대한흉부영상의학회 Korean Society of Thoracic Radiology

Discussion

Diagnosis With Brief Discussion

Diagnosis

Intrathoracic migration of lipiodol following gastric variceal obliteration

Radiologic Findings

Fig 1. Chest radiograph reveals a high-density nodular opacity in the left lower lung field, showing density significantly higher than the adjacent rib.
Fig 2. Contrast-enhanced chest CT reveals a high-attenuation nodule in the left supradiaphragmatic region, showing similar attenuation to the intrahepatic Lipiodol accumulation.
Fig 3. A: Chest radiograph obtained 2 years ago is unremarkable. B: Follow-up image obtained one day later reveals high-density material in the stomach and along the diaphragm.

Brief Review

Additional figure 1. Endoscopic variceal obturation (EVO) procedure involving the injection of Histocryl-Lipiodol mixture into the engorged varix at the gastric fundus.
Additional figure 2. A: Contrast-enhanced abdominal CT shows glue casts in the gastric cardia and the left supradiaphragmatic extrapleural space. B: Sagittal view reveals the glue cast extending superiorly along the course of the left inferior phrenic vein (arrow) and left supradiaphragmatic extrapleural space.

Endoscopic obliteration of gastric varices using an N-butyl-2-cyanoacrylate (NBCA)–lipiodol mixture is an established treatment in patients with portal hypertension, but it is associated with extra-variceal migration of radiopaque lipiodol.
Gastric fundal varices drain through portosystemic collateral pathways, most commonly via the gastrorenal shunt, which accounts for approximately 80–85% of cases. In this pathway, venous outflow from gastric varices passes through the inferior phrenic vein and predominantly drains into the left renal vein and inferior vena cava. Although the primary drainage is toward the systemic venous circulation, limited communications with peridiaphragmatic venous channels, including the pericardiophrenic or mediastinal veins, have been described, providing a less common potential route for cranial extension of migrated material above the diaphragm.
Consequently, the most frequently reported thoracic complication of NBCA–lipiodol migration is pulmonary embolism. In addition to intravascular embolization, pleuropulmonary reactions related to NBCA–lipiodol have been reported, including transient pleural effusion, localized pleuritis, and inflammatory changes in adjacent subpleural lung parenchyma. These reactions are thought to result from microembolization or direct contact of lipiodol-containing material with pleural surfaces, often remaining clinically silent.
In patients with liver cirrhosis or hepatocellular carcinoma, focal intrathoracic high-attenuation lesions on CT should prompt careful review of prior interventional history: right-sided lesions are more commonly related to transarterial chemoembolization, whereas left-sided supradiaphragmatic or pleural-adjacent lipiodol deposition should raise suspicion for migration after gastric variceal obliteration.

References

1. Tripathi D, Stanley AJ, Hayes PC, et al. UK guidelines on the management of variceal haemorrhage in cirrhotic patients. Gut. 2015;64:1680–1704.
2. Kiyosue H, Ibukuro K, Maruno M, et al. Hemodynamics of gastric varices: evaluation with multidetector CT and portography. Radiographics. 2013;33:87–100.
3. Kim YJ, Raman SS, Yu NC, et al. Pulmonary embolism of cyanoacrylate after endoscopic treatment of gastric varices: CT findings. AJR Am J Roentgenol. 2004;183:145–147.
4. Abdel-Aziz Y, et al. Pulmonary and pleural changes after cyanoacrylate injection for gastric varices. Int J Appl Res. 2015;1:79–83.

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