Figure 1. Norepinephrine (20 µg) was administered without response, but epinephrine (200 µg) rapidly restored blood pressure to 177/116 mmHg with tachycardia.
Figure 2. Findings on mid-esophageal four-chamber view and transgastric short-axis view. Arrows: numerous gas bubbles (carbon dioxide) are present in the right atrium and ventricle. The arial septum is displaced toward the left atrium. Signs of right heart pressure overload: elevated right heart pressure causes a right-to-left shift, with bulging of the interatrial and interventricular septum into the left chambers. Septal dyskinesia is a hallmark sign of acute cor pulmonale resulting from a massive gas embolism.
Figure 3. Findings on the transgastric inferior vena cava view. Arrows: multiple, discrete gas accumulations are observed in the liver parenchyma, and gas bubbles are seen passing through the inferior vena cava. Proposed pathophysiological mechanism: the gas likely originated from an inadvertent injury to a mesenteric vein during the establishment of the pneumoperitoneum. Explained systemic migration route: the entrapped gas traveled via the portal vein to the liver. While some gas was trapped locally, the remainder entered the systemic circulation through two potential pathways: (I) passing through the hepatic sinusoids into the hepatic veins and then to the inferior vena cava. (II) In the presence of portal hypertension, bypassing the liver via portosystemic collateral circulation to reach the inferior vena cava.
Figure 4. Findings on mid-esophageal four-chamber view and transgastric short-axis view. Arrows: the previously noted gas bubbles in the cardiac chambers have almost completely resolved; the interatrial and interventricular septum have returned to their normal convex curvature, bulging toward the right.
Figure 5. The transgastric inferior vena cava view reveals that the gas accumulations in the liver parenchyma have almost disappeared (arrow).
Figure 6. Findings on the chest ultrasound. Arrows: multiple B-lines are present in the lungs. Pathophysiological implication: this sonographic pattern is consistent with pulmonary interstitial edema, reflecting pulmonary complications impaired gas exchange.
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Chen et al. (2026) studied this question.
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