Asystole during percutaneous ethanol injection of symptomatic vertebral haemangioma.
Computed tomography guided percutaneous ethanol injection is frequently employed for treatment of symptomatic vertebral haemangiomas. The procedure is performed under monitored anaesthesia care in the prone position. It has several advantages over open surgery and other therapeutic modalities and is generally considered safe. There is no previous report of any significant haemodynamic disturbance attributable to alcohol ablation of vertebral haemangiomas. We report a case in which a patient of ASA physical status I developed asystole following injection of 100% alcohol into a vertebral haemangioma, and became apnoeic and unresponsive. He recovered following intravenous administration of atropine. All staff involved in this procedure should be aware of, and prepared for, this rare but potentially life-threatening complication.
Key Words: asystole, ethanol, percutaneous injection, vertebral haemangioma
Vertebral haemangiomas are congenital vascular malformations affecting almost 10% of the general population (1). They are most common in the thoracic spine and least common in the cervical spine. The majority of these lesions remain asymptomatic. Less than 1% become symptomatic, presenting with back pain or features of neural compression (1,2). Therapeutic options for symptomatic vertebral haemangiomas (SVH) include surgery, radiotherapy, arterial embolization, injection of methyhnethacrylate and/ or N-butyl cyanoacrylate into haemangiomatous vertebra, and percutaneous ethanol injection (PEI).
The technique of percutaneous alcohol ablation for treatment of symptomatic vertebral haemangiomas was first described by Heiss and colleagues (3), and later propounded by many others (4-8). Computed tomography (CT) guided instillation of 95-100% ethanol leads to intralesional thrombosis and destruction of the vascular endothelium of the haemangioma. It rapidly obliterates and shrinks the malformation, which is a critical requirement in the presence of progressive cord compression (3). The procedure is usually performed under monitored anaesthesia care (MAC) and immediate complications are rare; although pain is common following ethanol injection (3-8). We report a case of asystole during CT guided percutaneous ethanol injection under MAC, which was managed successfully.
A 32-year-old, 68 kg male of ASA physical status I presented with progressive weakness of both lower limbs. He was diagnosed as having a haemangioma of the eleventh dorsal vertebra and scheduled for CT guided percutaneous injection of absolute alcohol under MAC. He received no premedication and was allowed a light breakfast on the morning of planned intervention. In the neuroradiology suite he was monitored with 5-lead electrocardiography, non-invasive blood pressure (BP) and pulse oximetry. His baseline heart rate was 70 bpm, BP 130/80 mmHg and Sp[O.sub.2] 99%. After intravenous access was secured, the patient was positioned prone and vital parameters were recorded again. Fentanyl 150 [micro]g was administered intravenously to provide analgesia against the pain of alcohol injection and oxygen was administered by nasal prongs. CT scan was then performed in the prone position. With all aseptic precautions, after skin infiltration with lignocaine 2%, the interventional neuroradiologist inserted a 22G lumbar puncture needle to access the haemangiomatous cavity through the pedicle. When the needle was satisfactorily positioned, 8 ml of diluted non-ionic iodinated contrast (iohexol 300) was injected slowly, while CT was performed in the dynamic mode to enable visualization of the opacified soft-tissue component, and to exclude extravasation of contrast agent into the retroperitoneal/pleural space, paraspinal muscles, or into a vascular channel. After a satisfactory test injection, absolute alcohol was injected. Following injection of 10 ml absolute alcohol (100% ethanol), the heart rate decreased from 72 to 48 bpm, followed rapidly by disappearance of ECG and pulse oximetry waveforms. The patient became apnoeic and unresponsive, and peripheral pulses were not palpable. Atropine 0.6 mg was injected intravenously immediately and the interventional neuroradiologist was informed, who removed the needle and the patient was turned supine. Soon the heart rate was 120 bpm and BP 140/90 mmHg, and the patient regained consciousness. Oxygen was administered by facemask, 500 ml of dextrose normal saline was given rapidly and the patient was closely monitored for the next thirty minutes during which he remained haemodynamically stable. A 12-lead ECG showed normal sinus rhythm. It was then decided to continue with the procedure and the further course was uneventful. He was monitored in the intensive care unit for the next 24 hours, where a cardiological evaluation was performed and was unremarkable.
