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Published online before print April 15, 2005, 10.1148/radiol.2353040903
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(Radiology 2005;235:1072-1077.)
© RSNA, 2005

Vascular and Interventional Radiology

Multistage Ethanol Sclerotherapy of Soft-Tissue Arteriovenous Malformations: Effect on Pulmonary Arterial Pressure1

Byung Seop Shin, MD, Young Soo Do, MD, Byung Boong Lee, MD, Dong Ik Kim, MD, Ik Soo Chung, MD, Hyun Sung Cho, MD, Myung Hee Kim, MD, Gaab Soo Kim, MD, Chung Su Kim, MD, Hong Sik Byun, MD, Sung Wook Shin, MD and Kwang Bo Park, MD

1 From the Departments of Anesthesiology and Pain Medicine (B.S.S., I.S.C., H.S.C., M.H.K., G.S.K., C.S.K.), Surgery (B.B.L., D.I.K.), and Radiology and Center for Imaging Science (Y.S.D., H.S.B., S.W.S., K.B.P.), Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-Dong, Kangnam-Ku, Seoul, 135–710 Korea. Received May 20, 2004; revision requested August 3; revision received August 26; accepted October 15. Address correspondence to Y.S.D. (e-mail: ysdo@smc.samsung.co.kr).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To retrospectively investigate how repeat injections of absolute ethanol in therapeutic doses, required for multisession sclerotherapy of large high-flow soft-tissue arteriovenous malformations (AVMs) in patients with normal cardiopulmonary function, affect pulmonary arterial pressure (PAP).

MATERIALS AND METHODS: Study received approval and waiver of informed consent by institutional review board and was conducted in 16 male and 16 female patients with AVMs who underwent repeat sclerotherapy (142 sessions total) with absolute ethanol from July 1997 to December 2003. PAPs were monitored during first session in all patients. In subsequent sessions, PAP was monitored with pulmonary catheter when predicted single dose of ethanol exceeded 3 mL and total amount exceeded 0.25 mL/kg. PAP was measured in 104 sessions. Serum ethanol levels from blood samples obtained at end of each session were reviewed. PAP parameters were analyzed at beginning and end of each session, and highest value was recorded to assess any increase after repeat therapy. Difference between initial and highest PAP values recorded in a session ({Delta}max) was noted to determine any increase during repeat sessions. Possible relationship was reviewed between this value and amount of ethanol used. For sessions without PAP monitoring, mixed model was used for statistical analysis.

RESULTS: Total ethanol used was variable. In 43 sessions, highest mean PAP exceeded 25 mm Hg. Incidence of sustained pulmonary hypertension (mean PAP > 25 mm Hg) at end of each session was 30.8% (32 of 104 sessions). Initial PAP parameters did not increase or decrease during repeat sessions. No significant changes in {Delta}max of systolic and mean PAP were observed with increasing number of sessions. Rather, {Delta}max of diastolic PAP was reduced after repeat sessions (P = .03). There was no significant correlation between serum ethanol level and PAP parameters at end of sessions. Relationships between {Delta}max values of systolic, mean, and diastolic PAP and total ethanol used were not significant.

CONCLUSION: High incidence of acute pulmonary hypertension was observed in each sclerotherapy session without lasting effect on PAP.

© RSNA, 2005


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Although much valued effort is being made to improve the clinical management of congenital arteriovenous malformations (AVMs), they still present a major challenge, even to the most experienced clinicians (1–3). Many attempts to control AVMs with surgery during the past century often resulted in disappointing outcomes, such as recurrence, worsening, and/or life-threatening complications (4,5). With advances in instrumentation and imaging, sclerotherapy and embolotherapy now play a significant role in the treatment of AVMs and have been found to be effective for certain types of AVMs as a primary mode of therapy (6–9). In addition, the expanding roles of the different types of embolotherapy and sclerotherapy, which are designed to be integrated with surgery both pre- and postoperatively as part of a multidisciplinary approach, represent advanced management of AVMs (10).

