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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Diving-related pulmonary barotrauma

Respiratory · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Time-critical presentation

Sudden chest pain, dyspnoea, haemoptysis, subcutaneous emphysema, collapse, seizure, confusion or focal neurological deficit during ascent or immediately after surfacing can be pulmonary barotrauma with tension pneumothorax or cerebral arterial gas embolism. Call 999 or the Coastguard, give 100% oxygen by a tight-fitting system, keep the casualty horizontal and contact the current British Hyperbaric Association diving emergency service. Decompress a tension pneumothorax immediately before recompression or unpressurised air transfer.

Overview

Recognise lung over-expansion injury and arterial gas embolism after diving, stabilise immediately, and obtain urgent UK diving-medicine and hyperbaric advice.

Boyle's law explains pulmonary over-expansion: as ambient pressure falls on ascent, intrapulmonary gas expands. A closed glottis during panic ascent, equipment-related breath-holding, asthma, mucus plugging, bullae or another local obstruction can prevent gas escape and tear alveoli.

Gas tracking along tissue planes causes pneumomediastinum and subcutaneous emphysema; pleural entry causes pneumothorax. Gas entering pulmonary veins reaches the arterial circulation and can obstruct cerebral or coronary vessels. Neurological AGE and decompression sickness overlap clinically and are grouped operationally as decompression illness because both need urgent hyperbaric expertise.

The central decisions are whether a tension pneumothorax needs immediate decompression, whether neurological symptoms justify emergency recompression, and whether another diving illness or trauma coexists. Dive tables and imaging refine the assessment but never replace ABCDE resuscitation and early specialist contact.

Key points

Practice

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RespiratoryOriginal SBA

Neurology after surfacing

A scuba diver makes a rapid ascent and immediately develops aphasia and right-sided weakness. Symptoms improve after several minutes. Chest examination is stable. What is the best immediate action?

Choose one answer, then submit
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Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • British Hyperbaric Association diving emergency guidanceCurrent UK emergency contacts, oxygen and transfer advice.
  • NHS England HBOT decompression illness policyCommissioning framework for decompression illness and gas embolism.
  • UK Diving Medical Committee pneumothorax guidancePulmonary barotrauma risk and recreational return-to-diving boundaries.
  • HSE medical assessment of working diversStatutory occupational-diving medical assessment and return-to-work framework.
  • HSE certificate of fitness to dive at workApproved Medical Examiner responsibilities and restrictions for working divers.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
  • Compressed gas expands during ascent, with the greatest proportional volume change near the surface; breath-holding or regional airway trapping can rupture alveoli even after a shallow dive.
  • Escaped gas may cause pneumothorax, tension pneumothorax, pneumomediastinum, subcutaneous emphysema or entry into pulmonary veins with arterial gas embolism.
  • A stroke-like deficit, seizure, visual change, confusion or loss of consciousness within minutes of surfacing is arterial gas embolism until urgently assessed, even if symptoms improve spontaneously.
  • Chest pain, dyspnoea, voice change, neck crepitus or haemoptysis after ascent suggests pulmonary over-expansion injury; normal initial radiography does not exclude small mediastinal gas or gas embolism.
  • Give 100% oxygen immediately and call emergency plus diving-medicine services. Oxygen reduces bubble size and improves oxygen delivery; it should continue during transfer whenever safely possible.
  • Do not use Trendelenburg positioning, in-water recompression, commercial-air travel or unpressurised altitude transfer unless the diving and retrieval teams explicitly direct the safest option.
  • Tension pneumothorax is a resuscitation diagnosis and must be decompressed before hyperbaric chamber treatment because trapped pleural gas can expand and destabilise the patient.
  • Do not delay a compelling arterial gas embolism referral for extensive imaging; the hyperbaric specialist should help sequence CT, trauma care and chamber transfer.
  • Routine aspirin, anticoagulation, corticosteroid and prophylactic antibiotic treatment is not indicated for gas embolism or uncomplicated pulmonary barotrauma.
  • No further diving is permitted until specialist assessment. At-work divers require the HSE return-to-work process; recreational divers need a UKDMC-recognised diving medical opinion.

Aetiology

01

Breath-holding during ascent

Failure to exhale as ambient pressure falls allows expanding intrapulmonary gas to overdistend and rupture alveoli.

02

Air trapping

Asthma, mucus plugging, bullae or equipment-related breathing obstruction can create regional gas trapping even when the diver attempts a controlled ascent.

03

Rapid or uncontrolled ascent

Panic, buoyancy problems and emergency ascent magnify pressure change and reduce time for lung gas to escape safely.

04

Compressed-gas exposure

Pulmonary over-expansion can occur from shallow depth because relative pressure change is substantial near the surface; great depth is not required.

