Gas Embolism

Gas embolism here means arterial gas embolism: gas bubbles enter the arterial circulation and lodge in end-arteries of the brain, heart and other organs. It differs from venous embolism in its mechanisms, its target organs and its treatment.

Main causes

• Pulmonary barotrauma of ascent: a breath-holding diver or an escaping submariner (with an ascent of as little as 1 to 2 m from depth), where trapped gas expands and ruptures alveoli. Gas enters the pulmonary veins and left heart. Lung disease (asthma, bullae, cysts) raises the risk.
• Iatrogenic: positive pressure ventilation with high pressures, thoracic and lung biopsy, bronchoscopy with laser, cardiopulmonary bypass, intra-aortic and arterial lines, endoscopy with gas insufflation, hemodialysis, hydrogen peroxide irrigation of closed cavities and the ingestion of concentrated hydrogen peroxide.

The brain is the commonest target. Bubbles block cerebral arterioles, then damage the endothelium and activate platelets, complement and neutrophils, so secondary injury follows after the bubble has gone. Symptoms start within minutes, nearly always within 10 minutes of surfacing in divers. About 5% of divers with the condition die, and 30% have residual deficits. Complications: stroke syndromes, cerebral edema, seizures, myocardial infarction, arrhythmia, pulmonary barotrauma with pneumothorax and mediastinal emphysema, and death.

• Sudden loss of consciousness or collapse within minutes of surfacing or of the procedure
• Stroke-like deficits: hemiparesis, aphasia, visual loss, confusion, vertigo and focal or generalized seizures
• Chest pain, arrhythmia and cardiac arrest from coronary embolism
• Marbling of the skin or tongue, and froth in the retinal vessels or blood
• Signs of lung barotrauma: dyspnea, cough, hemoptysis, subcutaneous emphysema and pneumothorax
• Red flags: any neurological symptom within 30 minutes of surfacing, coma, seizures, chest pain, and a ventilated patient who deteriorates suddenly after a procedure

1. Clinical diagnosis from history and examination, with immediate treatment. Never delay recompression for imaging in a diver.
2. Neurological examination and a full record of times (depth, time at depth, ascent and symptom onset).
3. CT head: gas bubbles in cerebral vessels or sulci (often absent after minutes), cerebral edema and infarction. MRI diffusion-weighted imaging shows multiple small infarcts.
4. Chest imaging: radiograph or CT for pneumothorax, pneumomediastinum and cysts, since a pneumothorax needs drainage before recompression.
5. Transthoracic or transesophageal echocardiography for gas in the left heart and for the source in iatrogenic cases.
6. ECG and troponin for cardiac involvement, and arterial blood gas and creatine kinase (raised in divers).

Differentials: ischemic stroke, decompression sickness, hypoglycemia, seizure, intracranial hemorrhage and oxygen toxicity.

1. Resuscitation: airway, breathing, circulation, and high-flow 100% oxygen by a tight non-rebreather mask at 15 L/min (or via a ventilator), which shrinks bubbles by washing out nitrogen.
2. Position: flat supine. Head-down positioning is no longer advised, because it may worsen cerebral edema.
3. Hyperbaric oxygen therapy is the definitive treatment, and should begin as soon as possible, even when many hours have passed:
   • Pressurization to 2.8 atmospheres absolute (18 m of sea water) breathing 100% oxygen in cycles of three 20-minute periods separated by 5-minute air breaks, then two further periods at 1.9 atmospheres absolute (9 m), the first treatment lasting about 4 hours 45 minutes.
   • Extension of the table when deficits persist, and daily repeat treatments until improvement stops (usually 3 to 5, up to 10 sessions).
   • Treat a pneumothorax with a chest drain before compression, because gas expands on decompression.
4. Transport: to the nearest hyperbaric facility, with the patient supine and on oxygen, by ground transport or by an aircraft pressurized to sea level (or flying below 300 m).
5. Fluids: IV 0.9% saline or balanced crystalloid 1 L over the first hour, then 100 to 150 mL/h, avoiding glucose-containing solutions (they worsen cerebral injury). Keep a urine output over 1 mL/kg/h.
6. Seizures: lorazepam 4 mg IV (children 0.1 mg/kg), repeated once.
7. Adjuncts: lidocaine 1.5 mg/kg IV bolus then 1 to 2 mg/min infusion for 48 hours for cerebral involvement (monitor for toxicity), and normothermia, with avoidance of hyperthermia.
8. Cerebral edema: head of bed 0 to 15 degrees for the initial phase then 30 degrees once the airway is secured, hypertonic saline 3% 2 to 5 mL/kg IV over 10 to 20 minutes, and intubation with controlled ventilation to a PaCO2 of 35 to 40 mmHg.
9. Iatrogenic embolism: stop the source, and treat with 100% oxygen and early hyperbaric therapy.

Follow-up: neurological and cognitive review at 1 and 3 months, and counseling on diving (a diver should not dive again until cleared by a diving physician after a pulmonary assessment, and permanent exclusion is advised after lung barotrauma with an underlying cyst).