Cortical Vein Air Emboli With Gyriform Infarcts

Lai, Daniel; Jovin, Tudor G; Jadhav, Ashutosh P.

doi:10.1001/jamaneurol.2013.1949

Cited by 16 publications

(13 citation statements)

References 3 publications

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“…6 In our case, the MRI revealed multiple infarctions in different arterial territories, and also showed bihemispheric areas of restricted diffusion in a gyriform pattern along the cortical gray matter. As previously observed in other reports, this MRI finding may be seen in cases of cerebral venous air embolism and is thought to be related to the number and size of the air emboli.…”

Section: Oy-sterssupporting

confidence: 48%

“…Multiple small emboli may obstruct the blood flow in end-artery and cortical vein territories and cause infarctions. 6,7 The pathophysiology of retrograde venous air embolism is poorly understood, but it appears from laboratory data that air bubbles have a high probability of rising retrograde against venous blood flow when the patient is in the upright position. 8 Moreover, the contact of bubbles with the endothelium of the blood-brain barrier results in an inflammatory response leading to the breakdown of the barrier and cerebral edema, causing decreased blood flow, as was likely in our patient.…”

Section: Oy-stersmentioning

confidence: 99%

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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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Section: Oy-sterssupporting

confidence: 48%

Section: Oy-stersmentioning

confidence: 99%

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

Bartolini

Burger

2015

Neurology

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“…21 23 The latter survived, 23 but the former did not. 21 The course and management of the case in the former report is very sketchy and difficult to get a good picture, but a couple of case reports do not help us to select a course of treatment in a devastating condition. Patients with decompression illness (DCI) have bubbleinduced injury which has been treated with HBO for many decades.…”

Section: How Do We Treat Cvge?mentioning

confidence: 99%

II. Retrograde cerebral venous gas embolism: are we missing too many cases?

Bothma

Schlimp

2014

British Journal of Anaesthesia

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“…3,5 Some authors have also proposed that venous cerebral air emboli can migrate to the brain parenchyma in a retrograde pattern. 6 When air bubbles reach the brain parenchyma, they induce activation of neutrophils and promote stasis, which leads to an infarct. 1 The precise pathophysiology has not been delineated.…”

Section: Discussionmentioning

confidence: 99%