Complications of Regional Blocks

Spinal epidural hematoma after regional block

Signs and symptoms of spinal epidural hematoma after regional block include the following:

• Progressive loss of sensation and weakness in the lower extremities bilaterally
• Loss of bowel and bladder function
• Severe back pain (often not the presenting symptom)

Management of suspected spinal epidural hematoma includes the following:

• Emergency magnetic resonance imaging (MRI) of the spine for diagnosis
• If MRI is positive for epidural hematoma, notify neurosurgery immediately
• Definitive treatment consists of surgical decompression of the spine and evacuation of the hematoma

Measures for prevention of spinal epidural hematoma include the following:

• Proceed with caution in patients with known coagulation disorders, performing a careful risk-benefit analysis
• Follow the guidelines developed by the American Society of Regional Anesthesia (ASRA) for regional anesthesia in patients receiving antithrombotic or thrombolytic therapy ^[1]

Local anesthetic systemic toxicity after regional block

Signs and symptoms of local anesthetic systemic toxicity (LAST) after regional block include the following:

• Early neurologic symptoms - Tinnitus, oral numbness, metallic taste, lightheadedness
• Late neurologic symptoms - Seizures, respiratory arrest, coma
• Cardiac manifestations - Arrhythmias, cardiac arrest

Management of LAST includes the following:

• Airway management
• Treatment of seizures with benzodiazepines
• If cardiac arrest occurs - Modified advanced cardiac life support (ACLS) protocol (lower doses of epinephrine, < 1 μg/kg); avoidance of vasopressin, calcium-channel blockers, beta blockers, and local anesthetics
• Lipid emulsion (20%) therapy (patient < 70 kg) - Administer bolus of 1.5 mL/kg over 2-3 minutes; then infuse at 0.25 mL/kg/min (continue for 10 minutes after return of cardiovascular stability); repeat bolus if cardiovascular collapse persists; double the infusion rate
• Lipid emulsion (20%) therapy (patient >70 kg) - Give bolus of 100 mL over 2-3 minutes; then infuse 250 mL over 15-20 minutes; repeat bolus if cardiovascular collapse persists; infuse 500 mL over 15-20 minutes; upper limit for total dose is ~10 mL/kg over 30 minutes
• Report LAST events to www.lipidrescue.org and www.lipidregistry.org

Measures for prevention of LAST include the following:

• Use the lowest effective dose of local anesthetic possible
• Recognize factors that may increase the risk of LAST (eg, medical conditions and medications)
• Use a pharmacologic marker to show immediate signs of intravascular injection
• Aspirate before each injection of local anesthetic
• Inject local anesthetic incrementally, and watch for signs of toxicity in between injections

Hematoma can occur as a consequence of trauma to the epidural venous plexus during placement of a needle or catheter. Because the vertebral canal is a fixed space, the hematoma can compress the spinal cord and nerve roots and potentially cause permanent neurologic damage.

Spinal epidural hematoma after neuraxial anesthesia is exceedingly rare. A nationwide data analysis from 2016 reviewed more than 3.7 million instances of epidural analgesia over a period of 12 years and found the rate of spinal hematoma to be 0.6 per 100,000 in obstetric patients and 18.5 per 100,000 in nonobstetric patients. ^[2]

Although parturients, a cohort of patients that often receives neuraxial anesthesia, are generally in a hypercoagulable state, certain conditions of pregnancy (eg, gestational thrombocytopenia, HELLP [hemolysis, elevated liver enzymes, low platelets] syndrome, and complications of preeclampsia) can increase the incidence of epidural hematoma. ^[3] The incidence is also increased in patients who are taking anticoagulants, those who have coagulation disorders, and those who require multiple attempts for epidural placement. ^[4]

In a large meta-analysis of patients with spinal epidural hematomas from 1826 through 1996, idiopathic hematomas constituted the largest single group; those caused by anticoagulation were the next largest. ^[3] Factors that increased the risk included the following:

• Increased age
• Female sex
• History of gastrointestinal (GI) bleeding

The initial presentation of a spinal epidural hematoma often consists of progressive weakness and paresthesias of the lower extremities bilaterally, followed by loss of bowel and bladder function. Pain is not usually the initial symptom, but when it occurs, it tends to be sudden and very severe and is commonly aggravated by direct pressure on the spine.

