The authors describe a case of air embolism that developed during a plane flight in a woman who had a congenital cystic adenomatoid malformation. They review the pathophysiological mechanisms, risk factors, clinical features, and treatment of air embolism.
A 62-year-old woman was 20 minutes into a commercial airplane flight from Denver to Omaha when she suddenly became unresponsive and rigid. Her family and paramedics, who were incidentally on the airplane, attempted to arouse her without success. The patient demonstrated slow, sonorous, but spontaneous, breathing efforts. She remained with her eyes closed, exhibiting a few twitching movements of her left hand and leg and mild drooping of the left angle of her mouth for about 3 to 4 minutes.
An attempt to gain intravenous access failed. She was given diazepam, 10 mg, intramuscularly, for a presumed seizure episode and received oxygen via face mask. The airplane landed in 30 minutes without any further change in the patient's condition; she was transported to our hospital via ambulance within 20 minutes of landing.
On presentation, her vital signs were the following: temperature, 37.1°C (98.8°F); pulse, 124 beats per minute; blood pressure, 151/ 75 mm Hg; respiration rate, 20 breaths per minute; and oxygen saturation, 98% on 10 L/min oxygen by face mask. The patient was noted to be unresponsive to external stimuli. She was intubated for airway protection and placed on mechanical ventilatory support.
Physical examination of the patient revealed brisk pupillary reflexes with clonus in the left lower extremity; other findings were normal. A portable chest radiograph showed a large cystic radiolucency within the right lower lobe, which suggested a congenital cystic anomaly (Figure 1). A noncontrast CT scan of the head showed multiple intracranial parenchymal air bubbles consistent with air emboli, with no evidence of acute ischemic or hemorrhagic infarction (Figure 2). A CT scan of the chest with contrast revealed no evidence of pulmonary emboli, but it confirmed the presence of a large (10 3 9.5-cm) thin-walled cystic lesion with a small air-fluid level (Fig- ure 3). These radiological findings were consistent with the diagnosis of congenital cystic adenomatoid malformation.
A transthoracic echocardiogram with saline contrast showed a decreased left ventricular ejection fraction of 30% to 35%, with akinesis of the cardiac apex. No patent foramen ovale was demonstrated. The results of laboratory studies, including complete blood cell count, complete metabolic panel, and electrocardiography, were normal. Serial cardiac enzyme levels showed a rising trend of troponin I and creatine kinase isoenzyme MB fraction consistent with recent myocardial injury.
The patient was maintained on mechanical ventilation and given supportive care. Three days after the acute event, a CT scan of the head showed increasing cerebral edema. After consulting with neurosurgery and neurology teams, intravenous mannitol was administered for control of intracranial pressure. An MRI scan of the brain demonstrated bilateral acute infarcts with associated cerebral edema consistent with acute brain injury secondary to air emboli.
Her vital signs remained stable, and a second CT scan of the head demonstrated a decrease in cerebral edema. She was extubated 11 days after the acute event. She demonstrated 2/5 power in her left upper extremity and 4/5 power in the right upper extremity, with no movement in the lower extremities bilaterally. She was able to swallow without difficulty but had some slowing of speech. She was discharged to a rehabilitation facility in her hometown.
We concluded that the patient suffered an air embolism. Cabin decompression that occurred following the ascent of the airplane to cruising altitude resulted in an increased volume of the patient's cystic adenomatoid malformation with an increase in the transmural pressure across the cyst wall. This probably caused entry of air into the pulmonary venous circulation and systemic embolization, resulting in ischemic cerebrovascular accident as well as myocardial injury.
The development of air embolism requires an abnormal communication between air and the blood vessel and a pressure gradient that favors entry of air into the vessel.1 Occasionally, other gases used for medical purposes (such as carbon dioxide, nitrous oxide, and nitrogen) can lead to gas embolism. Trauma, surgical incisions, and intravascular catheters create the most common sources of venous air entry. Air travels to the right side of the heart and the lungs, where it may have circulatory or respiratory consequences.
Paradoxical embolism occurs when air reaches the arterial circulation via a patent foramen ovale or by overwhelming the filtering ability of the lungs,2 leading to systemic ischemic manifestations in the brain, heart, skin (livedo reticularis), and other organs.3 Arterial gas embolism is caused by the entry of gas into the pulmonary veins or directly into the arteries by decompression barotrauma.