Pathophysiology

  1. 1
    Expanding alveolar gas

    During ascent, decreasing environmental pressure expands gas within the lungs according to pressure-volume relationships, which links the underlying lesion to the observed respiratory dysfunction.

  2. 2
    Alveolar rupture

    When gas cannot escape, overdistension tears alveolar walls and releases air into interstitial, pleural or vascular compartments.

  3. 3
    Arterial gas entry

    Gas entering pulmonary veins travels to systemic arteries, where bubbles obstruct cerebral or coronary circulation, which links the underlying lesion to the observed respiratory dysfunction.

  4. 4
    Inflammatory vascular injury

    Beyond mechanical blockage, bubbles activate endothelium, platelets and inflammation, worsening tissue oedema and ischaemia, which links the underlying lesion to the observed respiratory dysfunction.

Clinical features and red flags

Pulmonary over-expansion eventRed flag

A rapid or uncontrolled ascent, breath-holding, out-of-air emergency or obstructive lung disease followed immediately by chest symptoms strongly supports barotrauma. It can occur despite apparently compliant computer profiles.

PneumomediastinumRed flag

Retrosternal pain, dysphagia, voice change, neck swelling or palpable crepitus after surfacing suggests mediastinal and subcutaneous gas. Haemodynamic stability does not exclude an associated pneumothorax or AGE.

Tension pneumothoraxRed flag

Severe respiratory distress, unilateral reduced air entry, hypotension, tachycardia, increasing ventilatory pressure or peri-arrest physiology after ascent requires immediate decompression without waiting for a radiograph.

Cerebral arterial gas embolismRed flag

Abrupt focal weakness, aphasia, visual loss, vertigo, seizure, confusion or coma during ascent or soon after surfacing is characteristic. Rapid spontaneous improvement does not remove the need for hyperbaric assessment.

Coronary gas embolismRed flag

Chest pain, dysrhythmia, shock or cardiac arrest immediately after ascent may reflect coronary gas, hypoxia or another cardiac event. Treat standard resuscitation needs while contacting hyperbaric medicine.

Investigations

  1. 01
    Dive profile and computer downloadFirst step
    Why
    Reconstruct pressure exposure and mechanism without delaying treatment.
    Interpretation and limitations
    Record maximum depth, bottom time, gas mixtures, stops, ascent rate, breath-holding, equipment failure, repetitive dives, flying, symptoms at depth and buddy observations. A normal profile does not exclude AGE.
  2. 02
    Serial full neurological examination
    Why
    Detect and track cerebral or spinal decompression illness.
    Interpretation and limitations
    Document consciousness, speech, cranial nerves, vision, limb power, sensation, coordination, gait and bladder function. Repeat before and after oxygen because fluctuating or resolved deficits still matter.
  3. 03
    Chest examination and point-of-care ultrasound
    Why
    Identify pneumothorax or haemodynamic compromise immediately.
    Interpretation and limitations
    Absent lung sliding can support pneumothorax but operator and context matter. A clinically unstable tension pneumothorax is decompressed without waiting for ultrasound or radiography.
  4. 04
    Chest radiograph
    Why
    Show pneumothorax, mediastinal gas and other pulmonary complications.
    Interpretation and limitations
    A normal film does not exclude small barotrauma or arterial gas embolism. Obtain it when it does not delay urgent recompression and repeat if symptoms evolve.
  5. 05
    CT chest
    Why
    Define subtle mediastinal, pleural or parenchymal injury in a stable patient.
    Interpretation and limitations
    CT is more sensitive for small gas collections, bullae and alternative pathology but transfer for compelling AGE should be sequenced with the hyperbaric clinician rather than delayed automatically.
  6. 06
    ECG and cardiac troponin
    Why
    Assess coronary embolism, ischaemia and dysrhythmia.
    Interpretation and limitations
    Abnormalities require monitored resuscitation and cardiology input but do not exclude concurrent cerebral AGE. Treatment choices should be coordinated with hyperbaric medicine.
  7. 07
    Blood gas and basic laboratory profile
    Why
    Assess oxygenation, ventilation, lactate and organ consequences.
    Interpretation and limitations
    Results support resuscitation but cannot rule out intravascular bubbles. Check glucose, full blood count, renal function and electrolytes for mimics and safe critical-care transfer.
  8. 08
    Trauma and ear examination
    Why
    Find concurrent injuries from ascent, impact or pressure change.
    Interpretation and limitations
    Assess cervical mechanism, tympanic membranes, vertigo and facial or chest trauma. Neurological symptoms should not be dismissed as middle-ear barotrauma without a complete examination.

