| | Prediction of the Effect of Injected Ethanol on Pulmonary Arterial Pressure during Sclerotherapy of Arteriovenous Malformations: Relationship with Dose of EthanolReceived 7 March 2008; received in revised form 3 October 2008; accepted 14 October 2008. published online 24 November 2008. PurposeTo prospectively evaluate the effect of injected ethanol on pulmonary artery pressure during embolosclerotherapy of arteriovenous malformations (AVMs). Materials and MethodsThis prospective study was conducted in 16 male and 14 female patients (37 sessions; mean age, 34 years; age range, 17–67 years) with AVMs during a 2-year period. The authors measured pulmonary artery pressure via a pulmonary artery catheter and ethanol levels from the pulmonary and radial arteries simultaneously within 3 minutes after each ethanol injection. The authors analyzed the relationship between pulmonary artery pressure and ethanol levels obtained from pulmonary and radial arteries with respect to both single and cumulative doses of ethanol injected. Retrospectively, patients were divided into two groups—those treated with and those treated without vascular occlusion techniques. ResultsThe radial arterial ethanol level showed good correlation with the pulmonary arterial ethanol level (r = 0.7). Single dose per injection was statistically related with pulmonary artery pressure (r = 0.5 vs 0.1 and P < .05 vs .29, respectively, in patients treated without and patients treated with vascular occlusion techniques), and the correlation coefficient between cumulative dose and pulmonary artery pressure was 0.2 and 0.3 in respective cases (P < .05 for both). The mean pulmonary artery pressure correlated with pulmonary arterial ethanol level irrespective of the use of vascular occlusion (r = 0.6 for both groups). ConclusionsPulmonary artery pressure reflected the pulmonary arterial ethanol level and was positively related to the dose of ethanol. Single dose per injection was predictive of pulmonary artery pressure only in patients treated without vascular occlusion techniques. ARTERIOVENOUS malformations (AVMs) are notorious for their resistance to treatment and high recurrence rate, often posing a great challenge to clinicians. The clinical management focuses on multidisciplinary approaches, including surgery and various pharmacologic agents (1). Recently, ethanol sclerotherapy has been considered to be a primary therapeutic choice for AVMs (1, 2, 3) because, when injected directly into the nidus, ethanol causes protein denudation and destruction of vessels within the nidus (1, 2, 4). Ethanol sclerotherapy for AVMs is usually performed with the patient under general anesthesia because of associated severe pain and physiologic changes (1, 2, 4, 5, 6, 7). Multiple injections of ethanol can result in various complications (1, 8). High concentrations of ethanol injected in the vascular malformations are known to be associated with adjacent tissue injury, intravascular hemolysis (6, 9), direct cardiovascular effects (1, 2, 10, 11, 12), and elevated systemic ethanol levels (13, 14). In this regard, many reports demonstrated disastrous cardiorespiratory manifestations related to ethanol therapy in vascular malformations (5, 11, 15). Unfortunately, in our center, we experienced sudden cardiac arrest in a 23-year-old patient after ethanol sclerotherapy of an AVM in the upper extremity in the recovery room. The pulmonary artery pressure was monitored, and a total of 0.7 mL/kg of ethanol was used. There was no remarkable elevation of pulmonary artery pressure during the procedure. After return of spontaneous respiration while in an intubated state, sudden bradycardia and desaturation were followed by asystole and cardiovascular collapse. The pulmonary artery pressure at the time of event was undetermined because the pulmonary arterial catheter had been removed before the patient was transported to the recovery room. The patient was recovered by means of resuscitative cardiopulmonary care, and pulmonary embolism was ruled out. We presumed that the existing subclinical pulmonary hypertension might have been aggravated by hypercapnia associated with delayed awakening. Previous reports regarding systemic levels of ethanol in vascular malformations have measured the peripheral blood ethanol level after the procedure (12, 13, 14). We hypothesized that, due to high flow rates, AVM embolization might be associated with a steep increase in the pulmonary arterial ethanol level and that this in turn might be correlated with increased pulmonary artery pressures. Our goal in this study was to investigate the pulmonary arterial ethanol level immediately after injection into AVMs and determine if this level correlated with an elevation in the pulmonary arterial pressure. Usually, it