In a meta-analysis of 613 patients with spinal hematomas, 65% had motor blockade, 8% had bowel or bladder dysfunction, and 27% had other symptoms (most often back or leg pain). ^[5] Associated neurologic symptoms (eg, weakness and numbness) may be difficult to elicit if the patient concurrently has a neuraxial blockade from spinal or epidural anesthesia. ^{[4, 6]}

Addressing the problem

If an epidural hematoma is strongly suspected, the diagnostic test of choice is MRI. If MRI is unavailable or contraindicated, computed tomography (CT) or CT myelography may be performed. ^[7] Other potential causes of neurologic symptoms include abscess, tumor, and vertebral fracture. If imaging confirms the presence of a hematoma, the patient should be evaluated by neurosurgery immediately.

If the patient's symptoms are improving or have resolved, conservative measures (close observation) may be considered. ^[8]  Otherwise, definitive treatment consists of surgical decompression of the spinal canal and evacuation of the hematoma to reduce the likelihood of permanent neurologic damage. ^[6]  For the best chance of neurologic recovery, such treatment should be carried out within 12 hours of the onset of symptoms. ^{[8, 7]}

In a review of 333 cases of spinal epidural hematoma, 44% had partial resolution of neurologic symptoms after surgical decompression, 34% had total neurologic recovery, and 15% had no improvement. ^[9]  The factors that appeared to have the most influence on the chance of recovery were as follows:

• Site of the hematoma
• Preoperative level of neurologic function
• Time between the onset of symptoms and surgical treatment

Generally, when patients with neurologic dysfunction are managed conservatively, there is little chance that symptoms will resolve. In a small study of eight patients with acute spontaneous spinal epidural hematomas, those with no neurologic symptoms at all had the best outcomes with conservative management. ^[10]

If a surgical option is not available or the patient refuses open surgical intervention, alternative approaches may be considered. Fujii et al reported two cases in which percutaneous drainage under fluoroscopy led to successful evacuation of spinal hematoma and complete recovery of neurologic function. ^[11]  

Evidence-based recommendations

It is essential to determine which patients are at risk for epidural hematoma. This determination requires a complete understanding of the patient's medical history, a full knowledge of the medications he or she is taking, and a careful risk-benefit analysis of whether regional or another type of anesthesia is the best option.

No current recommendations exist on the performance of regional anesthesia in patients with coagulation disorders. Because the incidence of spinal epidural hematoma in this setting is so low, it is very difficult to create guidelines on the basis of actual data. Instead, recommendations are based on case reports, expert opinion, and pharmacologic properties.

Guidelines formulated by the Association of Anaesthetists of Great Britain and Ireland, the Obstetric Anaesthetists' Association, and Regional Anaesthesia UK address special circumstances that can affect coagulation in patients (see Table 1 below). ^[12]  ASRA does not address specific coagulation disorders in its guidelines. Anesthetic management of coagulation disorders often involves replacement of deficient factors of each individual condition, usually in collaboration with a hematologist's recommendations. ^[13]

Table 1. Summary of Risks of Regional Anesthesia in Patients With Abnormalities of Coagulation in Special Circumstances ^[12] (Open Table in a new window)

There is no specific minimum platelet count that has been found to be acceptable for performing neuraxial anesthesia. Many practitioners consider 100,000/μL to be the minimum level. Monitoring trends in platelet count may be useful, especially for conditions such as HELLP or thrombocytopenia. Again, it is essential to review the clinical picture and do a risk-benefit analysis to optimize patient care. ^[3]

Acquired coagulation disorders from specific medications are becoming more common. As rare as bleeding complications from neuraxial anesthesia are, as many as 30% can occur as a result of anticoagulation. The incidence of spinal epidural hematomas increased significantly after the introduction of low-molecular-weight heparin (LMWH) to the United States in 1993, causing the US Food and Drug Administration (FDA) to issue a warning in 1998 about the performance of neuraxial anesthesia while LMWHs are being used. ^[14]

In 1998, ASRA created a set of guidelines for neuraxial anesthesia on patients taking anticoagulants, which have since been revised three times as the use of anticoagulants has become more prevalent. The third edition was published in 2010; the current (fourth) edition of the official recommendations was published in 2018 (see Table 2 below). ^[1]

Table 2. Summary of ASRA Recommendations for Regional Anesthesia in Patients Receiving Antithrombotic or Thrombolytic Therapy* (Open Table in a new window)

In summary, a careful risk-benefit analysis should be performed on any patient with acquired or inherent coagulation disorder who may receive neuraxial anesthesia in order to reduce the risk of spinal epidural hematoma. Once a spinal epidural hematoma is suspected, MRI should be performed as soon as possible. If the diagnosis of spinal epidural hematoma is confirmed, surgical decompression should occur urgently.

