Severe Refractory Hypoxemia 16 Years After a Gunshot Injury

Abstract

A 53-year-old man presented with a history of depressant syndrome. He had been hospitalized 16 years previously because of penetrating traumatic injury of the left hemithorax by bullet secondary to a suicide attempt. Recently, he came to the emergency department for an illness leading to the discovery of severe hypoxemia refractory to nasal oxygen therapy. The arterial blood gas measurements revealed a pH of 7.41, a PaCO 2 of 41 mm Hg, a PaO 2 of 45 mm Hg, and O 2 saturation of 83% on ambient air; the PaO 2 increased to 85 mm Hg on inspired oxygen of 100%. resulting in a shunt of 30%. Multidetector computed tomography-angiography of the chest showed clearly a giant proximal pulmonary arteriovenous fistula ( Figure 1A and B and Movies 1 and 2 of the online Data Supplement). Transthoracic contrast echocardiography (TTCE) showed a massive early (in the third cardiac cycle) passage of microbubbles to the left side of the heart (Movie 3 of the online Data Supplement) without evidence of pulmonary artery hypertension or ventricular cavity enlargement. The diagnosis was a laterolateral fistula between the laterobasal segmental pulmonary artery (6 mm in diameter) and an aneurysmal sac draining toward an enlarged pulmonary vein (8 mm in diameter) and the distal pulmonary artery (4 mm in diameter). Clinical examination did not reveal a continuous murmur in the left posterior thorax. The draining artery was occluded first by a plug 10 mm in diameter, and the feeding artery was then occluded by a plug 12 mm in diameter (Figure 2A and B). The PaO 2 increased to 75 mm Hg with a residual physiological shunt of 6%. Three-month multidetector computed tomography-angiography follow-up showed a decrease in the aneurysmal sac and the draining vein. One year later, TTCE showed extinction microbubbles (right to left passage) (Movie 4 of the online Data Supplement), and the O 2 saturation was 96% on ambient air. The patient recovered uneventfully and at present continues to do well. Although penetrating chest trauma is a common emergency, the development of traumatic pulmonary arteriovenous fistulas (PAVFs) is exceedingly rare. 1 Dairywala et Figure 1. A, Three-dimensional image shows clearly the feeding pulmonary artery and the draining pulmonary vein with a laterolateral fistula. B, Selective extracted three-dimensional image. Blue, pulmonary artery; red, draining vein. Figure 2. A, Selective pulmonary artery angiogram shows clearly the feeding pulmonary artery, the aneurysmal sac, the draining vein, and the distal portion of the pulmonary artery. B, Control pulmonary angiogram shows complete occlusion of the fistula by two plugs. From the Radiology Department

Late Presented Posttraumatic Pulmonary Arteriovenous Fistulea Occlusion With Septal Occluder Device

“…PAVF oluşumuna bağlı gelişen anatomik sağ-sol şant refrakter hipoksemi nedenidir. [5,16] Refrakter hipoksemi %100 oksijen desteğine rağmen PaO 2 ve SpO 2 değerlerinin yükselmemesi olarak tanımlanabilir. [16] Olgumuzda istirahat halinde PaO 2 50.6 mmHg, PvO 2 48 mmHg, SaO 2 %84.3 ve SpO 2 %84 olarak görülmüş ve %100 oksijen ile bu değerlerin yükselmedikleri gözlenmiştir.…”

“…[4] Sonradan gelişen PAVF ise siroz, metastatik troit karsinom, "schistosomiasis", "actinomycosis", fanconi sendromu, mitral stenoz ve penetran toraks travması sonrası oluşabilmektedir. [5] Penetran toraks travması sonrası akut dönemde veya geç dönemde PAVF oluş-tuğuna dair olgular bildirilmiştir. [6,7] En sık raslanan semptom %21-71 ile efor dispnesidir.…”