A 61-year-old African American woman with a past medical history of peripheral vascular disease (PVD), chronic venous insufficiency and pre-diabetes mellitus presented to our Emergency Department (ED) with worsening left lower extremity pain for the past 3 days. The pain was continuous, progressive and the patient denied any history of trauma. Examination showed a clean, shallow ulcer 2x3 cm with surrounding hyperpigmentation from stasis dermatitis; without discharges or signs of infection. Upon assessment, the pain was deemed to be due to chronic venous insufficiency. It improved with non-steroidal anti-inflammatory drugs and she was subsequently discharged from the emergency department. Three days later, the patient returned to the ED with worsening leg pain unresponsive to the oral analgesics. At this admission, she also reported inability to bear weight on the affected extremity. She denied fevers, chills, nausea, vomiting, abdominal pain, or urinary symptoms. Physical examination revealed erythema around the ulcer with increased warmth and mild tenderness. CT of her left lower extremity with intravenous (IV) contrast revealed subcutaneous edema and fascial thickening most prominently at the medial aspect of the lower extremity, compatible with cellulitis in the absence of a drainable fluid collection (). The patient was treated with IV ampicillin/sulbactam. There was evidence of symptomatic improvement and the patient was discharged with an oral course of antibiotics and zinc oxide compression bandages for local wound care. Her discharge diagnosis was lower extremity cellulitis with associated chronic venous insufficiency ulcer. Immediately upon leaving the hospital, the patient had a syncopal episode and collapsed; which prompted her to be rushed to the ED for further evaluation. In the ED, the patient presented with tachypnea and confusion and reported feeling short of breath. Physical examination revealed a blood pressure of 85/61 mmHg, heart rate of 131 beats per minute and respiratory rate of 32 breaths per minute with an oxygen saturation of 92% on non-rebreather mask 15 litres per minute. The patient was sedated and intubated due to dyspnea, increased work of breathing and hemodynamic instability. A central venous catheter was placed, along with initiation of vasopressors. CT scan of the head showed pneumocephalus within the cavernous sinus and clival venous plexus in the absence of skull base fracture, acute hemorrhage, mass effect or evidence of an acute ischemic infarct (). CT with IV contrast of pulmonary artery revealed saddle pulmonary embolus with pulmonary emboli extending into the right and left main pulmonary arteries, bilateral lobar and segmental arteries. The Figures also showed marked right heart strain with bowing of the interventricular septum and reflux of contrast within the IVC and hepatic veins, and pooling of contrast within the right heart. It also demonstrated air within the right ventricle as well as subcutaneous emphysema involving anterior chest wall and right supraclavicular fossa. Foci of air are also seen tracking into the hepatic vasculature likely iatrogenic from contrast administration (). Due to her clinical condition and imaging findings, the patient received thrombolytic therapy (recombinant Tissue Plasminogen Activator) for pulmonary embolism. Subsequently she was admitted to the critical care unit. Her initial laboratory results revealed lactate of 3 mmol/L (reference range 0.5-2.2), troponin I <0.01 ng/mL (reference range <0.01) and N-terminal pro B-type natriuretic peptide (NT-pro BNP) at 61 pg/mL (reference range <300 pg/mL). She was started on therapeutic anticoagulation with heparin drip afterwards. The patient was extubated next day and put on high flow 100% O2 as a trial to improve resorption of air in the vasculature. Once the patient was hemodynamically stable, there were no apparent neurological deficits noted as a result of cerebral air embolism. Two days after extubation, repeat CT head revealed resolution of air in cavernous system (). Venous duplex of her lower extremities revealed no evidence of thrombosis bilaterally (). Patient was transitioned to oral anticoagulation and discharged after two days of hemodynamic and clinical recovery.