Various agents have been introduced for sclerotherapy, and absolute ethanol has been shown to be one of the more effective agents for the treatment of AVMs (3). However, this ethanol sclerotherapy has been found to be accompanied by various complications, both acute and chronic, which are associated with serious morbidity. Complications include skin and/or mucous membrane bullae, skin and/or subcutaneous tissue necrosis, nerve damage, deep venous thrombosis and/or pulmonary embolism, massive muscle or cartilage necrosis, transient hemoglobinuria, and pulmonary hypertension (3,7,11). Although the ethanol washed out from the nidus of an AVM becomes diluted after being injected, it can strongly influence the pulmonary arterial pressure (PAP) (3). Moreover, most soft-tissue AVMs require multistage sclerotherapy, and the effect of repeat injection of absolute ethanol on the pulmonary vasculature remains a major concern to clinicians, especially in the case of a high-flow AVM, which carries an increased risk of morbidity (12). Thus, the purpose of our study was to retrospectively investigate whether repeat injections of absolute ethanol in therapeutic doses, which is required for multisession sclerotherapy of large high-flow soft-tissue AVMs in patients with normal cardiopulmonary function, have an effect on PAP.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Patients
A retrospective review, which received full approval and a waiver of informed consent by our institutional review board, was conducted in 34 patients diagnosed as having soft-tissue AVMs who underwent sclerotherapy at our center from July 1997 to December 2003. The patients included in this study were referred to interventional radiologists as a result of the inoperable state of their AVM lesions. They received sclerotherapy with absolute ethanol (99.6%) and required PAP monitoring more than once. Two patients were excluded from the study because they had dilated cardiomyopathy and moderate pulmonary hypertension before the start of sclerotherapy. The remaining 32 patients did not show any other disorder or disease at the beginning of sclerotherapy.

PAPs were monitored during the first session in all patients. In subsequent sessions, PAP was monitored by using a pulmonary catheter only when the predicted single injection dose of absolute ethanol was greater than 3 mL and the total amount exceeded 0.25 mL per kilogram of body weight. Thirty-two patients with AVMs (16 males and 16 females; mean age, 29.6 years; age range, 11–53 years) underwent a total of 142 sessions of ethanol sclerotherapy with general anesthesia. PAP was measured during 104 sessions for systolic, mean, and diastolic values by using a pulmonary artery catheter (7.5-F Swan-Ganz catheter [931HF-75; Baxter Healthcare, Irvine, Calif]). The mean number of therapy sessions per patient was 4.4 (range, 2–15) (Table 1).


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  		TABLE 1. Demographic Data for Patients with Soft-Tissue AVMs

 
Procedure
All sclerotherapy procedures that involved the use of absolute ethanol were performed with general anesthesia. Ethanol sclerotherapy was performed by two interventional radiologists (Y.S.D., H.S.B., with 7 and 10 years of experience in interventional radiology, respectively), who had been performing ethanol sclerotherapy since 1996. Cardiopulmonary monitoring was used by introducing a pulmonary artery catheter into the right internal jugular vein. Staged ethanol embolization was directed against the nidus itself, not against the vascular feeders; the goal was to embolize all or part of the nidus until the desired clinical result was achieved. Routes of vascular access to attack the nidus were chosen after an initial angiogram was obtained. Transarterial and transvenous catheterization with the use of a coaxial catheter and/or percutaneous direct puncture were required to reach the nidus for embolization. In some cases, proximal inflow occlusion was performed during the ethanol injection. To achieve vascular stasis, an intravascular occlusion balloon catheter was used for the trunk and pelvis area, and external pneumatic blood pressure cuffs were used for the extremities.