has been recommended that the pulmonary artery pressure be monitored during ethanol therapy for AVMs (1); however, the risks associated with the placement of a Swan-Ganz catheter cannot be overlooked (16). The criteria for the placement of a Swan-Ganz catheter have not been set up in AVMs. The mechanism of pulmonary artery pressure elevation during ethanol sclerotherapy for AVMs is not clear, but several purported mechanisms include ethanol-induced precapillary pulmonary artery vascular spasm (1), pain from ethanol injection causing sympathetic stimulation (17), and systemic absorption of ethanol during sclerotherapy (13, 14). The relationships between pulmonary artery pressure and blood ethanol level and dose of injected ethanol, however, are not clear (12, 17). Some radiologists have suggested that injection techniques (injection of small divided dose with intervals or a continuous rate injection under fluoroscopy) have an effect on the pulmonary artery pressure (11). In our center, the injection technique has not been set up in one way. Thus, we evaluated the effect of ethanol dose on the pulmonary artery pressure according to a single or cumulative dose per injection. The purpose of this study was to evaluate the effects of pulmonary arterial ethanol level, radial arterial ethanol level, and dose of ethanol on the pulmonary artery pressure and to suggest a guideline for pulmonary arterial catheter placement during emboloscleotherapy of AVMs. Materials and Methods  Patients The institutional review board on human study approved this study, and all patients provided written informed consent. This prospective study was conducted in 33 patients diagnosed with AVM undergoing ethanol embolization with a Swan-Ganz catheter for monitoring of pulmonary artery pressure under general anesthesia from September 2005 to August 2007. Patients younger than 16 years were excluded from the study (mean patient age ± standard deviation, 34 years ±10; age range, 17–67 years). Three patients (three sessions, 13 blood samples) were excluded from the analysis because of underlying moderate pulmonary hypertension and right heart failure. The remaining 30 patients (16 male and 14 female patients) underwent a total of 37 sessions of ethanol sclerotharapy. The vascular malformations were located in the upper extremity (n = 15), lower extremity (n = 11), head and neck (n = 7), and pelvic cavity and trunk (n = 4) (Table 1). Procedure and Data Acquisition All procedures were performed with the patient under general anesthesia, and 70%–100% ethanol was used for ethanol sclerotherapy. Anesthesia was induced with 5 mg/kg thiopental sodium and 0.6 mg/kg rocuronium and maintained with 1 L/min O2, 1 L/min medical air, 0.02–0.05 μg/kg/min remifentanil, and 1.0%–3.0 vol% sevoflurane. Patients were monitored with invasive blood pressure via the left or right radial artery, pulmonary artery pressure via the Swan-Ganz catheter inserted into either internal jugular vein, electrocardiography, peripheral oxygen saturation, end-tidal carbon dioxide level, body temperature, and urine output. Embolization of the AVM involved cannulation of the femoral or radial artery and selective catheterization of the supplying vessel with a guiding catheter. After angiography, transarterial or transvenous catheterization with use of a coaxial catheter and/or percutaneous direct puncture was required to reach the nidus for embolization. Ethanol embolization was directed against the nidus itself and not against the vascular feeders. Vascular occlusion techniques were always incorporated if possible to achieve vascular stasis, including inflow occlusion with balloons and venous occlusion with external pneumatic blood pressure cuffs, balloons, or coils. Then, ethanol was injected into superselected vessels. The injection dose was based on the amount of contrast medium required to fill the lesion without opacification of the normal vessels under fluoroscopic monitoring. The total amount of ethanol did not exceed 1.0 mL/kg of pure ethanol. After each bolus injection of ethanol, the pulmonary artery pressure and amount of ethanol used were recorded. Then, within 3 minutes, radial and pulmonary arterial blood was drawn simultaneously to measure respective ethanol levels. A total of 169 sets of blood samples were analyzed. Pulmonary artery pressure was measured by using a pulmonary arterial catheter (7.5-F Swan-Ganz catheter [931HF-75; Baxter Healthcare, Irvine, California]). After each ethanol injection, we waited for 5–10 minutes and then performed angiography to determine if the AVMs were properly embolized. Blood samples were analyzed to determine ethanol concentrations by using gas chromatography (model 5890; Hewlett-Packard, Waltham, Massachusetts). When the mean pulmonary