Stroke Snapshot: Stroke Due to Hemodialysis-Associated Air Embolism
Air emboli can cause iatrogenic stroke during a procedure when air has an opportunity to enter blood vessels. This is a rare occurrence that should be considered when a person who has had a procedure suddenly develops acute stroke symptoms. Clinical suspicion can help to identify stroke vs cerebral air embolism,1,2 which is important because the recommended treatment for air emboli is hyperbaric oxygen therapy (HBOT), not intracranial procedures.3
Etiology
Strokes from air emboli can be caused by air in the cerebral venous or arterial circulation and most commonly have iatrogenic causes,4,5 including but not limited to neurosurgery with the patient in a sitting position, fluid infusion, trauma, using positive end-expiratory pressure on a ventilator, hemodialysis, thoracentesis, intraoperative procedures, and deep-water dives.6,7 Venous air emboli (VAE) arise from air entering the venous circuitry and traveling through the right side of the heart into the pulmonary system.8 These can turn into an arterial air embolus when gas paradoxically enters the arterial circulation either through a pulmonary arteriovenous malformation, patent foramen ovale (PFO), or cardiac septal defects.8-10
For VAE to form, there must firstly be air-to-vessel communication. Secondly, the individual must be upright (usually sitting) during the procedure.5,11 For patients who undergo regular hemodialysis, the first condition is created to bypass the capillary bed and establish a direct connection from an artery to a vein. Gaseous particulates from the dialysis machine may enter the arteriovenous fistula without initiating the machine’s alarm system if a bubble is less than 50 mcL in diameter, or the flow rate is below the standard pump rate for infusion and dialysis.10 This air can travel to the cerebral vasculature because air has lower specific gravity than blood.
As described in the case report, a paradoxical VAE can occur when air enters the atrial circulation via a PFO. The prevalence of PFO in the adult population is approximately 20% to 25%, but prevalence rises to 40% to 50% in individuals who have had a stroke from uncertain causes, also termed cryptogenic.9,12 Individuals who experienced a cryptogenic stroke should be evaluated for PFO with transthoracic/transesophageal echocardiogram or contrast-enhanced transcranial Doppler (bubble-TCD).13 The route for the air emboli from the venous circulation via a PFO is from the right to left atrial cardiac shunt into the aorta and into the arterial circulation. Because of the lower specific gravity of air compared with blood, an air bubble will rise and can cause occlusion of the arterial cerebral vasculature.5,10 The air emboli in the vessel can also cause damage to the surrounding tissue via inflammation and platelet aggregation, which further contributes to the stroke.14
Mr P is 68 and was brought to the emergency department (ED) by emergency medical services with a chief complaint of left-sided weakness and numbness. He had been at a dialysis center that day receiving routine hemodialysis when, 30 minutes into the treatment, he complained to his wife about these symptoms. At that time, he also developed left-sided facial weakness and incoherent speech. Mr P’s wife called 911 and he was transported by EMS in an ambulance to the ED for suspected stroke.
On arrival to the ED, Mr P was alert and interactive with blood pressure of 127/60 mm Hg, pulse 89, and normal temperature of 98.3º. He had slurred speech and was confused, with left-sided vision loss and weakness in the upper and lower extremities (upper>lower). The ED stroke alert workup was done, and Mr P had a National Institutes of Health Stroke Scale (NIHSS) score 14. Mr P’s wife was able to share relevant medical history of end-stage renal disease treated with regular hemodialysis via AV fistula in the left arm for the last 22 years, hypertension, and thyroid neoplasm. Mr P also has a pacemaker implanted for treatment of sick sinus syndrome and was taking the following prescribed medications: 81 mg/ day aspirin, 80 mg/day atorvastatin, 175 mcg/ day levothyroxine, 5 mg midodrine 3 times daily, and 1,334 mg calcium acetate 3 times daily.
Diagnostic Studies and Diagnosis
While Mr P was in the ED, blood was taken, and complete blood cell count, serum chemistry, and coagulation test results were obtained urgently (Table). Mr P had immediate head CT as per the stroke protocol, which showed hyperlucency of the right frontal parietal region on the brain windows that were also hyperlucent on bone windows, indicating air emboli (Figure). Mr P’s pacemaker made MRI contraindicated.