Among the 104 total sessions of ethanol sclerotherapy, 43 sessions were performed with the direct puncture method, 49 sessions with the transcatheter method, and the remaining 12 sessions with both methods. Arteriograms were acquired to determine the exact flow characteristics of the AVMs. Moreover, to determine the volume of ethanol used during embolization and the rate of injection, test injections of the contrast material were performed with fluoroscopic monitoring. The amount of ethanol used was based on the amount of contrast material required to fill the fistula without opacifying the normal vessels. After ethanol injections, we waited for 10 minutes and then acquired arteriograms to determine whether the therapy was successful. Complete embolization of at least one compartment of the AVMs required meticulous repetition of the previously described technique (3). The single ethanol dose per each injection during the sessions ranged from 2 to 10 mL. The total amount of absolute ethanol used per session was less than 1.01 mL/kg. PAP values were recorded at the start and end of each procedure, and the highest PAP value was recorded after injection of absolute ethanol or after deflation of an intravascular occlusion balloon or external pneumatic cuffs.

When the mean PAP exceeded 25 mm Hg, nitroglycerine was administered as either a bolus injection (50–100 µg) or by means of continuous infusion (0.3–3.0 µg/kg/min) intravenously. When increased PAP was sustained at the end of the session, the patient was kept at the intensive care unit for close PAP monitoring and for continuous administration of nitroglycerine.

Data Acquisition
The initial, maximum, and final PAP values (systolic, mean, and diastolic) were investigated and compared with the total amount of absolute ethanol used at each session and the serum ethanol level measured from a blood sample acquired at the end of each session. We also investigated the incidence where the highest mean PAP exceeded 25 mm Hg, where nitroglycerine was required to control the increased PAP during the sessions, and where there was sustained pulmonary hypertension (mean PAP > 25 mm Hg) at the end of each session. The complications that occurred in the 142 sessions were reviewed. Data acquisition was performed by two of the authors (B.S.S., Y.S.D.).

Data Analysis
We analyzed the data to determine whether the initial, maximum, and final PAP values (systolic, mean, and diastolic), as well as the difference between the initial-session PAP measurement and corresponding maximum PAP measurement ({Delta}max) for each session, increased at the repeat sessions (M.H.K., G.S.K.). We compared the relationship between the {Delta}max values and the total amount of ethanol used per session. We reviewed whether the highest PAP occurred during the session or at the end of the session. The correlation between the serum ethanol level and PAP parameters (systolic, mean, and diastolic) at the end of the sessions was also investigated. Data analysis was performed by two of the authors (M.H.K., G.S.K.).

Statistical Analysis
To consider the bias caused by the sessions without PAP monitoring, a mixed model was used for statistical analysis with SAS version 8.1 software (SAS Institute, Cary, NC) to analyze the changes in PAP during each session, since individual patients underwent different numbers of sessions. The primary hypothesis in this study was that the difference between the highest values of the systolic, mean, and diastolic PAP and the initial PAP values are positively correlated with the number of sessions. If we suppose that the coefficient of correlation is greater than 0.5 (beyond a moderate correlation), 30 patients were required under the significant level of .05 and a power of .8. By using a mixed model, the relationship between the {Delta}max values and the total amount of ethanol used per session and the correlation between the serum ethanol level and PAP parameters (systolic, mean, and diastolic) at the end of the sessions were also analyzed. A P value of less than .05 was considered to indicate a statistically significant difference. All statistical analyses were performed by one author (M.H.K.) and a statistician.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 
The total amount of absolute ethanol used to control the AVM nidus varied: 6.0–69.0 mL was used per session (range, 0.14–1.01 mL/kg), with a mean of 32.2 mL. The mean serum ethanol level at the end of the sessions was 42.8 mg/dL (9.3 mmol/L) (range, 5.4–118.7 mg/dL [1.2–25.8 mmol/L]) (Tables 2, 3). Serum ethanol level greater than the legal intoxication level at the end of the session (>80 mg/dL [17.4 mmol/L]) occurred in 11.5% of sessions (12 of 104). The initial mean values of systolic, mean, and diastolic PAPs were 22.6 mm Hg ± 6.4 (standard deviation), 16.3 mm Hg ± 5.1, and 11.6 mm Hg ± 4.4, respectively. The highest mean values of systolic, mean, and diastolic PAPs were 33.3 mm Hg ± 11.1, 24.8 mm Hg ± 8.2, and 18.4 mm Hg ± 7.5, respectively. The mean PAP values at the end of the sessions were 28.9 mm Hg ± 9.2, 21.8 mm Hg ± 7.0, and 16.4 mm Hg ± 6.4, respectively.