Clinical scenario

A 32-year-old G3P2 female at 39 weeks' gestation with no significant past medical history receives epidural analgesia for labor. She delivers a healthy neonate and is transferred to the postpartum unit. The epidural catheter remains in place; the plan is to use it for anesthetic management during the scheduled postpartum tubal ligation the following day. The case proceeds uneventfully, and the epidural catheter is removed at the end of the case. The patient and her newborn are discharged home in the afternoon.

Later that evening, the patient returns to the emergency department (ED) after having fallen at home. She reports that her legs "gave out" when she was getting up from a nap to feed the baby. Examination reveals that she has 3/5 strength in her right lower extremity and 2/5 strength in her left on manual muscle testing (MMT). In her upper extremities, she has 5/5 strength bilaterally. She is sent for immediate MRI of the spine. On the way to the MRI suite, she starts to complain of severe low back pain. MRI identifies an epidural hematoma in the lumbar region.

Resolution

When the MRI results were received, neurosurgery was immediately called to evaluate the patient. She continued to have symptoms, and the lower back pain was worsening. She was brought to the operating room (OR) for emergency surgical decompression of her lumbar spine. She was extubated at the end of an uneventful case.

The patient was still sedated in the postanesthesia care unit (PACU) and was unable to move her legs when she arrived in the PACU. After a couple of hours, however, she started to regain strength in her lower extremities. She was sent to the neurosurgical intensive care unit (ICU).

The patient remained in the hospital for another 4 days, with daily physical and occupational therapy, and was ambulating with human assistance upon discharge. She was discharged home with home physical and occupational therapy. She was seen for follow-up 3 weeks later, by which time she had regained complete motor function in her lower extremities.

Clinical scenario

A 76-year-old male patient with a past medical history of atrial fibrillation, hypertension, stage IV lung cancer, and diabetes mellitus has been in a high-velocity motor vehicle accident, in which he sustains multiple right-rib fractures and a fractured distal femur. A thoracic epidural catheter is placed to ameliorate the difficulty in breathing that he is experiencing as a result of the rib fractures. His respiration improves with adequate epidural analgesia.

A few hours later, the patient becomes hemodynamically unstable, and CT reveals a suspected liver laceration and hematoma. He is sent to the OR for an emergency exploratory laparotomy. Intraoperatively, he receives eight units of packed red blood cells and two units of fresh frozen plasma (FFP). He returns to the surgical ICU (SICU) intubated but is extubated the next day.

A repeat CT scan to evaluate for perihepatic hematoma is negative, but a small epidural hematoma is noted in the midthoracic region. Emergency MRI confirms the presence of an epidural hematoma. The patient is immediately evaluated at the bedside. He is able to move all four extremities without difficulty. He does not complain of any back pain. 

Resolution

The neurosurgeon consulted with the patient and his family and discussed the option of urgent surgical decompression of the spine. However, because the patient had no neurologic symptoms, conservative management was also considered. In view of the other acute injuries the patient had sustained and his terminal cancer diagnosis, he and his wife opted for conservative management.

The patient's INR was elevated, and his platelet count was below 100,000/μL. He was given additional FFP and platelets to prevent expansion of the hematoma. He remained in the SICU and underwent neurologic evaluation every 4 hours.

Repeat MRI 3 days later showed that the epidural hematoma had decreased in size. The patient continued to demonstrate complete neurologic recovery. The epidural catheter was removed 5 days after placement, when his coagulopathy had resolved. He was discharged to a skilled nursing facility for rehabilitation.

LAST is a rare but well-known complication of local anesthetic use. It was first observed in the 1880s, when the use of cocaine for clinical purposes was found to cause seizures and respiratory depression. Most of what is understood about LAST comes from animal models; the severity of the known complications makes it unethical to perform randomized clinical trials on human subjects. On the basis of data from these animal models, it appears that local anesthetics inhibit cardiac conduction by binding to and inhibiting sodium channels. ^[15]

The likelihood of cardiac and neurologic toxicity is dependent on the potency of the individual local anesthetic. Clarkson et al compared the effects of lidocaine and bupivacaine on cardiac conduction in guinea pigs and found that the two agents differed with respect to action potential duration, frequency of impulses, and possibly, affinity for the sodium channel. ^[16] These findings led them to suggest that differences in activity on the receptor caused bupivacaine to be more cardiotoxic than lidocaine.

