculationUse intrapleural therapy selectivelyDrainage has ceased but a clinically important infected collection remains.

1Confirm tube position and patency and review bleeding risk, anticoagulation, recent surgery and consent.
2Give combined intrapleural tPA and DNase through the trained pleural service using the current BTS/local regimen; never give either intravenously for this purpose.
3AlternativeUse saline irrigation as an alternative in selected patients when combined treatment or surgery is unsuitable.
4Measure clinical, inflammatory and imaging response and stop ineffective treatment rather than repeating it indefinitely.

04FailureEscalate to thoracic surgery in timeEscalationSepsis, collection or lung restriction persists despite adequate antibiotics and drainage.

1Discuss early with thoracic surgery, particularly with extensive loculation, pleural peel, fistula or deteriorating organ function.
2Optimise nutrition, thrombosis prevention, analgesia and comorbidity without delaying necessary source control.
3Use VATS access where appropriate for debridement and, when required, decortication; operative extent is an expert decision.
4If surgery is not appropriate, agree a realistic prolonged-drainage, antimicrobial and palliative plan with clear review endpoints.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Treats pleural and parenchymal infection while drainage provides source control.

Empirical antimicrobial therapy

Start intravenous treatment promptly using the current local pleural-infection guideline, distinguishing community from hospital acquisition and including anaerobic cover where indicated.

Adjust for allergy, renal and liver function, resistant-organism risk and cultures. Review route and total duration with microbiology; antibiotics alone are inadequate for frank pus or high-risk complicated fluid.

Breaks fibrinous septation and reduces fluid viscosity when a residual infected collection is not draining.

Intrapleural alteplase plus dornase alfa

A BTS-supported adult regimen is alteplase 10 mg plus dornase alfa 5 mg intrapleurally twice daily for three days; use the current local protocol and consider reduced alteplase in higher bleeding risk.

This is specialist, consented intrapleural use. Assess bleeding risk and anticoagulation; pain and pleural bleeding occur. Do not substitute either drug alone or administer by the wrong route.

Supports deep breathing, coughing, mobilisation and tolerance of an intercostal drain.

Analgesia

Use regular multimodal analgesia with carefully titrated opioid rescue when needed, adjusted for frailty, respiratory failure, renal function and bleeding risk.

Avoid oversedation and respiratory depression. NSAIDs may be unsuitable with kidney injury, anticoagulation or gastrointestinal risk; uncontrolled pain can also signal drain malposition.

Reduces thrombosis during sepsis, immobility and prolonged admission.

Venous-thromboembolism prophylaxis

Use the approved inpatient prophylaxis regimen unless bleeding or procedure risk contraindicates it, with renal and weight adjustment.

Coordinate timing with drain insertion, fibrinolytics and surgery. Reassess pharmacological versus mechanical prophylaxis daily.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Sepsis

An inadequately drained collection acts as a persistent infectious focus causing bacteraemia, shock and organ dysfunction.

Trapped lung

An organised visceral rind prevents re-expansion, leaving chronic restriction, space and breathlessness, particularly when baseline cardiopulmonary reserve is limited.

Bronchopleural fistula

Necrosis can connect bronchial tree and pleura, producing persistent air leak and difficult infection control, particularly when baseline cardiopulmonary reserve is limited.

Chest-wall spread

Chronic pus can rarely erode through parietal pleura into soft tissue as empyema necessitans, with severity determined by its extent and the patient's underlying reserve.

Drainage-related harm

Poorly positioned drains, bleeding, organ injury and blockage can delay source control and worsen clinical decline.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track temperature, haemodynamics, oxygen need, pain, mental state, urine output and organ dysfunction as part of sepsis care.
Review CRP or other inflammatory markers with clinical trajectory; one slowly falling result does not prove adequate source control.
Document drain output, character, bubbling, flushes, patency, fixation and insertion-site findings every shift.
Repeat ultrasound or CT when improvement stalls, not merely on a fixed schedule, to find residual locules or malposition.
During antibiotics monitor cultures, renal and liver function, blood count, allergy and line complications, narrowing treatment when possible.
During intrapleural treatment monitor pain, haemoglobin, pleural bleeding and drainage response and maintain a clear escalation plan.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

pH technique changes treatment

Lidocaine contamination lowers pH, while air and processing delay can shift it. A misleading sample can cause an unnecessary drain or missed empyema.

The drain treats anatomy

A correctly placed small tube in the main locule often outperforms a large tube outside it. Image guidance and patency matter more than size alone.

Culture-negative is still infection

Prior antibiotics and anaerobes reduce yield. Pus, low pH and a compatible syndrome remain actionable even without organism growth.

tPA and DNase are a pair

Evidence supports combined therapy when residual collection persists; using one agent alone is not an equivalent evidence-based shortcut.

Surgery is not a final defeat

Early VATS discussion can shorten ongoing sepsis and avoid chronic trapped lung. Referral should occur before profound deconditioning and organ failure.

11Common pitfallsFrequent interpretation and management errors.

01
Failing to ultrasound a pneumonia patient with persistent sepsis.
02
Measuring pleural pH from a lidocaine-contaminated or delayed sample.
03
Using antibiotics alone for frank pus or a high-risk complicated effusion.
04
Assuming no drain output means the cavity is empty.
05
Giving intrapleural alteplase without DNase as if it were equivalent treatment.
06
Persisting with ineffective drainage for days before surgical discussion.
07
Clamping a bubbling chest drain without a specific specialist instruction.