June 2022


November 2022

C.S. van Dam (1), S. Tarasevych (2), D. Verschure (3), F. van Hoorn (4), S.C.E. Koster (5) Departments of 1. Internal Medicine, 2. Respiratory Medicine, 3. Cardiology, 4. Radiology, and 5. Intensive Care Medicine, Zaans Medical Center, Zaandam, the Netherlands


S.C.E. Koster -
Case Report

Air embolism after lung biopsy: A case report


Air embolism is the entry of gas into vascular structures. It is a rare life-threatening complication of several medical procedures, in particular lung biopsy and central catheter insertion. The prevalence is 0.06%, but may be underestimated. It can have an asymptomatic course. Symptomatic air embolism can be accompanied by respiratory insufficiency and myocardial or cerebral infarction. We present a 78-year-old woman with acute hypotension and unconsciousness after lung biopsy. A CT scan showed air embolism in both the pulmonary and systemic circulation, followed by myocardial infarction and stroke. She was admitted to the intensive care unit for stabilisation and hyperbaric oxygen therapy. The patient improved, but a hemi-paralysis remained. Recognising air embolism is important to prevent further embolisation and to start treatment. Treatment is mostly supportive. In severe cases, 100% oxygen is supplied to expel air, thereby limiting permanent injury. In case of neurological and cardiac complications, hyperbaric oxygen is indicated.

Air embolism - the entry of gas into the vascular structures - is a rare, but life-threatening complication of invasive medical or surgical interventions.[1] Air introduction in veins can occur with several medical procedures, but the risk is greatest with lung biopsy and central catheter insertion.[2,3] The overall estimated prevalence is 0.06%, but it is probably higher as it can have an asymptomatic course.[2,4,5] Some studies reported an incidence ranging from 0.21 to 3.8% after percutaneous transthoracic lung biopsy, based on the inclusion of asymptomatic patients with extensive surveys of post-biopsy CT examination. Although air embolism is mostly asymptomatic, it can be accompanied by respiratory insufficiency and myocardial or cerebral infarction may occur.

A 78-year-old woman was referred to hospital for a transthoracic lung biopsy because of a growing pulmonary nodule on the right dorsal pulmonary lobe. Her medical history included an acute anterior and inferior myocardial infarction treated with a primary percutaneous coronary intervention (PCI) of the left anterior descending artery (2001) and followed by PCI of the right coronary artery (RCA) several years later (2006), diabetes mellitus type 2, non-specific interstitial lung disease (NSIP) with severe diffusion disorder and diffuse large B-Cell lymphoma treated with chemotherapy and in complete remission (2020).

CT-guided biopsy was performed with the patient in a prone position under local anaesthetic using an 18-gauge semi-automatic biopsy gun. A CT scan of the thorax was performed directly after biopsy to exclude a pneumothorax (figure 1). After the CT scan, the patient coughed up a little blood so she was put in an upright position, after which she suddenly became haemodynamically unstable and lost consciousness. She was immediately put back in the supine position and the resuscitation team was paged.

The patient’s vital signs were: obstructed airway, opened by jaw thrust, SpO2 98% without extra oxygen supply, blood pressure 90/60 mm Hg, sinus rhythm 50/min, and cold marble-like extremities. The Glasgow Coma Scale score was E4M1V1 with normal pupil size, responsive to light. Heart and lung sounds were normal. The initial ECG showed signs of acute myocardial infarction with ST-segment elevation suggesting an inferolateral infarction with possible right ventricular involvement (figure 2).

Laboratory investigations were performed and showed normal blood gases (pH 7.42, pCO2 32 mmHg, pO2 89 mmHg, HCO3 20.8) with an elevated lactate of 5.6 mmol/l and troponin 39 ng/l. Electrolytes and glucose were normal. An emergency CT scan showed intravascular air in both the pulmonary and systemic circulation including the jugular vein and both mammary veins, the ventral part of the pulmonary artery, the apex of the left ventricle and ventral part of the ascending aorta. Also an air embolism was seen in the proximal RCA, explaining the acute ST elevation and troponin release. No pneumothorax was seen. The CT scan of the brain at that time showed a normal parenchyma.