Differential diagnosis

01

Decompression illness

Inert-gas bubble disease often follows longer or deeper exposure and may cause joint, skin or neurological symptoms, but overlap requires diving-medicine advice.

02

Primary neurological event

Stroke, seizure or intracranial haemorrhage may occur coincidentally, yet sudden deficits immediately after surfacing strongly raise arterial gas embolism.

03

Pneumothorax unrelated to barotrauma

Underlying cystic lung disease can cause spontaneous pleural air, though the timing during ascent suggests pressure-related rupture.

04

Aspiration or immersion pulmonary oedema

Cough and hypoxaemia after a dive without focal neurological signs may reflect water aspiration or immersion-related oedema rather than over-expansion injury.

Additional chapter-specific clues

Important differentialRed flag

Decompression sickness, immersion pulmonary oedema, aspiration, salt-water inhalation, myocardial ischaemia, stroke, seizure, hypoglycaemia and trauma can mimic or coexist; none justifies withholding emergency oxygen or specialist advice.

Management

01Dive incidentStart oxygen and specialist contactFirst stepAny serious chest, neurological or cardiorespiratory symptom during ascent or after surfacing.+
  1. 1Call 999 or Coastguard at sea, give 100% oxygen by tight-fitting mask, keep the casualty lying horizontally, warm and monitored, and use the live BHA emergency contact.
  2. 2Perform ABCDE assessment with glucose and a documented neurological examination, treating arrest, hypoxaemia, seizure, trauma and shock in parallel.
  3. 3Preserve the dive computer and record profile, gas and symptom timing, but do not postpone evacuation or oxygen to complete a perfect history.
  4. 4Agree destination, imaging and pressure-safe transport with the diving physician; avoid altitude exposure and never attempt in-water recompression.
02TensionRelieve pressure before chamber transferHaemodynamic or severe respiratory compromise with suspected pneumothorax after ascent.+
  1. 1Diagnose clinically, continue high-concentration oxygen and perform immediate pleural decompression using the current trauma protocol and trained operator.
  2. 2DefinitiveInsert definitive thoracic drainage when indicated and secure it for transport, checking function and recurrence rather than clamping a bubbling system casually.
  3. 3Inform the hyperbaric service because AGE and decompression sickness may coexist; an untreated tension pneumothorax makes pressure changes dangerous.
  4. 4Use lung-protective ventilation if intubation is required and reassess for bilateral injury, mediastinal gas, haemorrhage and equipment-related complications.
03Neurological AGEExpedite recompression assessmentFocal deficit, seizure, confusion, visual disturbance or loss of consciousness at or soon after surfacing.+
  1. 1Continue 100% oxygen, place supine or in a comfortable horizontal position, protect the airway and treat seizures while avoiding head-down positioning.
  2. 2Contact the National Diving Accident service immediately and describe the exact onset, evolution, examination, dive profile and possible pneumothorax.
  3. 3Do not cancel referral because symptoms resolve or CT brain is normal; bubbles may have moved while tissue injury remains and early HBOT can still be indicated.
  4. 4Coordinate imaging for trauma or haemorrhage only when it changes immediate safety, with the hyperbaric and retrieval teams controlling any delay to recompression.
04RecoveryPrevent premature return to divingAcute symptoms have resolved after conservative care, drainage or HBOT.+
  1. 1Arrange follow-up with a diving-medicine physician to review lung imaging, pulmonary function, mechanism, neurological recovery and risk of recurrence.
  2. 2Prohibit diving, flying and altitude exposure for the interval specified by the treating hyperbaric team; generic waiting periods are unsafe after serious injury.
  3. 3For a diver at work, use an HSE Approved Medical Examiner of Divers and statutory return-to-work process; recreational clearance follows current UKDMC standards.
  4. 4Address asthma, bullae, smoking, equipment practice, panic or training issues before any decision about future compressed-gas exposure.
Key medicines and prescribing safety5 treatments · regimens, roles and cautions+
Improve tissue oxygenation, promote inert-gas washout and reduce bubble volume before HBOT.

Normobaric 100% oxygen

Deliver continuously through a tight-fitting non-rebreather or secured airway at the highest feasible inspired concentration during transfer and consultation.

Do not interrupt for unnecessary tests. Ensure adequate cylinder supply and ventilation, observe fire precautions, and remember oxygen does not decompress a tension pneumothorax.

Correct dehydration and support circulation when clinically present during decompression illness care.

Isotonic crystalloid

Give cautious boluses or maintenance guided by perfusion, oral tolerance, urine output and the diving or critical-care specialist plan.

Avoid routine aggressive loading, particularly with pulmonary oedema or cardiac disease. Oral electrolyte fluid is suitable only if fully alert with safe swallowing and no urgent anaesthetic need.