A 22-year-old previously healthy female was the unrestrained passenger in a highway MVA. Upon impact, a mailbox penetrated the passenger front windshield and struck the patient's face, resulting in severe facial trauma. The patient was intubated in the field for a Glasgow Coma Scale score of 5. She was emergently airlifted to the hospital and, en route, was resuscitated with crystalloid and two units of whole blood.\nThe patient arrived hemodynamically unstable—tachycardic and hypotensive complicated by severe metabolic acidosis (lactate 3.42 mmol/L, reference range: 0.6–2.3 mmol/L). Her right eye was ruptured, and her left pupil was dilated to 5 mm and minimally responsive to light. Three additional units of packed red blood cells (pRBCs) and two units of fresh frozen plasma (FFP) were rapidly administered via a Level 1 rapid infuser in the right 18-gauge antecubital intravenous catheter with stabilization of her hemodynamic status. Trauma series computerized tomography (CT) revealed facial trauma with ruptured right globe, temporal bone fracture, temporomandibular joint-line fractures, and mixed subdural and epidural hematomas with an 8 mm midline shift and effacement of the anterior horn of the right lateral cerebral ventricle. A large amount of air within the right ventricle (RV) extended to the right axillary vein (Figures and ) with air collection under the pulmonary valves () but no immediate RV outflow tract obstruction. The air entrainment was thought to be due to transfusion of products through the Level 1 rapid infuser given that there were no pneumothoraces or air in the superior and inferior vena cava.\nA multispecialty conference was held between the trauma surgery, neurosurgical, cardiac intensive care, and anesthesia teams regarding the optimal treatment plan. The concern was RV air burden may risk embolization and would compound hemodynamic collapse during emergent craniotomy. Aspiration of air via a central line was considered, but the impending risk of brain damage expedited the decision to proceed emergently to the OR for intracranial decompression. While the patient was in the CT scanner, vital signs included bradycardia (50s–60s) and occasional hypertension (systolic blood pressure reaching 150s–160s mm Hg), indicating presence of Cushing's triad. These vital signs along with physical exam findings of left dilated pupil and imaging evidence of an 8 mm cerebral midline shift were consistent with possible critically elevated intracranial pressures. With relatively stable hemodynamics but critical cerebral herniation risk, the decision was made to proceed with emergent craniotomy.\nThe patient arrived to the OR directly from diagnostic radiology, with heart rates between 80 and 90 beats/min and mild hypotension with systolic blood pressures of 90–100 mm Hg without any vasopressor support. She was maintained on inhaled sevoflurane at a minimum alveolar concentration <1.0 with nondepolarizing muscle relaxant. A right radial arterial line was placed. For access, the patient had a previously placed 18-gauge peripheral intravenous and intraosseous catheters. The patient was positioned in pins in the reverse Trendelenburg position. The degree of reverse Trendelenburg position was small (about 10–15 degrees) and was performed to decrease intracranial pressure and for optimum surgical visualization.\nTwenty-five grams (200 mg/kg) of intravenous mannitol was administered. At this point, the patient had approximately 2–2.5 L of estimated blood loss and had received four units of red blood cells (two whole blood, two pRBCs) and four units of FFP. Since intraoperative hemoglobin (9.7 g/dl), coagulation panel, and lactate (normalized to 2.0 mmol/L) were normal, further transfusions were deferred.\nApproximately 28 minutes after incision, end-expiratory CO2 (EtCO2) and mean arterial pressure abruptly fell concomitantly with loss of pulse oximetry waveform. She maintained an organized rhythm but distal pulses could not be palpated. The neurosurgeons were able to palpate intracranial pulsation; therefore, chest compressions were not initiated. Obstructive VAE physiology was assumed, and repeated intravenous epinephrine doses (10 mcg per injection) and 1 L fluid bolus were administered. After the first 30 mcg of epinephrine was administered over approximately 30 seconds, EtCO2 and blood pressure increased and the pulse oximetry waveform returned. An epinephrine infusion was initiated to maintain hemodynamic stability. In aggregate with hemodynamic resuscitation, the patient was immediately placed on 100% inspired oxygen and taken out of reverse Trendelenburg position to a more neutral position.\nThe patient remained hemodynamically stable on the epinephrine infusion and did not have a recurrence of such an event for the rest of the procedure. At the conclusion of the right hemicraniectomy and hematoma evacuation, intraoperative transesophageal echocardiography (TEE) showed hyperdynamic contractility and persistent, though nonobstructive air in the right ventricle. The intracardiac air burden was substantially less compared to the amount visualized on preoperative CT scan. There was no patent foramen ovale or regional wall abnormalities. At this point, the patient had displayed normal and stable vital signs for two hours. Thus, in the presence of hemodynamic stability in a patient without cardiac or other major comorbidities, the decision was made to proceed with the remainder of planned surgery. Furthermore, the ophthalmology and plastic surgery teams indicated that urgent surgical intervention may potentially preserve function of the patient's right eye while decreasing chance of infection.\nOnce the TEE probe was removed, the ophthalmology and plastic surgery teams performed a right eye enucleation, repair of brow and facial lacerations, complex repair of nasal laceration and cartilage, repair of upper and lower eyelid lacerations and reduction and fixation of numerous, complex frontozygomatic fractures, and irrigation and debridement of open wound, which collectively took 90 minutes of additional operating time.\nTotal OR time totaled 569 minutes. Using a goal-directed transfusion threshold of 8.0 g/dL, the patient received a total of two units of pRBCs and two units of FFP intraoperatively. Additionally, a total of 5,000 cc of crystalloid and two grams of intravenous calcium chloride were administered. Estimated blood loss for the procedure was 300 mL with 4000 mL of urine output. The epinephrine infusion was weaned off by the end of the procedure (highest dose 0.1 mcg/kg/min).\nA postoperative head CT revealed expected postoperative changes with complete resolution of midline shift. The patient was then transported to the neurological intensive care unit intubated for ongoing cares. Given her age, lack of preexisting cardiac comorbidities, and resolution of her hemodynamic instability, further cardiac evaluation was deferred. She remained intubated for airway protection but was extubated within 36 hours of admission. The patient exhibited no gross neurological deficits and was able to verbally communicate shortly after extubation. She continues to progress with traumatic brain rehabilitation in the outpatient setting.