Risk factors for catheter-related venous air embolism include detachment of a catheter connection, failure to occlude the needle hub on a catheter during removal, dysfunction of valves and connectors, persistent catheter tract, deep inspiration and upright position during catheter removal, and hypovolemia.4 Air embolism has also been reported as a complication of mechanical ventilation, from coughing while using continuous positive airway pressure, and as a complication of diving.
Air embolism during an airplane flight is rare, but the presence of preexisting pulmonary pathology, such as a pulmonary bulla, bronchogenic cyst, or cystic adenomatoid malformation, increases the likelihood of occurrence.5-9 It usually occurs during rapid ascent when the airplane climbs to cruising altitude in a short span of about 20 minutes, with the cabin decompressed to 560 mm Hg (an equivalent altitude of 8000 feet) from 760 mm Hg (at sea level).10 This decrease in ambient pressure can result in an increase in the volume of the cyst or bulla by as much as 35%, according to Boyle-Marriotte's law (pressure 3 volume = constant).6 This marked increase in volume may result in tears in the cyst wall and subsequent air embolization to the arterial or venous circulation.
Congenital cystic adenomatoid malformations are pulmonary hamartomas consisting of overgrown terminal bronchioles11 that can occur anywhere in the lung, most commonly in the left lower lobe. Most of these malformations are recognized in early life, but a few remain undiscovered until later adult life.12 Pulmonary pathology such as cystic adenomatoid malformation or bronchogenic cyst offers a mechanism for the entry of air into the venous/arterial circulation. This usually occurs when there are sudden, significant changes in the air pressure within these lesions, such as would occur in underwater diving13,14 or decompression during airplane flight.5-9
When the pulmonary circulation is involved, air embolism usually presents as acute hypoxemic respiratory failure. If systemic embolization occurs, signs of acute hypoperfusion or peripheral embolization may be noted. Cerebral air embolism results in symptoms identical to those of a cerebrovascular accident from ischemic causes and depends on the region of the brain that is involved.
Diagnosis of cerebral air embolism requires a high index of suspicion. Demonstration of intraparenchymal/intravascular air on a CT scan of the head is diagnostic. As is our case, the primary lesion (cystic adenomatoid malformation or bronchogenic cyst) should be demonstrable on a chest radiograph or a chest CT scan. Laboratory studies may show evidence of ischemic injury to organs, such as elevated levels of cardiac biomarkers, indicating ischemic myocardial injury, or elevated levels of creatinine kinase, reflecting skeletal muscle injury. The creatinine kinase level can be markedly elevated if skeletal muscle injury is diffuse.14
Immediately after the occurrence of air embolism, the patient may benefit from recompression of the passenger cabin.6 Significantly improved outcomes have been noted on administration of hyperbaric oxygen, although no randomized control trials have been conduct- ed to evaluate this.5,8,15-17 Therapy should be administered as soon as possible after the event.
Hyperbaric oxygen therapy is hypothesized to work because it decreases the size of the gas bubbles and thereby decreases the ischemic complications as well as increases the surface area of the gas bubble available for gas exchange relative to its volume.5 Using pure oxygen or heliox mixture in the hyperbaric chamber would also result in more rapid absorption of the gas bubble.5 Hyperbaric oxygen therapy benefits the patient even if it is administered late in the course. This is believed to be because of the persistence of gas bubbles in distal cerebral circulation, even 40 hours after the initial event, as a result of poor circulation.17,18 Long-term outcomes depend on the extent of brain and end-organ injury.
Susceptible patients with pulmonary pathology such as bronchogenic cysts, cystic adenomatoid malformations, or pulmonary bullae should be treated with resection of these lesions to avoid complications such as infection, pneumothorax, and air embolism.11,13,19,20 Patients who are not surgical candidates should be advised to avoid significant changes in ambient air pressure, as would occur with underwater diving or airplane flights. Patients who have a known history of conditions likely to be worsened by hypoxia (such as chronic obstructive pulmonary disease, coronary artery disease, and pulmonary fibrosis) or who have dyspnea may require pre-flight screening.21 However, pre-flight screening of asymptomatic patients for lung pathologies is not feasible because of the considerable costs with minuscule benefits.22
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