Abstract
Catheter ablation for atrial fibrillation is associated with a low rate of complications, with few reports of intracranial hemorrhage in the literature. Additionally, subarachnoid hemorrhage with spinal hematoma is also an uncommon pathology with less than 200 total cases to date described. A 78-year-old female with hypertension and atrial fibrillation on warfarin presented for catheter cryoablation and experienced periprocedural hypertension. Subsequently, post-procedure, the patient developed severe back pain, nausea, vomiting, altered consciousness, and paraplegia. Imaging demonstrated subarachnoid hemorrhage with hematoma compressing cord at the T4/5 level and infarction inferior to this level. The rare nature as well as presentation of this pathology, in the setting of a safe procedure, emphasizes the importance to re-evaluate diagnostic plans when patient presentation is inconsistent with expected post procedural course.
〈Learning objective: The rare nature as well as presentation of subarachnoid hemorrhage with spinal hematoma, in the setting of a safe catheter cryoablation for atrial fibrillation, emphasizes the importance to re-evaluate diagnostic plans when patient presentation is inconsistent with expected post procedural course.〉
Keywords: Catheter ablation, Atrial fibrillation, Subarachnoid hemorrhage, Spinal hematoma, Intracranial hemorrhage
Introduction
Below is a presentation of a subarachnoid hemorrhage leading to cord compression which presented post catheter cryoablation for atrial fibrillation. On review of the literature, it appears that this is the first descriptive case report of subarachnoid hemorrhage associated with this procedure. Additionally, it appears to be the first report of a spinal subarachnoid hematoma associated with a procedure not involving spinal anesthesia.
Case report
A 78-year-old female with a history of persistent atrial fibrillation, well-controlled hypertension, and New York Heart Association class II heart failure with preserved ejection fraction, presented 1 month previously to the emergency department for symptomatic atrial fibrillation with rapid ventricular response. At this time the patient received pharmacological treatment and spontaneously converted to sinus rhythm. She was subsequently referred for catheter ablation to our academic medical center.
The patient's surgical history was significant for distant appendectomy, hysterectomy, and tonsillectomy. Family history was non-contributory and social history was negative for tobacco, alcohol, and drug use. Medications included warfarin, losartan, metoprolol succinate, and atorvastatin. The patient was allergic to aspirin.
Five days prior to catheter cryoablation, the patient was seen in the clinic with vital signs: heart rate 55 bpm, blood pressure (BP) 112/77 mmHg, weight 65.1 kg, and body mass index 27.1 kg/m2. Complete blood count showed hemoglobin/hematocrit of 11.8 g/dL/35.1% with platelets of 171 k/μL. Basic metabolic panel was notable for potassium 4.8 mequiv./L, and creatinine 0.8 mg/dL. Thyroid stimulating hormone was 1.4 μU/mL, hemoglobin A1C 5.6%, and urine microalbumin <7 mg. Lipid profile showed total cholesterol 113 mg/dL, triglycerides 50 mg/dL, low-density lipoprotein 70 mg/dL, and high-density lipoprotein 45 mg/dL. International normalized ratio (INR) at this time was therapeutic at 2.4.
A previous transthoracic echocardiogram was significant for diastolic dysfunction with ejection fraction of 66%, and mild left atrial dilation.
On the day of cryoablation, the patient had INR 1.79, was non-hypertensive, non-tachycardic, in sinus rhythm with normal neurological examination. The patient was managed under monitored anesthesia care while the procedure was completed via a right femoral vein approach. Prior to transeptal puncture, the patient received a 11,800 unit bolus of heparin followed by infusion of 2065 units per hour. Activated clotting times (ACT) throughout the procedure were 307 s, 312 s, and 329 s, respectively.
Eight minutes after anticoagulation, the patient had a brief hypertensive episode with BP 166/74 mmHg which spontaneously resolved without treatment. At 36 min after anticoagulation another hypertensive episode occurred, which lasted for 29 min with peak blood pressure of 208/93 mmHg. Again, this episode resolved without treatment. At 98 min after initial anticoagulation a 50 mg bolus of protamine was administered with post ACT of 142 s. The patient remained with stable vital signs for the remainder of the procedure and was transferred to the post anesthesia care unit (PACU).
In the PACU, the patient experienced hypertensive emergency with systolic blood pressures peaking over 230 mmHg. The patient complained of severe back pain and headache. Intensive measures were taken to reduce blood pressure, including arterial line placement, nicardipine infusion, and intensive care unit admission. A timeline of operative events can be seen in Fig. 1.
Fig. 1.
Blood pressure and heart rate trends – intraoperative events.
Five hours post procedure, the patient had variable burning sensations on the left side of the body as well as nausea which was treated with morphine and ondansetron. Thirteen hours post-ablation, the patient was somnolent, with decreased lower extremity strength and no rectal tone. Urgent magnetic resonance imaging of the head and spine was completed and was significant for hydrocephalus, diffuse cerebral subarachnoid hemorrhage, as seen in Fig. 2, extending into cervical and thoracic thecal sac, and 6-mm associated mass effect at T4/5 with associated spinal cord infarction inferior to this level, as seen in Fig. 3. Additionally, grade 1 anterolisthesis was noted at the C7 level. It is unclear if bleeding first occurred in the brain or at the spine.
Fig. 2.