The diagnosis of air embolism was confirmed. A small amount of air in the apex of the left ventricle had already partly moved to the RCA, and there was still a high risk of embolisation to the brain. Therefore, the patient was directly placed in the Trendelenburg position to prevent ascending air and 100% oxygen was given. She was admitted to the ICU for further stabilisation.

After 15 minutes her vital parameters and the ST segments on the ECG had improved significantly, but an altered consciousness remained with aphasia and left-sided Babinski. A control CT scan showed right-sided frontoparietal infarction and diminished air in the apex of the left ventricle, suggesting embolisation of air from the apex of the left ventricle to the brain. Therefore, the patient was transferred to the Amsterdam University Medical Center for hyperbaric oxygen therapy. Unfortunately the first hyperbaric oxygen therapy was complicated with an epileptic seizure probably secondary to ischaemia of the brain, and possible aspiration because of vomiting. The seizure was treated with midazolam and levetiracetam. Her neurological status improved to E4M5V3 with persistent left-sided paralysis.

Transthoracic echocardiogram was performed because of the rare finding of air embolism in both the pulmonary and systemic circulation. The echocardiogram showed moderate left and right ventricular function without any sign of a permanent foramen oval (PFO) or atrial septum defect (ASD).

During her stay in the ICU high-flow oxygen therapy, antibiotics and methylprednisolone were indicated due to poor oxygenation because of aspiration and flaring of pre-existent NSIP. After one week the patient was discharged to the neurology ward for further recovery. After several days a repeated ECG showed signs of an evolving myocardial infarction with a return to normal of the ST segments, but with new negative T-waves in the inferior and lateral leads.

The pathology of the lung biopsy showed a non-small cell lung carcinoma. Stereotactic radiotherapy was not applied, because of the high mortality associated with radiotherapy in the case of NSIP with the current flare and pre-existing severe diffusion disorder. Best supportive care was given, in addition to a high-dose corticosteroid regimen. Unfortunately, two months later, the patient died of a Sars-COV-2 pneumonia.

The most common type of gas embolism is air embolism, although the medical use of other gases such as carbon dioxide, nitrous oxide, nitrogen and helium can also result in embolisms.[6] Risk factors for the development of air embolisms are underlying lung disease (NSIP, carcinoma, lymphoma), the use of a ≥19 gauge needle, aspiration biopsy, and supine position.[4]

Gas embolism may originate in the systemic venous system as well as in the systemic arterial circulation, but after lung biopsy the pulmonary circulation can also be involved. Systemic venous air embolism occurs when gas enters the systemic venous system and is transported to the lungs via the pulmonary arteries.[6] Air embolism may lead to trapping of air bubbles in the pulmonary capillary bed, which can cause decreased gas exchange, pulmonary hypertension, and sometimes systemic arterial gas embolism.[6] Systemic venous air embolisms may reach the arterial circulation due to overflow of air from the pulmonary arteries to the pulmonary veins, or shunting through a cardiac right to left shunt, for example via a PFO or ASD, which are present in 20-34% of the population.[2,7,8]


When the gas embolism enters the systemic arterial circulation, it may cause transient arterial obstruction with subsequent ischaemia and reperfusion injuries resulting in neurological or myocardial damage. Cerebral arterial air embolism can arise when air is directly introduced in the arterial circulation between the heart and brain, for example during left-sided cardiac catheterisation, lung surgery, cardiac surgery or carotid surgery.[8]

In our patient, there was air in both the systemic arterial and venous circulation, and in the pulmonary circulation without the presence of a right to left shunt. A possible explanation could be that both the pulmonary and systemic venous circulation were punctured during biopsy.