Treatment
After discovery of cerebral air embolism, Mr. P was placed in a hyperbaric oxygen chamber, which is the recommended management for neurologic sequelae of an air embolism. The chamber was decompressed to 2.8 atmospheric pressures for 6 hours with intermittent breaks. Mr. P began to recover from his left-sided hemiparesis and numbness after HBOT. At 4 hours, his neurologic condition was rechecked during a 15-minute break and his NIHSS score had decreased to 6; he had mild left-sided facial asymmetry with dysarthria and upper/lower extremity hemiparesis.
Follow-up Care and Outcome
After 6 hours of HBOT, Mr P was admitted to the intensive care unit and his neurologic symptoms were monitored. He had mild left upper incoordination and left upper extremity motor weakness (4/5). Motor strength of his left lower extremity was normal (5/5). Mr P had a transthoracic echocardiogram (TEE) with bubble study and CT angiography (CTA) to evaluate for conditions underlying his cerebral ischemia secondary to air embolism. CTA showed resolution of the right frontoparietal gas embolism and minimal carotid atherosclerosis without stenosis and calcified plaques in the intracranial vertebral and basilar arteries without stenosis. TEE with bubble revealed a patent foramen ovale (PFO), which explained how an air embolus entered his cerebral circulation.
After continued care and close monitoring, Mr P was discharged with only a mild deficit of left arm weakness. He was referred to an outside tertiary care center for evaluation related to PFO closure.
Clinical Presentation and Diagnosis
Individuals experiencing VAE have symptoms that range from subtle headache to tachyarrhythmias, stroke symptoms, and unresponsiveness.5,10 Air emboli can go unnoted because there may be no symptoms. A high index of suspicion should be maintained for anyone with acute stroke symptoms who has just had a procedure or hemodialysis.
The differential diagnosis of an acute neurologic change begins with acute stroke and also includes seizure, migraine, toxic and metabolic causes (eg, hyper- or hypoglycemia), infection, tumor, and migraine. Acute ischemic stroke may be from ischemic causes including venous, arterial, or hemorrhagic. Individuals with end-stage renal disease (ESRD) are more prone to hemorrhagic stroke because of the increased risk of bleeding from frequent use of heparin for dialysis and impaired platelet function from uremia.15
Diagnosis is made with head and brain CT and is indicated by hyperlucency that appears the same on both brain and bone windows (see Figure). Accurate diagnosis is essential because treatment of air emboli is time dependent as described in the case and following section.
Treatment
Treatment of air emboli is 100% oxygen followed by immediate transfer to a facility with HBOT.3,16 There are no guidelines for using HBOT in people who have cerebral air embolic strokes, although several case reports and case series suggest HBOT is associated with better outcomes. Administration of 100% oxygen reduces nitrogen content of air bubbles to, in turn, reduce or compress the size of the bubbles.4,5,17 HBOT improves oxygenation to the cerebral tissue and reduces cerebral edema and thus, intracranial pressure.5 If no hyperbaric chamber is available, it is recommended to transport the patient to a facility with HBOT. Treatment should begin within 6 hours.3 Resolution of neurologic damage from air embolus is highly associated with initiating HBOT as early as possible.18 Full neurologic recovery has been seen when HBOT was initiated with 3 to 5 hours of the inciting incident, whereas after a delay of 9 to 20 hours, only 1 of the 8 individuals had full neurologic recovery.18 In another case series, 75% of individuals treated within 5 hours had little to no disability at 6-month follow-up.19
Prevention
Intraoperative maneuvers such as lowering the head during a procedure may reduce the risk of venous air emboli because of the lower specific gravity of air vs blood, making it less likely that an embolism will rise to the cerebral vasculature. In some surgical procedures, pericardial Doppler may be used to detect VAE; however, proper placement of the probes and close attention to the event by an anesthesiologist can be challenging.20,21 Air emboli often lead to hemodynamic instability because of the resulting strain on the cardiopulmonary systems that may result in hypoxia, hypercapnia, and even a decrease in cardiac output.5
Summary
Cerebral air embolism can occur during a routine hemodialysis procedure through an arteriovenous graft and is an emergency. Hemodialysis should be immediately stopped. Once stabilized, the patient should be transferred urgently to a facility with HBOT available. HBOT should be started within 6 hours. In the case presented, the individual with cerebral air embolism had HBOT for 6 hours, which reduced his NIHSS score from 14 to 6 with subsequent resolution of all symptoms except residual left arm weakness.
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