At higher doses, local anesthetics can also bind to other ion channels, enzymes, and drug receptors. ^[17]  Despite differences in the likelihood of causing LAST, all local anesthetics have the potential to cause it. Local anesthetics can also inhibit oxidative phosphorylation, which may explain why LAST predominantly affects organs with the highest oxygen demand. ^[15]

In the 1920s, after it had become clear that LAST can be fatal, the American Medical Association (AMA) created the Committee for the Study of Toxic Effects of Local Anesthetics, emphasizing the need to establish and maintain an airway in these situations.

Although bupivacaine had been linked with fetal demise after paracervical block in the 1960s, it was not associated with fatal cardiac events in adults until the 1970s. The bupivacaine enantiomers ropivacaine and levobupivacaine were introduced in the late 1980s as agents with reduced cardiotoxicity; however, mortality from local anesthetic toxicity continued to occur with these agents.

In the mid-2000s, lipid emulsions were found in a few case reports to reverse cardiac toxicity from LAST. ^[15]

Addressing the problem

It is essential to recognize the signs and symptoms of LAST immediately. Patients who are at risk include anyone who has received a local anesthetic intraspinally, perineurally, subcutaneously, or topically. Even those who have received very low doses of local anesthetic are at risk; errors in the administration of the dose may have occurred, and patients may actually have received a much higher dose than was ordered. Other patient factors can affect the incidence of central nervous system (CNS) toxicity from local anesthetics, including decreased protein binding and clearance, acidosis, and hypercapnia. 

The initial symptoms of LAST are usually neurologic. ^[17]  Local anesthetics cross the blood-brain barrier with ease. CNS symptoms are dose-dependent. At lower plasma concentrations, patients may experience tinnitus, circumoral numbness, metallic taste, or lightheadedness; at higher concentrations, they may experience seizures, loss of consciousness, or respiratory arrest. Unfortunately, if the patient is sedated or under general anesthesia, these symptoms may be very difficult to recognize; often, seizure or cardiac toxicity is the presenting symptom. ^{[15, 18]}  (See Table 3 below.)

Table 3. Summary of Recommendations for Diagnosing LAST ^[15] (Open Table in a new window)

CNS toxicity is exceedingly rare. Surveys from France and the United States that included more than 280,000 cases found the incidence of seizures to be 1/10,000 with epidural analgesia and 7/10,000 with peripheral nerve blockade. ^[18]  However, an analysis of the American Society of Anesthesiologists (ASA) Closed Claims Database found that one third of cases of brain damage or death associated with regional anesthesia were related to LAST. ^[19]

Cardiac toxicity usually occurs at higher plasma concentrations. As mentioned previously, elevated levels of local anesthetic delay cardiac conduction by blocking sodium channels. This causes prolongation of the PR interval and QRS complex, ^[20] leading to severe cardiac dysrhythmias and potential cardiac arrest. Although CNS symptoms may be recognized first, sometimes the first noted sign is cardiac arrest, especially if the patient is receiving general anesthesia and in cases of direct intravascular local anesthetic injection. ^[18]

Evidence-based recommendations

The most important step is to prevent the toxicity from occurring. According to the 2010 ASRA practice advisory on local anesthetic toxicity, ^[15] there is no single specific intervention that can eliminate the risk. (See Table 4 below.)

Table 4. Summary of ASRA Recommendations for Prevention of LAST ^[15] (Open Table in a new window)

One of the key factors is limiting the dose of local anesthetic, especially in those at the extremes of age (< 4 mo or >70 y) and those with known cardiac conduction problems. Weight-based dosing is not the best predictor of the amount of local anesthetic in the plasma; block location, epinephrine use, and the patient's medical history are better predictors. Unfortunately, there are no specific recommendations regarding how much to reduce the dose.