artery pressure exceeded 25 mm Hg, nitroglycerine was administered either as a bolus (50–100 μg) or as a continuous intravenous infusion (0.5–3.0 μg/kg/min). Vital signs, central venous pressure, peak airway pressure, and peripheral oxygen saturation (Spo2) were recorded. Retrospectively, patients were divided into two groups, those treated with vascular occlusion techniques (ie, external pneumatic blood pressure cuff, coil) and those treated without vascular occlusion techniques, and data were compared between the two groups. We performed arterial blood gas analyses after the procedure. Blood ethanol levels were obtained for the first four injections in every session. The mean number of injections per session was 5.1 (range, 1.0–11.0). Statistical Analysis To compensate for the bias caused by the number of ethanol injections per session, a mixed liner model was used for statistical analysis with software (SAS version 8.1; SAS Institute, Cary, North Carolina). The primary hypothesis of this study was that pulmonary artery pressure values are positively correlated with the pulmonary arterial ethanol level. Under a significance level of .05 and a power of 0.8, 30 patients were required to satisfy the coefficient of correlation to be greater than 0.5 (ie, coefficient of 0.4 is a moderate correlation). By using a mixed model, the relationship between pulmonary artery pressure and the blood ethanol level and amount of ethanol per injection were analyzed. The unpaired t test (Mann-Whitney U test) and χ2 test were used for comparing patients treated with and without vascular occlusion techniques. The difference was regarded as statistically significant when the P value was less than .05. Statistical analyses were performed by one author (J.A.K.) and a statistician from our institute. Results The amount of ethanol per injection was 0.06 mL/kg (range, 0.01–0.19 mL/kg). The average pulmonary and radial arterial ethanol levels were 44.5 and 48.2 mg/dL, respectively (range, 1.7–124.5 and 1.0–198.8 mg/dL, respectively) (Table 2). The pulmonary and radial arterial ethanol levels showed good correlation with each other (r = 0.7) (Fig 1). The systolic, mean, and diastolic pulmonary artery pressures obtained after each ethanol injection were 29, 23, and 13 mm Hg, respectively (range, 20–59, 14–49, and 5–33 mm Hg, respectively). The dose of ethanol per injection was significantly higher in patients treated without vascular occlusion techniques. Pulmonary and radial arterial ethanol levels and mean pulmonary artery pressure were significantly higher in patients treated without vascular occlusion techniques than in those treated with vascular occlusion techniques (Table 2). The single and cumulative dose of ethanol per injection was respectively related with pulmonary artery pressure; however, the relationship between single injection dose and pulmonary artery pressure was most obvious in the patients treated without vascular occlusion techniques (r = 0.5). The mean pulmonary artery pressure showed good correlation with the pulmonary arterial ethanol level. The cumulative dose of injected ethanol was related to the pulmonary arterial ethanol level. The mean blood pressure increased after ethanol injection; however, it was not significantly related to the pulmonary artery pressure (Table 3). The degree of pulmonary artery pressure elevations from that before ethanol injection to that at the time of maximum pulmonary artery pressure after the injection (average, 5.6 mm Hg) showed no correlation with the dose of ethanol, mean blood pressure, or pulmonary and radial arterial ethanol levels (data are not shown). The changes in mean blood pressure, central venous pressure, Spo2 and peak airway pressure before and after each ethanol injection were not statistically significant (Fig 2). A pulmonary arterial ethanol level of more than 80 mg/dL after each injection was observed in 14 of the 169 samples (8.3%). In those cases, the average amount of ethanol used was 0.11 mL/kg ± 0.03. Serum glucose, potassium, and base excess measurements obtained after the procedure were 95 mg/dL ± 17, 4.0 mEq/L ± 1.2, and −3.9 ± 3.2 mMol/L, respectively. Complications were observed in 19 of the 37 sessions (51%). Skin lesions such as bullae, discoloration, and necrosis were observed in seven of the 37 sessions (19%), but no further management was required. Two events (5.4%) of distal embolism and nine cases (24%) of hematuria were observed. Permanent peripheral nerve injury occurred in one case, which did not recover during follow-up. Discussion The injected ethanol in vascular malformations induces direct tissue toxicity that leads to endothelial damage, severe vascular spasm, and denudation of proteins, which, in turn, leads to the entrapment of erythrocytes in arteries (1, 2). The result of ethanol embolization of AVMs was reported as a 40% cure rate, 28% partial remission, 18% no remission, and 2% of aggravation (18). Ethanol has been favored over other embolic agents because of its relatively good results and low chance of recanalization (1, 3). The complication rate of ethanol embolization in AVMs has been reported to range from 31% to 48% (19, 20). Systemic absorption of ethanol in sclerotherapy is well known, and the dose-response relationship between the injected ethanol dose and the systemic level is relatively accepted (13, 14). A high blood ethanol concentration causes cardiac arrhythmias (21) and decreased heart rate variability (22). However, there has been some doubt about the pulmonary artery pressure reaction to the injected ethanol (12, 17). For instance, several cases reported incidences of ethanol-related cardiovascular complications by using small total injection amounts and low levels of blood ethanol (5, 11, 15). In those cases, however, the blood ethanol level was measured after the procedure, so there was a temporal delay between the events and the blood ethanol level measurements. In addition, the injected amount of ethanol related to the event was not elucidated. Ingested alcohol is excreted in first-order kinetics at a speed of 100–200 mg/kg/h, and, after saturation of the enzyme system, zero-order (time-dependent) excretion occurs (23). The pharmacokinetics of intravenously injected ethanol is still unclear. However, it is certain that systemic ethanol level measured at the end of the procedure is not an accurate reflection of systemic ethanol levels at the time of events. The mechanism of pulmonary artery pressure elevation relating to the ethanol injection is still not clear. In dogs, ethanol caused dose-dependent contraction of pulmonary artery smooth muscle (24, 25). In healthy volunteers (26), the orally ingested ethanol led to pulmonary artery pressure changes. The important finding of this study was that increases in pulmonary artery pressure correlated with rapid increases in the pulmonary arterial ethanol levels after the administration of ethanol into peripheral AVMs. On the basis of this result, it may be deduced that an elevation in pulmonary artery pressure may reflect the direct effect of ethanol on the pulmonary vasculature. It has been suggested that ethanol induces pulmonary vasospasm, resulting in elevation in pulmonary artery pressures as a cause behind cardiovascular collapse in patients undergoing ethanol sclerotherapy (1). However, idiosyncratic anaphylactic and/or anaphylactoid reactions (eg, to contrast dye or ethanol), local thrombosis of small pulmonary artery branches, and embolization of materials from the damaged vasculature of the AVM may also be considered as other contributing factors. A prominent elevation in pulmonary artery pressure has been reported in patients with AVM when compared to those without AVMs (17), and this may be explained by the direct drainage of some injected ethanol from the AVM into the heart via draining veins through the nidus and/or by the systemic absorption through the damaged vascular endothelium. In this regard, we presumed that two routes show an incongruent ethanol flow rate into the heart. Accordingly, we retrospectively divided the patients into two groups depending on the presence of vascular occlusion techniques, and the results showed different responses in pulmonary artery pressures to ethanol injections between two groups. The relationship between pulmonary artery pressure and the cumulative or single dose of ethanol was different depending on the use of a vascular occlusion technique. Vascular occlusion techniques are very helpful for effective ethanol sclerotherapy because they reduce the massive washout of ethanol into the systemic circulation in AVMs. However, this study showed that single-dose pulmonary artery pressure response was unclear in this situation (r = 0.1); therefore, the predictive effect of a single dose of ethanol per injection on the pulmonary artery pressure could be also abolished. The lack of correlation between the cumulative ethanol dose and pulmonary artery pressure in patients without vascular occlusion techniques is interesting. Various factors, including different time intervals between each ethanol injection and a different single dose per injection, may influence the effect of cumulative ethanol dose on the pulmonary artery pressure. The same amounts of ethanol could be injected in small, divided doses with intervals or by bolus injection with an appropriate speed according to the fluoroscopic dye behavior (11). This study showed the relationship between pulmonary artery pressure and single injection dose was more direct than it and cumulative dose. From