Pulmonary embolism is a known complication after trauma. Menaker et al. 1 reported that pulmonary embolism (PE) after trauma was more likely to occur after blunt trauma with up to 37 per cent of those cases being early in onset (detected between hospital day 1 and day 4) and as many as 15 per cent in the first 48 hours. Traditional teaching has been that PE stems from the formation of a deep vein thrombosis (DVT) originating with Virchow’s triad of hypercoagulability, stasis, and vessel injury. Patients at high risk of developing a fatal PE include those $60 years old, operative times $1 hour, prolonged immobility, polytrauma, and hip and/or knee surgery. 2 We report a case of a massive PE that is unique in that it occurred in a young patient after penetrating trauma, was early in onset, and occurred in the absence of deep venous thrombosis. A 22-year-old obese, African American man status postgunshot wound to the left thoracoabdomen was transported to Grady Memorial Hospital, a Level I trauma center in Atlanta, Georgia. The patient had no prior medical or surgical history and was taking no medications. He was taken immediately to the operating room due to ballistic trajectory and underwent a left chest tube thoracostomy and an exploratory laparotomy. He was found to have a left hemopneumothorax, two injuries to the left diaphragm (grade II), a liver laceration (grade I), an anterior and posterior gastric injury (grade II), a transverse colon injury (grade I), and a splenic injury (grade III). He underwent splenectomy and primary repair of his diaphragmatic, gastric, and transverse colon injuries. Sequential compression devices were used during the case, which lasted two hours.

The patient was admitted to the intensive care unit for ongoing resuscitation and ventilator management. Sequential compression devices were placed for mechanical prophylaxis but he was not started on chemoprophylaxis. Approximately 18 hours postoperatively, the patient developed hypoxia with oxygen saturations in the 80s. At that time chest X-ray was unremarkable. Arterial blood gas demonstrated hypercarbia with a pH 7.25, pCO2 54, pO2 91, and base deficit–4.7. Serial hemoglobin measurements did not decrease, making postoperative hemorrhage an unlikely etiology of his symptoms. The patient then developed sinus tachycardia with a heart rate documented as high as 160. Urine output remained 0.5 cc/kg/hr throughout postoperative day 0 and his base deficit corrected to–2.8 with crystalloid resuscitation. A noninvasive cardiac output monitor suggested adequate preload based on stroke volume variation. However, on postoperative day 1 the patient became hypotensive requiring norepinephrine and vasopressin infusions. Our team considered massive PE at this time. Electrocardiogram (EKG), troponins, transthoracic echocardiogram, and a CT PE protocol scan were ordered. The EKG demonstrated sinus tachycardia with an S1Q3T3 pattern with ST elevation in the right precordial leads suggestive of acute right heart strain. Transthoracic echocardiogram was significant for right ventricular dilation and systolic dysfunction with elevated right ventricular systolic pressures (30–40 mm Hg) and flattened septum, in addition to a positive McConnell’s sign (regional wall motion abnormalities sparing the right ventricular apex). His troponin was elevated at 1.01 ng/mL. Subsequently, CT PE protocol identified extensive bilateral pulmonary emboli extending from the main pulmonary arteries through the subsegmental pulmonary arteries bilaterally (saddle embolus)(Fig. 1). After consultation with the multidisciplinary PE Team, the patient underwent emergent surgical pulmonary …