Theoretically, using ultrasound guidance to perform nerve blocks should reduce the incidence of inadvertent intravascular injection. However, there have been case reports of inadvertent intravascular injection even with ultrasound-guided nerve block placement. ^[15]

A retrospective review of 25,336 peripheral nerve blocks performed with a local anesthetic (80% under ultrasound guidance and 20% using only anatomic landmarks and nerve stimulation) found that 22 patients (0.87/1000) developed LAST, with 12 cases occurring in the ultrasound-guided group and 10 in the landmark/stimulator group. ^[21] The risk of LAST was reduced by 65% when ultrasound was used to guide peripheral nerve blocks.

The authors of the study suggested that their results may be due to the ability of ultrasonography to visualize vascular structures and the possibility that direct viewing of local anesthetic surrounding the nerve may result in the use of lower anesthetic doses. ^[21] Although the incidence of LAST was incredibly low in this study, it is the largest study to date that suggests a reduced frequency of LAST with ultrasound guidance. As yet, there have been no randomized clinical trials specifically investigating this subject.

Once LAST is suspected, it must be treated immediately. (See Table 5 below.) The most essential step is to ensure a patent airway and adequate oxygenation and ventilation.

Table 5. Summary of ASRA Recommendations for Treatment of LAST ^[15] (Open Table in a new window)

The ASRA has also developed a concise checklist to help guide treatment of LAST (see the image below). ^[22]

If seizures occur, treat appropriately with benzodiazepines. If seizures are refractory to benzodiazepines, consider giving small doses of succinylcholine or another neuromuscular blocker to prevent likelihood of acidosis and hypoxemia from repeated muscle contractions.

If LAST causes cardiac dysrhythmias, a specific pathway should be followed. Typically, ACLS guidelines are employed for any patient in cardiac arrest. Patients with cardiac arrest as a result of LAST do not respond as well to the ACLS algorithm as those with traditional cardiac arrest do. For this reason, it is essential that practitioners recognize LAST as the cause of the cardiac arrest.

Animal studies have shown that subjects treated with epinephrine, a standard drug for treatment of cardiac arrest per ACLS guidelines, fared worse than subjects treated with lipid emulsion, the standard treatment for LAST. Administration of vasopressin, which had been used in previous ACLS cardiac arrest algorithms, resulted in worse outcomes and led to pulmonary hemorrhage in animal studies. ^[15]

Lipid emulsion therapy consists of a 20% emulsion of triglycerides and phospholipids, ^[23] which "soaks up" the highly lipid-soluble local anesthetics, thereby preventing the molecules from interacting with the ion channels. Although lipid emulsion therapy was first studied as a treatment for cardiac arrest from LAST, case reports have suggested using it at the first sign of prolonged seizures, arrhythmia, or rapid progression of toxicity, on the grounds that it can prevent the progression to cardiac arrest.

Per current ASRA recommendations, 20% lipid emulsion is given as a bolus of 1.5 mL/kg, followed by infusion at 0.25 mL/kg/min, to be continued for 10 minutes after hemodynamic stability is achieved. If there is no clinical improvement, the bolus can be repeated and the infusion rate raised to 0.5 mL/kg/min, up to a maximum recommended total dose of 10 mL/kg over 30 minutes.

Although propofol is a lipid emulsion, it is only 10% lipid and therefore lacks sufficient lipid content to reverse the effects of a large quantity of local anesthetic. It can also cause cardiac depression, which is contraindicated in a patient on the verge of or in cardiac arrest. ^[15]

Clinical scenario

A 56-year-old 65-kg man with a past medical history of congestive heart failure (CHF) who has an ejection fraction (EF) of 35%, chronic kidney disease (CKD) stage 3, hypertension, and diabetes mellitus presents for open reduction and internal fixation (ORIF) of his right distal radius. A supraclavicular nerve block of the brachial plexus is performed in the preoperative holding area with 25 mL of 0.5% bupivacaine with no additives.

The patient is brought to the OR, and intravenous (IV) sedation is started with propofol at a rate of 50 μg/kg/min, preceded by bolus IV injection of midazolam 2 mg and propofol 30 mg. Shortly after the bolus injection of propofol, the patient reports feeling lightheaded. Blood pressure and heart rate are stable. The anesthesia resident reassures the patient that this is a normal sensation after receipt of anesthesia medications, and the patient promptly falls asleep.