Magnetic resonance imaging brain flair – arrows indicate areas of subarachnoid hemorrhage.
Fig. 3.
Magnetic resonance imaging spine T2 – arrow indicates spinal hematoma at T4/5.
Subsequent cerebral and spinal angiography at 2 and 4 days post ablation demonstrated a 2.08 mm × 1.24 mm saccular aneurysm without dissection at the right posterior communicating artery, and no obvious abnormalities in spinal arteries. No neurosurgical intervention was attempted to decompress the cord because of evidence of infarction on initial imaging. The patient had an external ventricular drain placed for management of hydrocephalus in the setting of subarachnoid bleed. On hospital day 16, the patient was discharged with complete sensory and motor deficits below T4, to rehabilitation, on clopidogrel, without anticoagulation.
At outpatient follow-up a month after discharge, the patient was found to be in atrial fibrillation which was treated with amiodarone 200 mg daily.
Review of literature/discussion
Complications associated with catheter ablation for atrial fibrillation have been well described in the literature, and estimated at 2.9%. These events mainly have included vascular complications, cardiac tamponade/effusion, and ischemic neurological complications. The incidence of neurological complications overall was low at 0.4% [1]. Limited reports of catheter ablation-associated intracranial hemorrhage can be found in the literature, with reviews of tens of thousands of patients, at most identifying a few patients with this pathology [2]. When identified, bleeds were intraparenchymal with poor outcomes [3].
Although long-term anticoagulation has been associated with central nervous system bleeding, population-based studies of anticoagulated patients suggest a 0.4% per year incidence [4]. Because of the rarity of this pathology associated with catheter ablations, studies have demonstrated that patients with previous intracranial hemorrhages can be safely anticoagulated in the periprocedural and postprocedural period [5].
Furthermore, it is estimated that the incidence of subarachnoid hemorrhage in the general population is 1 per 10,000 [6]. In samples of patients anticoagulated with apixaban or warfarin, these rates increase to 4.6 per 10,000 [7]. With consideration of the very low observed incidence of subarachnoid bleeds and the very low central nervous system complication rate of catheter ablations for atrial fibrillation, it was not surprising that on extensive review of the literature, no reports of subarachnoid hemorrhage in association with catheter ablation could be found.
Studies observing risk factors for intracranial bleeding in temporal relation to this procedure have come to conflicting results. Some suggest a relationship to thrombolytic therapy and aspirin use, while others argue no association with intensity of anticoagulation or INR values [2], [3], [7].
Within the population of patients with subarachnoid hemorrhages, those with associated spinal hematomas are extremely uncommon.
Case series of subarachnoid hemorrhages with spinal hematomas have been published with a total number of less than 200 patients. These series found anticoagulation to be a major risk factor, especially in the setting of spinal anesthesia. Other etiologies included vascular malformations, tumors, autoimmune conditions and trauma. Interestingly, a large number of cases were without an identifiable cause [8], [9].
The pathology behind the development of these hematomas has not been elucidated in the literature. Hypertension was considered a cofactor in disease pathology, as the prevalence in case series was the same as the general population. Additionally, it was speculated that spondylothesis was a risk factor, impairing the flow of cerebrospinal fluid, leading to hematoma formation [8].
Clinical presentation for hematoma related to subarachnoid bleeds was variable as described in the literature. Common features were divided into two main categories, meningeal/cerebral features and back/radicular features. Severe back pain in a radicular distribution initially presented without motor or sensory deficits. Meningeal signs included headache, nausea, vomiting, and nuchal rigidity. Additionally, features of increased intracranial pressure, such as altered level of consciousness were also possible if extension into the cerebral space occurred [8], [9].
Treatment for this pathology has been suggested to be primarily surgical, with a large number of patients experiencing full recovery with surgical intervention. Rapid onset of symptoms, and mild deficits at presentation were associated with better outcomes. Mortality in non-operative patients was high and patients with severe deficits at presentation were unlikely to experience improvement with surgical intervention [9].
The case of the 78-year-old above was notable for the features described in the literature for this rare pathology: severe back pain, headache, nausea, lateralized radicular/burning pain, and altered consciousness. Additionally, risk factors such as anticoagulation, intraoperative hypertension, and spondylothesis may have contributed to subarachnoid bleed with spinal cord compression. Treatment was appropriate and aligned with literature based on neurological deficits. This case with rare pathology was unique in that it occurred in temporal relationship to an electrophysiology procedure where intracranial bleeding is uncommon.
Conclusion
Diagnostic reasoning is the cornerstone to medical decision-making. The process of evaluating a patient's condition, integrating information into an expected disease or procedure course, and adapting a diagnostic and treatment plan, is as much of an art, as it is a science [10]. The presented case above, a rare pathology in the setting of a safe procedure, underscores the importance of identifying an unexpected patient trajectory and the need to rapidly expand a diagnostic plan to capture an underlying disease process.
Additionally, in the setting of anticoagulation and hypertension, both conditions common in patients with atrial fibrillation undergoing catheter ablation, it is important to consider the rare possibility of central nervous system hemorrhage. The case presented demonstrates an example of this rare complication. With knowledge that such an event is possible, future clinicians can be alert and respond appropriately to allow for timely intervention and quality patient care.
Conflict of interest
The authors declare no conflict of interest.
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