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Symptom: Left-Sided Weakness

Leccese, Paul MD

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doi: 10.1097/01.EEM.0000529877.20592.82
    air embolism, cerebral infarction
    air embolism, cerebral infarction:
    Noncontrast CT scan of the brain showing a punctate embolism of free air and hypodensity in the precentral gyrus consistent with acute stroke in an area that anatomically correlates with the patient's symptoms.

    A 53-year-old woman two weeks after a double-lung transplant for end-stage COPD presented three hours after a sudden onset of weakness and shakiness. Her family said she was acting normally when she awoke. They said she took some unknown medications for her lung transplant, and then slumped over and became unresponsive. She was given two 1 mg doses of IV naloxone by paramedics prior to arrival in the emergency department, which yielded no response. She remained unresponsive for several minutes before slowly becoming more alert. Her blood sugar in the field was normal.

    She was afebrile, tachycardic to 128 bpm, hypotensive to 94/61 mm Hg, and had a respiratory rate of 20 bpm and oxygen saturation of 94% on 4L/min of oxygen. She was alert, oriented to person, place, and time, and was noted to have equal and reactive pupils. She had a right gaze preference, left-sided hemineglect, left-sided weakness and sensory deficits, and a left facial droop that spared the forehead.

    Her incision sites, all closed with surgical staples, were in place and well-appearing without dehiscence, drainage, or surrounding erythema. Her lungs were clear and equal throughout, and she had no increased work of breathing. She was tachycardic and regular, and had no murmurs on auscultation.

    The patient was taken emergently for a CT scan, which is shown. What is the diagnosis?

    Find the diagnosis and case discussion on p. 18.

    Diagnosis: Air Embolism and Cerebral Infarction

    Air embolism is a rare but highly morbid condition that occurs when free air enters the vasculature in a quantity greater than what can be absorbed by the capillary beds in the pulmonary vasculature. Air emboli are classified by the site of entry into the circulation as venous or arterial air embolism. (N Engl J Med 2000;342[7]:476.) The emboli tend to lodge in anatomically distinct parts of the circulation based on their site of entry. Venous air emboli will pass through the right-sided heart circulation and lodge in the lungs, causing pulmonary arterial occlusion. (Prog Cardiovasc Dis 1994;36[6]:447.) Left-sided (arterial) emboli, on the other hand, can lead to obstruction of systemic vessels and resultant end-organ ischemia, including stroke. (N Engl J Med 2000;342[7]:476.)

    Numerous causes of air embolism have been reported in the literature, with the most common being vascular access procedures such as central venous lines or peripheral intravenous procedures, neurosurgical, or otolaryngological operations performed with the patient in an upright or a semi-upright position, intrathoracic procedures, including lung resection or endobronchial lung biopsy and cardiopulmonary bypass. (N Engl J Med 2000;342[7]:476; Neurocrit Care 2009;11[3]:381.) Barotrauma, such as that sustained during mechanical ventilation or rapid ascent during scuba or other kinds of underwater diving, also places patients at risk of systemic air emboli. Cases of lung transplantation leading to air emboli have been reported in the literature, but these are rare, and a definitive cause of embolization is often not identified in these cases. (Neurocrit Care 2009;11[3]:381; J Heart Lung Transplant 2008;27[6]:692.)

    The definitive management of systemic air embolism is with hyperbaric oxygen. Temporizing measures can include high-flow oxygen, mechanical ventilation in the event of respiratory failure, fluid resuscitation and vasopressors to remedy circulatory compromise, and patient positioning to avoid further entry of air into the circulation. Patients with venous emboli should be placed in the left lateral decubitus position to avoid propagation of the emboli out of the right ventricular outflow tract, while those with arterial emboli should be positioned supine and flat. (Eur Respir J 2009;34:452.)

    Hyperbaric oxygen has been shown to improve outcomes in a time-dependent manner, with earlier treatment leading to improved outcomes. (Intensive Care Med 2002;28[5]:559; J Thorac Cardiovasc Surg 1999;117[4]:818.) The mechanism is thought to be a dramatic increase in the partial pressure of oxygen in the blood, which leads to decreased partial pressure of nitrogen. This, in turn, allows for faster re-absorption of the nitrogen-rich gas in the air bubbles trapped in the bloodstream. (Undersea Hyperb Med 1998;25[1]:43.)

    The patient was emergently transferred to a nearby center with a hyperbaric oxygen chamber where she underwent four hours of hyperbaric oxygen therapy. A follow-up CT scan revealed resolution of the air emboli. She subsequently underwent CT angiography of the head, neck, and chest to evaluate for a surgically correctable source of the embolism, but this was unrevealing. Transthoracic echocardiography was also performed and did not reveal any evidence of interatrial shunt. She was medically stabilized and later transferred to acute rehab, where she slowly began to regain some strength, though her left-sided weakness persisted. She was slowly continuing to improve at her last follow-up visit, though her ultimate prognosis remains unknown. No definitive cause of embolism has yet been found.

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