While the surgeons are preparing the right arm for surgery, the anesthesia resident notes that the patient has had a few premature ventricular contractions (PVCs). The PVCs become more frequent, and as the surgeons are inflating the tourniquet, the resident observes a widening QRS complex and a shortened PR interval. The resident notifies the surgeons and calls the attending anesthesiologist to the room immediately. When the attending arrives, the patient is in asystole.

Resolution

ACLS protocol was initiated immediately. The surgical resident initiated chest compressions. The attending anesthesiologist, suspecting cardiac arrest due to LAST on the basis of the recent peripheral nerve block, called for the code cart and 20% lipid emulsion. Before the arrival of the lipid emulsion, 50 μg of epinephrine was given IV per modified ACLS protocol, and the patient was intubated by the anesthesia resident without difficulty and placed on the ventilator with a fraction of inspired oxygen (FiO₂) of 1.0.

When the lipid emulsion arrived, 100 mL was given as a bolus, followed by infusion at a rate of 16 mL/min. After 6 minutes of ACLS protocol, two pulse checks, and two more 50-μg doses of epinephrine, the patient remained in asystole. A second 100-mL bolus of lipid emulsion was given, and the infusion was continued. After 8 minutes of ACLS protocol, the patient had converted to sinus tachycardia with a weak carotid pulse and a blood pressure of 98/62 mm Hg. Chest compressions were halted.

The lipid emulsion infusion was continued for another 15 minutes. The patient's blood pressure remained stable, and he remained in sinus tachycardia, with a heart rate in the low 100s. The surgical procedure was canceled, and the patient was brought to the PACU intubated.

The patient began to respond by spontaneously ventilating appropriately and opening his eyes and following commands. His hemodynamics remained stable. He was extubated to 2 L by nasal cannula without difficulty. He had no recollection of the events and reported a sore throat and numbness in his right arm. He remained in the PACU for another 2 hours, with continued hemodynamic stability and occasional PVCs. He was sent to the SICU for close monitoring, with only a few PVCs reported overnight.

Two days later, the patient returned to the operating room for the ORIF of his right distal radius. He refused a peripheral nerve block, and general anesthesia was performed uneventfully. He was discharged home the following day.

Clinical scenario

A 22-year-old woman with a past medical history of poorly controlled asthma and morbid obesity (120 kg) presents for excision of a Bartholin cyst. Because of her asthma, the patient does not want to be intubated, and the surgeon offers to use local anesthetic at the site. The patient is brought to the OR, and a low-dose propofol infusion is started at a rate of 25 μg/kg/min, preceded by midazolam 2 mg and fentanyl 50 μg IV. The surgeon injects 20 mL of 0.5% bupivacaine. The excision is more difficult than expected, and additional bupivacaine is injected.

The case proceeds uneventfully and is completed 90 minutes later, with the patient awake upon transport to the PACU. Ten minutes later, the PACU nurse reports that the patient is complaining of dizziness. The anesthesiologist arrives at the bedside. The patient reports continued dizziness and a "funny" taste in her mouth. During the discussion, she becomes less responsive until she no longer responds to voice. At this point, she cannot be aroused, even by sternal rub.

Resolution

Airway assessment revealed that the patient was spontaneously ventilating, with a patent natural airway and an oxygen saturation of 100%. Hemodynamics were stable, and electrocardiography (ECG) showed normal sinus rhythm. A face mask with 10 L of oxygen was placed on the patient. Pupils were 2 mm wide.

The patient had received 250 μg of fentanyl in the OR and 0.5 mg of hydromorphone IV in the PACU. Concerned about possible narcotic overdose, the anesthesiologist administered naloxone 0.04 mg IV, with no response. The dose was repeated three times without effecting any change in arousal. The anesthesiologist then arranged to send the patient for a CT scan to rule out acute stroke.

The surgeon was notified and arrived at the bedside. The anesthesiologist asked how much local anesthetic had been given. The surgeon consulted with the surgical technician, who reported that a total of 52 mL of 0.5% bupivacaine had been given at the surgical site. The anesthesiologist, immediately suspecting LAST, administered a 180-mL bolus of 20% lipid emulsion and started infusion at a rate of 30 mL/min.

After a few minutes, the patient began to regain consciousness. Five minutes later, she was fully awake, alert, and appropriate. The CT scan was canceled. ECG continued to show sinus rhythm the entire time. The patient was admitted to a telemetry unit for monitoring overnight. No ECG changes were noted. The patient was discharged home the next day.