Air embolism can present in many ways. Embolisms can occur in every organ system, but the effects are particularly profound in the cerebral or coronary circulation.[9] The severity of symptoms depends on the patient’s position, the volume and type of gas, the size of the bubbles and the rapidity of gas entry into the arteries.[3,6,7]

Cerebral ischaemia can occur when embolisms lodge in the arterioles of the brain. This resembles solid embolisms, as gas can lead to endothelial damage with an inflammatory response.[8] Neurological symptoms include motor symptoms (hemiparesis, tetraplegia), seizures, and altered consciousness. Although the prevalence of cerebral arterial air embolism is low (5.7/100,000 hospital admissions), the neurological sequelae and mortality rates are severe.[8]

Cardiopulmonary symptoms are also frequent, and sometimes even proceed and potentially mask neurological symptoms.[3,6] Entrapment of venous bubbles in the pulmonary micro-circulation may also lead to cellular injury and lung oedema, resulting from the release of vasoactive mediators following pulmonary vascular obstruction.[6]

The diagnosis is made clinically when sudden neurological, pulmonary or cardiac abnormalities occur during invasive procedures.[2] In the early stages, the diagnosis can be difficult if a small amount of gas is involved or if the patient is anaesthetised or sedated.[9] CT can be used to confirm air embolism, however a normal CT scan does not rule out air embolism.[8] Literature shows that gas embolisms up to 1 cm3 may not be visualised via any imaging modality once diffusely distributed.[5] More subtle cases may be diagnosed by echocardiography and transcranial Doppler, while electro-encephalography and transcranial oximetry can be useful in the diagnostic process.[2,8]

The mainstay of acute management is rapid recognition and termination of further entrainment of air.[5,8,9] Further treatment consists of supportive care.[8] Administration of 100% oxygen is important to treat hypoxaemia and improve the oxygenation of affected tissues but also to decrease air bubble size by establishing a diffusion gradient that favours the elimination of gas from the bubbles by lowering the arterial nitrogen pressure.[3,6] If intubated, airway pressures should be limited to prevent a persistent airway-to-vein-pressure differential.[5]

Hyperbaric oxygen in a recompression chamber should be considered in all patients with (probable) air embolism, especially in case of severe neurological or circulatory symptoms.[8-10] Hyperbaric oxygen therapy is suppletion of 100% oxygen at a high ambient pressure. The air bubble volume may be reduced by the high pressure and by inducing blood denitrogenation.[2] Hyperbaric oxygen raises the arterial oxygen pressure up to 1500 mmHg, leading not only to a favourable gradient and diffusion of nitrogen, but also higher oxygen pressure in the brain. Lastly, hyperbaric oxygen therapy has anti-inflammatory features.

Potential disadvantages of hyperbaric oxygen therapy include risks associated with the transport of critically ill patients, hyperoxic seizures, claustrophobic reactions and barotrauma.[2] An absolute contraindication is a pneumothorax, because of the possible evolution to a tension pneumothorax when the ambient pressure decreases at the end of the treatment. Therefore, a chest tube will be placed upfront in cases of lung injury.[11,12] A relative contraindication is delay between the onset of symptoms and the start of treatment. A clear time cut-off is not exactly known, but previous literature suggests unfavourable outcomes after seven hours due to irreversible damage.[11,13] Amsterdam UMC maintains a 24-hour limit. Other relative contraindications are difficulty in equalising ear pressure (a paracentesis will be performed before treatment), recent eye surgery when a gas or air bubble is still present in the eye and devices in general (e.g. pacemakers, neurostimulators, epidural pumps) which might malfunction due to altered pressure.[12] Pulmonary comorbidity is also a relative contraindication because hyperbaric oxygen can lead to alveolar inflammation and subsequent decreased oxygenation.[12] In patients with chronic obstructive pulmonary disease, an increased oxygen saturation can lead to oxygen-induced hypoventilation and increased ventilation/perfusion mismatch.[12]