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  		TABLE 2. Sclerotherapy Data

 

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  		TABLE 3. Sclerotherapy Data according to AVM Location

 
Increases of more than 10 mm Hg for systolic, mean, and diastolic PAP immediately after injection occurred in 49.0% of sessions (51 of 104), 37.5% of sessions (39 of 104), and 25.0% of sessions (26 of 104), respectively. The highest PAP values were recorded within 3 minutes of ethanol injection. In 30.8% of sessions (32 of 104), the highest PAP value was recorded at the end of the session, and in 64.4% of sessions (92 of 104), it was recorded during the sessions.

In 43 sessions, the highest mean PAP exceeded 25 mm Hg. Nitroglycerine was required to control pulmonary hypertension in these patients. The incidence of sustained pulmonary hypertension (mean PAP > 25 mm Hg) at the end of each session was 30.8% (32 of 104 sessions). These patients were transferred to the intensive care unit (20 of 32 patients; range, one to four times), and PAP levels returned to baseline levels within a maximum of 10 hours.

Repeat Session Findings
There was no increase or decrease in the initial PAP parameters (systolic, mean, diastolic) during repeat sessions (P = .26, .09, and .61, respectively) (Fig 1). No increase in the {Delta}max values of the highest and initial systolic and mean PAPs were observed when increasing the number of sessions (P = .52 and .21, respectively) (Fig 2). The relationship between the {Delta}max values of initial systolic, mean, and diastolic PAPs and the total amount of absolute ethanol used was not statistically significant (P = .38, .22, and .22, respectively). Similar to the findings of Mason and colleagues (13), we found statistically significant correlations between injected serum ethanol levels acquired at the end of session and total amount of ethanol injected (P < .05), but there was no significant correlation between the serum ethanol level and PAP parameters (systolic, mean, and diastolic) at the end of sessions (P = .30, .26, and .29, respectively) (Fig 3).



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  		Figure 1. Lines on each graph represent changes in initial PAP (systolic, mean, and diastolic) values of each individual patient with respect to number of repeat sclerotherapy sessions. There were no statistically significant changes in initial PAP parameters when sessions were repeated (P = .26, .09, and .61 for systolic, mean, and diastolic PAP, respectively).

 


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  		Figure 2. Lines on each graph represent changes in difference ({Delta}max) between initial and highest PAP values (systolic, mean, and diastolic) in each patient with respect to number of repeat sclerotherapy sessions. There were no statistically significant changes in {Delta}max between initial and highest PAP values of systolic and mean PAPs with increasing number of sessions (P = .52 and .21, respectively). Rather, differences between initial and highest values of diastolic PAP were reduced after repeat sessions (P = .03).

 


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  		Figure 3. Scatterplot shows no statistically significant correlation between mean PAPs and serum ethanol level at end of sclerotherapy sessions (P = .26).

