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.
An 18 year-old female patient was scheduled for a craniotomy and excision of a mid-brain ependymoma in a seated position. Her clinical, biochemical and coagulation parameters were normal. In the operating theatre, standard monitors (electrocardiograph [ECG], non invasive blood pressure, pulse oximeter) were attached. General anesthesia was induced with fentanyl and thiopentone and intubation was facilitated with vecuronium. Anesthesia was maintained with oxygen, air, isoflurane, fentanyl and atracurium with controlled ventilation using a tidal volume of 500 ml and respiratory rate (RR) of 12 breaths/min to achieve normocarbia. Intra-operative monitoring (using a Datex Ohmeda S5) included heart rate, ECG, oxygen saturation by pulse oximetry, RR, end-tidal carbon dioxide (EtCO2), central venous pressure (CVP) (via the basilic vein), invasive blood pressure, airway pressure, volume of intravenous fluids infused, urine output, nasopharyngeal temperature, arterial blood gas (ABG), blood glucose and blood loss. Transesophageal echocardiography was not monitored as this was not available in our institute. There were no hemodynamic changes during moving the patient to a seated position. Baseline ABG analysis and CVP were normal.\nAt the time of opening of the dura, there was a sudden decrease in EtCO2 from 36 to 20 mmHg and then, further, to 15 mmHg. Concurrently there was a small tear in the occipital sinus. A VAE was therefore suspected. The EtCO2 changes observed during the VAE, with corresponding arterial blood gas analyses, are depicted in . There were no associated changes in hemodynamics or oxygenation. The EtCO2 returned to normal within a few minutes, following measures such as administration of 100% oxygen and prevention of further air entrainment through packing of the surgical site with saline-soaked gauze. The tear in the occipital sinus was identified and clipped.\nExcision of the tumor was uneventful, and intra-operative blood loss during the excision was around 500 ml. CVP was maintained at around 11-14 cmH2O. The patient remained hemodynamically stable. During the final stages of dura closure, application of the Valsalva maneuver was requested by the surgeon to check for cerebrospinal fluid leaks and assess the adequacy of hemostasis. Immediately after releasing the sustained positive pressure during the Valsalva maneuver, the EtCO2 again suddenly decreased from 30 to 9 mmHg, followed by a reduction in blood pressure to 62/30 mmHg and ST-T depression by 1 mmHg. Precordial auscultation at the apex of the heart revealed a mill-wheel murmur. The PaCO2 to EtCO2 gradient was 39 mmHg (). A massive VAE was contemplated and the surgeon was cautioned.\nImmediately, 100% oxygen was administered and the incision site was packed with saline-soaked gauze pieces. The patient was then repositioned in a left lateral recumbent position. About 50-60 ml of air was aspirated from the central venous catheter. She was resuscitated with 1 L of intravenous voluven® (6% hydroxyethyl starch 130/0.4 in 0.9% sodium chloride injection) and an injection of 6 mg mephenteramine. Blood pressure and EtCO2 returned to normal. The mill-wheel murmur disappeared. Soon afterwards, the rest of the surgical procedure was continued in the lateral position.\nAt the time of wound closure, bleeding was noted from the suture line and the wound was therefore reopened to check for the source of the bleeding. The bleeding from the wound was diffuse, with no identifiable bleeding site. An abnormality in coagulation was suspected. Since blood loss was high and hemostasis could not be obtained surgically, two units of packed red blood cells (PRBCs), four units of fresh frozen plasma (FFPs) and four units of platelet-rich plasma (PRPs) were administered without waiting for the coagulation profile report. Initially, the blood began to clot and the bleeding stopped. The patient was shifted to the neurosurgical intensive care unit for post-operative ventilation and observation. Later, there was continued oozing from the operative site and from the external ventricular drain (EVD). A post-operative computerized tomography scan of the brain showed a hematoma at the operative site, which was evacuated on the first post-operative (PO) day. Surgical findings showed further oozing from the operative site and surrounding cerebellar surfaces. These were corrected with blood and blood products. The patient's blood parameters and coagulation profile, with interventions made in the following PO days are shown in . There was continued oozing at the operative site and also from other intravenous and arterial cannulation sites. She deteriorated neurologically, showing clinical features of raised intracranial pressure and an EVD persistently draining blood. On the fourth PO day, inotropic support was initiated, as the patient developed persistent hypotension along with a decreasing Glasgow Coma Scale value and absent pupillary reaction. Finally, on the fifth PO day, she passed away despite resuscitative measures.