In the Netherlands, hyperbaric oxygen treatment is possible at the Antonius Hypercare Center in the Antonius Hospital in Sneek, and at Amsterdam UMC.[11] During office hours hyperbaric oxygen treatment is also provided at the Admiraal de Ruyter Hospital in Goes.[11] Patients on mechanical ventilation can only be treated in Amsterdam UMC.[10,11] Referrals can be made by attending physicians (mostly intensive care physicians and pulmonologists) after telephone consultation with the on call specialist of the hyperbaric treatment department.[10,11]

In our patient the Trendelenburg position was used to prevent air ascending to the aorta and brain because of the large amount of air in the apex of the left ventricle. Also the patient had been moved into the supine position after biopsy while vomiting, leading to possible embolisation. However, recent literature suggests that air embolisms are too small to overcome the blood pressure and that the Trendelenburg position can have negative effects on intracranial pressure.[9] Further cerebral damage should be prevented by maintaining normocapnia, normotension, hypothermia and treatment of possible epileptic seizures.[9]

Little is known about the morbidity and mortality associated with iatrogenic gas embolism, because the diagnosis may be difficult in conditions other than high-risk surgery.[2] Full recovery of neurological complications varies in the literature from 7% to 77%;[8] also the range of described mortality is wide from 5% to 23%.[2]

Air embolism is an uncommon, but life-threatening complication of lung biopsy. Healthcare workers should be especially attentive to neurological and cardiopulmonary symptoms after procedures with a high inherent risk of embolisation. In all cases of proven or suspected arterial gas embolism, a hyperbaric facility should be consulted immediately.

All authors declare no conflict of interest. No funding or financial support was received. Written informed consent was obtained from the patient’s relatives for the publication of this case report and the accompanying images.


  1. Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000;342:476-82.
  2. Bessereau J, Genotelle N, Chabbaut C, et al. Long-term outcome of iatrogenic gas embolism. Intensive Care Med. 2010;36:1180-7.
  3. Hatling D, Høgset A, Guttormsen AB, Müller B. Iatrogenic cerebral gas embolism–A systematic review of case reports. Acta Anaesthesiol Scand. 2019;63:154-60.
  4. Lee JH, Yoon SH, Hong H, Rho JY, Goo JM. Incidence, risk factors, and prognostic indicators of symptomatic air embolism after percutaneous transthoracic lung biopsy: a systematic review and pooled analysis. Eur Radiol. 2021;31:2022-33.
  5. Swenson KE, Shaller BD, Duong K, Bedi H. Systemic arterial gas embolism (SAGE) as a complication of bronchoscopic lung biopsy: A case report and systematic literature review. J Thorac Dis. 2021;13:6439-52.
  6. van Hulst RA, Klein J, Lachmann B. Gas embolism: Pathophysiology and treatment. Clin Physiol Funct Imaging. 2003;23:237-46.
  7. Smithuis JW, Müller MCA, Smithuis FF, Weenink RP. A case of cerebral and coronary air embolism after flushing of a pleural drain. Neth J Crit Care. 2021;29:41–4.
  8. Weenink RP. Anesthesiologische Aspecten Van Een Duikmedisch Ziektebeeld. Ned Tijdschr Anesth 2013;5-12.
  9. Intensive Care Society Guideline. Management of Patients With Gas Embolism: Guidance For Intensive Care And Resuscitation Teams. August 2022.
  10. Department Hyperbaric oxygen Amsterdam UMC. ‘Protocol Gas embolism: logistics and treatment with hyperbaric oxygen. 2022.
  11. Weenink RP, van Hulst RA. Preventie , detectie en behandeling van iatrogene gasembolieën. A& I. 2020;29-35.
  12. Gawdi R, Cooper JS. Hyperbaric Contraindications. Treasure Island (FL): StatPearls Publishing; 2022.
  13. Blanc P, Boussuges A, Henriette K, Sainty J, Deleflie M. Iatrogenic cerebral air embolism: Importance of an early hyperbaric oxygenation. Intensive Care Med. 2002;28:559-63.