this finding, it might be deduced that there is a positive effect of small, divided ethanol injection on pulmonary artery pressure, especially in the cases without vascular occlusion techniques. However, when ethanol is injected in small, divided doses, there was a suggestion that a sclerosing effect of ethanol could be diluted and that the possibility of obliteration of lesions in the immediate vicinity of the needle tip exists (11). There is no practical guideline for pulmonary artery pressure monitoring in patients with AVMs, and, as a general rule, placement of a pulmonary artery catheter is indicated if a large amount of ethanol is required or the patient has a history of increased pulmonary artery pressure. However, there are some concerns about the placement of a pulmonary artery catheter because many pulmonary artery catheter-related complications have been reported (16, 27) and it requires time and some expertise. Detected pulmonary hypertension could be properly treated by using various methods; however, if it is not treated or even if it is aggravated by injection of ethanol, the result would be disastrous. Pulmonary artery pressure elevation is known to induce an increase in peak airway pressure, right ventricular dysfunction, ventricular septal deviation, and decreased cardiac contractility (28). These conditions could be aggravated by hypercapnia, acidosis, hypoxemia, increased sympathetic tone, and hypothermia. Therefore, the treatment of increased pulmonary artery pressure should be directed to avoid these conditions. The hemodynamic management of right ventricular failure should focus on the support of right ventricular output to allow adequate filling of the left ventricle (28). Supplemental oxygen and hyperventilation to decrease carbon dioxide tension levels will lower pulmonary artery pressure, and isoproterenol increases right ventricular contractility and causes pulmonary vasodilatation. Vasodilators such as nitroglycerine and prostaglandin E1 are useful. However, systemic hypotension and increases in left-to-right shunt could result from the use of vasodilators. Inhaled nitric oxide has some efficacy as a selective pulmonary vasodilator (28). There was a report that injected ethanol especially aggravated hypoxic pulmonary vasoconstriction, so additive oxygen was more helpful in this situation (29). At the time of restoration of spontaneous respiration after general anesthesia, patients are usually left under a state of compromised respiratory function due to a residual anesthetic effect and an increased sympathetic tone secondary to tracheal irritation, hypercapnia, and pain (30, 31, 32). These factors may contribute to the aggravation of already elevated pulmonary artery pressures after ethanol injection. Therefore, we believe that the maintenance of pulmonary artery pressure monitoring during the recovery period may be beneficial in this selective group of patients because early detection of an increase in pulmonary artery pressure and prompt management may prevent any detrimental complications. The limitation of this study is that the correlation of increased pulmonary arterial ethanol levels and pulmonary artery pressures may not be causal because the elevation of pulmonary artery pressure could also be related to embolization of materials such as thrombus and sloughed endothelium from the damaged vasculature of the AVM. In conclusion, elevations in pulmonary artery pressures immediately after bolus injection of ethanol showed strong correlation with pulmonary arterial ethanol level, and, in turn, pulmonary arterial ethanol level was correlated with the dose of ethanol. In particular, a single dose of ethanol was predictive of pulmonary artery pressure elevations in cases treated without vascular occlusion techniques, and, therefore, small, divided injection of ethanol may be recommended with respect to pulmonary artery pressures. References 1. 1Yakes WF, Rossi P, Odink H. How I do it: arteriovenous malformation management. Cardiovasc Intervent Radiol. 1996;19:65–71. 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a Department of Anesthesiology and Pain Medicine, Samsung Medical Center, Sungkyunkwan University, School of Medicine, 50, Irwon-dong, Gangnam-gu, Seoul, Korea 135-710 b Radiology and Center for Imaging Science, Samsung Medical Center, Sungkyunkwan University, School of Medicine, 50, Irwon-dong, Gangnam-gu, Seoul, Korea 135-710 c Department of Anesthesiology and Pain Medicine, Dankook University, Cheonan, Korea  Address correspondence to J.A.K.
None of the authors have identified a conflict of interest. PII: S1051-0443(08)00928-7 doi:10.1016/j.jvir.2008.10.012 © 2009 SIR. Published by Elsevier Inc. All rights reserved. | |
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