Gas embolism: pathophysiology and treatment

Hulst, Rob A. van; Klein, Jan; Lachmann, Burkhard

doi:10.1046/j.1475-097x.2003.00505.x

Cited by 197 publications

(227 citation statements)

References 117 publications

(142 reference statements)

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“…The entry of gas into vessels was first described by Morgagni, whose post-mortem findings were published in 1769 [243,244]. The first clinical report dates to 1821 [244].…”

Section: Gas Embolismmentioning

confidence: 97%

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Nonthrombotic pulmonary embolism

Jorens¹,

Marck²,

Snoeckx³

et al. 2009

Eur Respir J

162

127

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Nonthrombotic pulmonary embolism (NTPE) is defined as embolisation to the pulmonary circulation of different cell types (adipocytes, haematopoietic, amniotic, trophoblastic or tumour), bacteria, fungi, foreign material or gas. The purpose of this article is to describe the clinical signs, pathogenesis, diagnosis and treatment of the different NTPE subtypes.The complex and diverse pathogenesis of different subtypes of emboli is subject to continuing speculation and is certainly far more complex than ''simple'' mechanical obstruction after embolisation of vascular thrombi. Nonthrombotic emboli may also lead to a severe inflammatory reaction both in the systemic and pulmonary circulation, as well as in the lung.NTPE presents a formidable diagnostic challenge, as the condition often presents with very unusual and peculiar clinical signs that are frequently overlooked. They range from very dramatic acute presentations such as acute respiratory distress syndrome to signs observed late in the disease course. Pathological observations play a key role in the exact diagnosis, and sometimes carefully aspirated blood from the pulmonary artery or specific staining of cells recovered from bronchoalveolar lavage fluid may be helpful. Frequently, lung biopsies revealing severe granulomatous reaction or unfortunate post-mortem pathological investigations of pulmonary tissue are necessary to confirm the diagnosis. Here, we also aim to familiarise the reader with the atypical radiological features of NTPE. Thin-section computed tomography of the lungs showing peculiar radiographic findings, such as a feeding vessel, the so-called tree-in-bud pattern or the appearance of micronodules distributed at the termination of bronchovascular bundles, may be observed in certain forms of NTPE.Increased awareness of NTPE as an underestimated cause of acute and chronic embolism, which may result in acute and chronic pulmonary hypertension, is needed. Despite the fact that detailed descriptions of several forms of NTPE have existed for nearly 100 years, well-designed trials have never been performed to evaluate therapy in the different subsets of these patients.

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“…The entry of gas into vessels was first described by Morgagni, whose post-mortem findings were published in 1769 [243,244]. The first clinical report dates to 1821 [244].…”

Section: Gas Embolismmentioning

confidence: 97%

“…The first clinical report dates to 1821 [244]. Gas embolism (GE) is mainly air embolism (AE), although the use of other gases used in medical procedures or diving, such as carbon dioxide, nitrous oxide, nitrogen and helium, can also provoke these symptoms [245].…”

Section: Gas Embolismmentioning

confidence: 99%

Nonthrombotic pulmonary embolism

Jorens¹,

Marck²,

Snoeckx³

et al. 2009

Eur Respir J

162

127

View full text Add to dashboard Cite

show abstract

“…Immediately after removing the catheter, an impermeable dressing should be applied to the site and pressure should be held for at least 5 minutes. 10 The diagnosis of cerebral venous air embolism can be challenging, as no imaging technique alone has shown sufficient diagnostic accuracy, 2 and the diagnosis mainly relies on clinical presentation and temporal correlation with catheter manipulation. Head CT can be diagnostic if done immediately after the onset of symptoms, before air is reabsorbed.…”

Section: Oy-stersmentioning

confidence: 99%

Pearls & Oy-sters: Cerebral venous air embolism after central catheter removal

Bartolini

Burger

2015

Neurology

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Too much air can kill PEARLS 1. Cerebral air embolism is a rare but potentially catastrophic consequence of central venous catheter removal. 2. Treatment is often supportive; hyperbaric therapy should be considered but is not readily available in most hospitals and its efficacy for cerebral venous air embolism is unknown. OY-STERS1. Place the patient in the Trendelenburg position before removing the catheter to minimize the risk of air emboli going to the brain. 2. Clinical suspicion of this diagnosis is essential, as signs and symptoms are not specific and brain imaging may not show the presence of air in the cerebral vasculature. 3. Even patients without patent foramen ovale are at risk for cerebral air embolism.CASE REPORT A 95-year-old woman with a history of hypertension presented from a long-term care facility for altered mental status in the context of dehydration and hypoglycemia. Multiple attempts to obtain a peripheral IV failed, and a triple lumen catheter was placed into the right internal jugular vein using the Seldinger technique under ultrasound guidance. No complications followed the procedure. The patient was then rehydrated and given multiple ampules of D50, leading to prompt resolution of the hypoglycemia and improvement in her mental status. After resolution of symptoms, the central line was removed, with the head of the bed at 30°. Within minutes of removal of the central line, the patient developed severe respiratory distress and hypoxia with desaturation to 80% on a nonrebreather mask with 100% oxygen. On examination, the patient was unconscious and gasping for air with severe suprasternal retractions; she was tachypneic and tachycardic, and her blood pressure was 210/100 mm Hg. All limbs were flaccid. She was placed in the left lateral decubitus position as resuscitation efforts were activated. She was then intubated and transferred to the intensive care unit.A stat CT angiogram of the head and neck did not show signs of stroke, bleeding, or vascular occlusion. Chest CT with contrast showed dilation of the distal esophagus with fluid and debris within the distal trachea and left mainstem bronchus, without evidence of pulmonary embolism, and consistent with aspiration. An echocardiogram revealed an ejection fraction of 79%, normal left ventricular function, and mildly dilated left atrium, but no thrombi, vegetations, or evidence of patent foramen ovale (PFO) with agitated saline contrast. Troponin I peaked about 8 hours after the event (0.468, normal range 0-0.034), simultaneous creatine kinase MB was elevated (4.92, normal range 0-2.30), and multiple EKGs were consistent with non-ST elevation myocardial infarction. Prolonged cardiac telemetry failed to show atrial fibrillation. Brain MRI showed areas of restricted diffusion bilaterally in the cerebellum, temporal lobes, frontal lobes, left occipital lobe, and thalami, consistent with different arterial vascular territories, including middle, anterior, and posterior cerebral arteries. It also showed restricted diffusion in the left more th...

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“…Gas embolism is related to many specialities. It can be caused by central venous catheterization, mechanical ventilation with high pressure, chest trauma, thoracentesis, hemodialysis, and several other invasive vascular procedures [2,3] (Figure 3). Air embolism in the watershed area, between anterior and middle right cerebral arteries has a complication of endoscopy procedure [4].…”

Section: Discussionmentioning

confidence: 99%