Although the blood ethanol level was not measured in our patient, in view of the temporal relationship between the ethanol injection and asystole, the most likely cause of asystole in this patient appears to be a direct depressant effect of ethanol on the sinus node. Since the patient had received adequate analgesia and did not complain of pain, the possibility of vasovagal reflex owing to pain from the needle or ethanol injection seems unlikely. Though the mechanism of rhythm disturbances following ethanol injection remains obscure, a cardiorespiratory reflex comprising bradycardia, hypotension and temporary apnoea has been described following other intravenous ethanol injections, which is caused by vagal stimulation in the right atrium and which can be inhibited by atropine (9). Although there is no previous report of significant haemodynamic disturbance following PEI for SVH, Ferlitsch and colleagues (10) have reported sinoatrial and atrio-ventricular block in 42% of patients following PEI for hepatocellular carcinoma and attributed the development of heart blocks to vasovagal reactions and the direct effect of ethanol on the sinus node or the right atrial conduction system. In their series, unconsciousness and seizure-like symptoms were seen in two of eleven patients who developed heart block following PEI, one of whom suffered respiratory arrest requiring mechanical ventilation. They observed that the development of heart block appeared to be more common in patients with slower heart rates at rest and with larger amounts of instilled alcohol (10). Another mechanism of circulatory depression with alcohol injection is acute increase in pulmonary vascular resistance causing right ventricular dysfunction, which can precipitate cor pulmonale in susceptible individuals (11,12). Tsutsui and colleagues have described alcohol ingestion-induced sinus bradycardia and hypotension in two patients with carotid sinus hypersensitivity, suggesting a paradoxical increase in parasympathetic activity and/or decrease in sympathetic activity (13). It is possible that such patients might be more prone to develop serious complications after alcohol injection as well.
There is considerable difference of opinion amongst interventional radiologists regarding the technique of alcohol injection into a haemangioma. While some prefer to inject alcohol in increments of 2 ml every 10 to 15 minutes (3), others inject 10 to 15 ml continuously at a rate subjectively decided by the rate of opacification and clearing of contrast material from the epidural soft tissue, as seen on CT images taken in dynamic mode during the test injection (5). Interventional neuroradiologists at our institution use the latter technique because in their experience, continuous injection leads to better distribution of alcohol in the haemangiomatous cavity, with less chance of obliteration of the haemangioma in the immediate vicinity of the needle tip. It is possible that during a continuous injection, moderate to large amounts of alcohol can inadvertently escape into the systemic circulation, leading to systemic complications. This might have been the cause of asystole in our case.
Although the recent American Heart Association guidelines support the use of atropine for treatment of asystole (14), Ferlitsch and colleagues (10) observed that patients recovered spontaneously from alcohol induced sinus arrest after stopping the ethanol injection, without any pharmacological intervention. For management of asystole, restoration of venous return is imperative. Since the prone position may be associated with decrease in venous return due to inferior vena caval compression or decreased left ventricular compliance due to increased intrathoracic pressure, it is mandatory to turn the patient supine for resuscitation.
Our patient recovered from asystole after injection of atropine and turning supine. He was closely monitored for half an hour after the episode. There was no sign of further deterioration in his clinical status (neurological or otherwise) and he remained haemodynamically stable. As he had already received 10 ml of alcohol, it was decided to continue with the treatment but limit his second injection to 5 ml. The second injection was performed in two increments with a gap of five minutes between them, and the procedure was uneventful. We speculate that the slower speed of injection and prior administration of atropine contributed to the procedure being uncomplicated on the second occasion.
This case demonstrates that anaesthetists providing monitored anaesthesia care during percutaneous ethanol injection for treatment of symptomatic vertebral haemangiomas should be aware of and prepared for the rare but potentially life-threatening complication of asystole associated with the alcohol injection. Patients with carotid sinus hypersensitivity and lower resting heart rates might be more susceptible. The amount and rate of injection of alcohol should be carefully considered. Prophylactic administration of atropine might be useful. Adequate analgesia should be provided, although the association between opioids and bradycardia should also be recognized. Appropriate resuscitation facilities and the ability to turn the patient supine rapidly must be readily available.
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D. SHARMA *, V. JAIN *, G. P. RATH [dagger]
Department of Neuroanaesthesiology, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi, India
* M.D., Senior Resident.
[dagger] M.D., D.M., Assistant Professor.
Address for reprints: Dr G.P. Rath, Assistant Professor, Department of Neuroanaesthesiology, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi, 110029, India.
Accepted for publication on July 11, 2006.
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|Title Annotation:||Case Report|
|Author:||Sharma, D.; Jain, V.; Rath, G.P.|
|Publication:||Anaesthesia and Intensive Care|
|Date:||Oct 1, 2006|
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