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 65-year-old lady with morbid obesity, hypertension, and rheumatoid arthritis was planned for total hip replacement under combined spinal and epidural anesthesia. Spinal anesthesia with 3 ml 0.5% of bupivacaine and 25 mcg of fentanyl was given at L3-4 interface with 26G Quinke's needle. Epidural space was identified at L2-3 level with a 18G Tuohy canula using loss of resistance technique with air (1 ml). The air filled syringe was disconnected soon after the loss of resistance. A 20G epidural catheter was introduced and fixed at 12 cm at the skin level. 5 min after the test dose, infusion was established at 2 ml/h with bupivacaine 0.125% and fentanyl (2 mcg/ml). Surgery lasted for around 8 h and epidural infusion was stopped at 6 h of surgery due to hypotension mostly due to bleeding (1100 ml). It was managed with fluids and blood transfusion through a peripheral cannula. In Intensive Care Unit for severe pain, she was prescribed an epidural bolus of 10 ml of 0.125% bupivacaine with 20 mcg of fentanyl along with IV tramadol 50 mg and promethazine 12.5 mg. With a lot of resistance, only 8 ml of the mixture could be injected over around 2 min. There was sudden bradycardia (73/min) and hypotension (systolic pressure 86 mmHg). She started jerking and gasping with suddenly diminished level of consciousness. Blood sugar was 242 mg% (13.44 mmol). Left pupil was noticed to be dilated and fixed. She was resuscitated with fluids and low dose noradrenaline and intubated.\nAn urgent computed tomography (CT) brain was done, which revealed air around the brain stem and no bleeding. Within 1 h she was awake but left pupil still remained dilated and fixed. She was extubated the next day. The mildly altered sensorium lasted for 2 days.