 
Complications
Twenty-three (16.2%) complications occurred in 142 procedures. Nineteen (19 of 142 procedures, 13.4%) minor complications (17 skin blisters or necrosis and two transient peripheral nerve injuries) occurred in 14 patients (43.8%). All of these minor complications responded to conservative treatment. There were five major complications (five of 142 procedures, 3.5%) in five patients (15.6%): an infection caused by severe skin necrosis, acute renal failure due to muscle necrosis, permanent median nerve injury of the arm, focal urinary bladder necrosis, and pulmonary hypertensive crisis accompanying a bronchospasm.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
REFERENCES
 
Currently, many agents such as absolute ethanol, sodium tetradecyl sulfate, N-butyl cyanoacrylate, and isobutyl 2-cyanoacrylate are used for the treatment of AVM. These are applied by using either a direct puncture technique into the nidus or a superselective catherterization technique to deliver embolotherapy or sclerotherapy agent selectively to the nidus of the lesions (14). Of these agents, absolute ethanol has a unique ability to induce protein denaturation of the endothelial cells with subsequent vessel wall denudation and interruption, which results in the complete obliteration of the vessel lumen rather than simple obstruction. Ethanol does not allow recanalization as a result of permanent damage to the endothelium of the AVM nidus (15–17).

Therefore, a multistage approach by using absolute ethanol, which has the lowest recurrence rate of available techniques, is considered to be more effective than methods involving the use of other embolotherapy or sclerotherapy agents currently available (14,18). Also, ethanol is readily available, has a long shelf life, and is inexpensive.

However, many clinicians who have used absolute ethanol have been alarmed by the various complications as a result of its chemical toxicity, even though the method has produced excellent results with promising outcomes and an increased chance of cure (3,13,19). These events were the result of various conditions, such as dysrhythmia, cardiac collapse, and/or acute and severe pulmonary vasospasm induced by the ethanol. A fatal outcome in a 3-month old boy with end-stage renal disease was reported after arterial injection of 4.5 mL of absolute ethanol for renal ablation (20). In one of our cases involving right-thigh and large pelvic AVM lesion, the PAP values abruptly increased to 72/49/40 mm Hg (systolic/mean/diastolic), mechanical ventilation became impossible as a result of high resistance of the airway, and peripheral oxygen saturation (SpO2) decreased to 60% after injection of 10 mL of absolute alcohol. PAP values were promptly restored to 24/19/10 mm Hg, however, and mechanical ventilation and SpO2 returned to normal after four repeated bolus injections of nitroglycerine in conjunction with continuous infusion and hyperventilation with 100% oxygen. Even though we have experienced only one case of pulmonary hypertensive crisis among a total of 142 sessions, we do not consider it an insignificant incidence, because the patient with AVM must undergo multiple sessions of sclerotherapy that can result in life-threatening complications.

Pulmonary vasospasm caused by absolute ethanol, even though it is diluted by the time it reaches the pulmonary vasculature, results in acute pulmonary hypertension at the precapillary level, which in turn increases right ventricular afterload and leads to right ventricular failure (21). The right ventricle begins to fail when the systolic pressure is acutely increased by a factor of two—that is, by more than 50 mm Hg. This results in decreased left-sided heart filling, decreased left-sided cardiac output, systemic hypotension, and finally cardiopulmonary collapse (15,21). Therefore, the rapid correction of pulmonary hypertension should be absolutely warranted before the cascade of events reaches the final stage of pulmonary hypertension—cardiopulmonary collapse. In case of high-flow AVM, the importance of having PAP cautiously monitored by an experienced anesthesiologist for the prompt prevention of serious pulmonary hypertension cannot be overemphasized to prevent such a disastrous outcome.

Hypoxia, acidosis, and hypercapnia can aggravate pulmonary hypertension by means of hypoxic pulmonary vasoconstriction. Cockrill et al (22) noted that supplemental oxygen induced a mild degree of pulmonary vasodilatation and reduced PAP. Therefore, adequate ventilatory management is mandatory during ethanol sclerotherapy. In addition, an adequate depth of anesthesia is needed, because sympathetic stimulation caused by severe pain during injection of absolute ethanol contributes to the increase in PAP (23).