Relieve pleuritic or chest-wall pain while definitive pulmonary injury treatment proceeds.

Analgesia

Titrate paracetamol or an opioid to pain and physiology under the emergency formulary, preserving serial neurological assessment and ventilation.

Sedation can obscure neurological deterioration and suppress breathing. Avoid nitrous oxide because it can expand trapped gas spaces; adjust opioid choice for shock and renal function.

Stop seizures caused by cerebral arterial gas embolism

Complications

01

Cerebral arterial gas embolism

Bubbles in cerebral vessels cause abrupt confusion, focal deficits, seizure, coma or death and require immediate specialist hyperbaric coordination.

02

Coronary gas embolism

Gas entering coronary arteries may cause myocardial ischaemia, arrhythmia and cardiac arrest, with severity determined by its extent and the patient's underlying reserve.

03

Tension pneumothorax

Pleural air can expand further during ascent or positive-pressure ventilation and produce obstructive shock, and potentially prolonging treatment and functional recovery.

04

Pneumomediastinum

Interstitial air may track centrally into the mediastinum and neck, causing chest pain, voice change and subcutaneous emphysema.

05

Persistent neurological disability

Delayed bubble clearance and secondary inflammation can leave cognitive, motor or balance impairment despite initial stabilisation.

Monitoring and follow-up

  • Repeat a structured neurological examination during oxygen, transport and after HBOT; transient recovery does not mean the emergency has resolved.
  • Track respiratory rate, SpO2, work of breathing, chest symmetry, crepitus and haemodynamics for evolving or recurrent pneumothorax and pulmonary oedema.
  • If a chest drain is present, monitor swinging, bubbling, output, connections and securement across pressure and transport changes under the specialist plan.
  • Use continuous ECG monitoring when there is collapse, chest pain, dysrhythmia or possible coronary gas, trending troponin and perfusion as indicated.
  • Document oxygen concentration and cylinder reserve throughout retrieval so treatment is not inadvertently interrupted during transfer between services.
  • After treatment, follow cognitive, vestibular, pulmonary and functional recovery and ensure written restrictions on diving, flying, work and driving are explicit.

Special situations

The last metres carry large expansion

Ambient pressure changes proportionally most near the surface, so a shallow emergency ascent with a held breath can cause major over-expansion despite a modest maximum depth.

A compliant profile does not exclude AGE

Decompression computers model inert-gas exposure; they cannot prevent a local lung segment from trapping expanding gas during ascent. Mechanism and immediate symptoms remain decisive.

Improvement does not cancel recompression

Arterial bubbles can move or fragment and neurological findings can fluctuate. Tissue ischaemia and inflammatory injury may persist after a normal examination returns.

Chest gas and neurological gas coexist

The same alveolar rupture can produce pneumothorax and AGE. Searching for pleural pressure is essential before chamber pressurisation or altitude transfer.

Immersion pulmonary oedema is different

Dyspnoea and frothy sputum developing during a dive without ascent injury may reflect immersion pulmonary oedema. It still needs emergency oxygen and assessment but has different recurrence evaluation.

Common pitfalls

  1. 01

    Withholding oxygen because pulse oximetry is normal or neurological symptoms have improved.

  2. 02

    Placing a patient head-down in the outdated belief that it keeps bubbles away from the brain.

  3. 03

    Waiting for CT brain or a visible bubble before contacting hyperbaric medicine.

  4. 04

    Sending an unstable tension pneumothorax into a chamber or altitude transfer before decompression.

  5. 05

    Attempting in-water recompression without a specialist operational system and creating drowning or hypothermia risk.

  6. 06

    Assuming a normal dive-computer profile excludes pulmonary barotrauma or AGE.

  7. 07

    Giving aspirin, anticoagulation or corticosteroid reflexively for a stroke-like presentation caused by gas.

  8. 08

    Allowing return to recreational or occupational diving without the appropriate diving-medicine clearance.

or another acute insult.

Anticonvulsant rescue treatment

Treat an ongoing seizure using the current emergency benzodiazepine and status-epilepticus protocol while securing oxygenation and expert help.

Respiratory depression may necessitate intubation. Seizure control does not treat the gas embolism and must not delay hyperbaric referral or pneumothorax assessment.

No established routine role in removing intravascular gas or healing alveolar rupture.

Anticoagulants and corticosteroids

Do not administer routinely for pulmonary barotrauma or arterial gas embolism unless a separate confirmed indication has specialist support.

Anticoagulation can worsen traumatic or pulmonary bleeding, while steroid toxicity adds risk without replacing oxygen and HBOT. Investigate alternative stroke or thrombotic diagnoses carefully.