Nitroglycerine, prostaglandin E1, prostaglandin I2, and inhaled nitric oxide are highly selective pulmonary vasodilators with low systemic effects (24–27). In our study, the incidence of pulmonary hypertension was high. Nitroglycerine was used in 43 (41.3%) of the 104 sessions by following our regimen described previously. The incidence of sustained pulmonary hypertension (mean PAP increase > 25 mm Hg) at the end of each session was 30.8% (32 of 104 sessions). Although the incidence of pulmonary hypertension in our study was high, our findings show that repeated sessions of absolute ethanol injections did not elevate initial PAP. From these findings, we can derive the conclusion that repeated ethanol injections within the limited dosage of less than 0.5–1.0 mL/kg absolute ethanol per session and less than 10 mL of single ethanol dose per injection do not seem to cause increasing tendencies of PAP in multisession sclerotherapy.

As Yakes et al (3) recommended, it is important to perform ethanol sclerotherapy within the maximum volume of less than 0.5–1.0 mL/kg absolute ethanol per session. By following this recommendation, our results did not show any statistically meaningful relationship between PAP increase (between highest and initial values of systolic, mean, and diastolic) and the total amount of absolute ethanol used. Furthermore, in 30.8% of sessions, the highest PAP value occurred at the end of sessions, and in 64.4%, it occurred during the procedure. It is important to realize that in two-thirds of the interventions, the highest PAP occurred during the session because the highest single absolute ethanol dose was administered during and not at the end of ethanol sclerotherapy.

In our experience, increases in PAP were higher in subsequent sessions than in previous sessions in some patients, and we questioned whether the highest PAP increases with the repetition of the sessions. We investigated the difference ({Delta}max) between the initial and the highest PAP in each session and whether it increased during repeat sessions. Statistical analysis showed that there were no increasing or decreasing tendencies, which meant that the reactivity of pulmonary vasculature to the injected ethanol did not increase during multistage ethanol sclerotherapy.

The main limitation of this study is that, even though we used a mixed model to take into account the sessions without PAP monitoring, the bias caused by the 38 sessions without PAP monitoring could not be ruled out completely. In addition, these results failed to show any statistically meaningful relationship between PAP increase and the total amount of absolute ethanol used within the maximum volume of less than 0.5–1.0 mL/kg absolute ethanol per session. It was assumed that the highest PAP may be primarily influenced by a single injection dose rather than the total amount of absolute ethanol. However, the correlations between a single ethanol injection dose and PAP increase were not examined as a result of the limitation of our retrospective study. Also, we could not determine the effect of high PAP increase on cardiac output. Further study may be required to find these correlations.

In conclusion, a high incidence of acute pulmonary hypertension was observed in each session without lasting effect on PAP during multistage ethanol sclerotherapy. Since a tendency toward significantly increasing or decreasing PAP was not shown, we believe that the risk of pulmonary hypertensive crisis may still exist in subsequent sessions.


   ACKNOWLEDGMENTS
 
The authors thank Seon Woo Kim, PhD, of Samsung Biomedical Research Institute, Seoul, Korea, for her assistance with statistical analysis.


   FOOTNOTES
 
Abbreviations: AVM = arteriovenous malformation, PAP = pulmonary arterial pressure

Authors stated no financial relationship to disclose.

Author contributions: Guarantors of integrity of entire study, B.S.S., Y.S.D., B.B.L.; study concepts, B.S.S., Y.S.D., B.B.L.; study design, B.S.S., Y.S.D., D.I.K.; literature research, I.S.C., K.B.P.; clinical studies, B.S.S., Y.S.D., H.S.C., H.S.B., S.W.S.; data acquisition, B.S.S., Y.S.D.; data analysis/interpretation, M.H.K., G.S.K.; statistical analysis, M.H.K.; manuscript preparation, B.S.S., Y.S.D., C.S.K.; manuscript definition of intellectual content, B.S.S., Y.S.D.; manuscript editing, B.S.S., B.B.L., Y.S.D.; manuscript revision/review and final version approval, all authors


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 

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