Ann Thorac Surg 1998;65:1158-1160
© 1998 The Society of Thoracic Surgeons
How to Do It
Prostaglandin E1 From the Tip of an Intraaortic Balloon Catheter for Lower Limb Ischemia
Toshihide Nakano, MDa,
Ryuji Tominaga, MDa,
Kiminori Shiraishi, CEa,
Hisataka Yasui, MDa
a Division of Cardiovascular Surgery, Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan
Accepted for publication October 14, 1997.
Address reprint requests to Dr Tominaga, Division of Cardiovascular Surgery, Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku Fukuoka 812-82, Japan
e-mail: (tnakano{at}heart.med.kyushu-u.ac.jp)
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Abstract
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A method to treat lower limb ischemia associated with the insertion of an intraaortic balloon catheter is herein reported. A low dose of prostaglandin E1 was administered into the descending aorta continuously from the tip of the intraaortic balloon catheter. Immediately after the administration of prostaglandin E1 in patients whose lower limbs were ischemic due to obstruction with the catheter, the peripheral circulation of the ischemic limbs recovered with minimal changes in the systemic arterial blood pressure. This method is simple and noninvasive and was found to induce a satisfactory effect.
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Introduction
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Intraaortic balloon pumping (IABP) has been used with increasing frequency in the management of unstable angina, cardiogenic shock, and a postoperative low cardiac output syndrome. However, lower limb ischemia is still the most common vascular complication, and is reported to occur in 10% to 20% of these patients despite continuing refinements in catheter design and insertion techniques [1]. Although the main cause of this complication is vascular occlusion of the femoral artery with the catheter, arterial spasms induced by mechanical stimulation with the catheter and thromboembolism also contribute to lower limb ischemia. We administered prostaglandin E1 (PGE1) continuously from the tip of an intraaortic balloon catheter and succeeded in achieving improved lower limb perfusion.
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Technique
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Three male patients who underwent cardiac operations and intraaortic balloon catheter insertion at our institution were enrolled in this study. The mean age was 64.3 years, the mean weight was 60.8 kg, and none of the patients had any peripheral arterial occlusive disease. The indication for IABP consisted of a perioperative low cardiac output in all patients. A 9.5F dual-lumen sheathed intraaortic balloon catheter (Datascope Corp, Montvale, NJ) was percutaneously inserted into the right femoral artery by the Seldinger technique. Administration of PGE1 (Ono Pharmaceutical Co, Ltd) was started when lower limb ischemic signs such as a loss of the pulse in the dorsalis pedis artery, a decrease in the skin temperature, a change in skin color, and the presence of edema were detected. The central lumen of the intraaortic balloon catheter was used to drip PGE1 while IABP was triggered by an electrocardiogram. The hemodynamic changes in the lower limb were checked by the blood flow velocity measured by a Doppler ultrasound flow probe in the dorsalis pedis artery and the hallux skin temperature on both sides simultaneously; the systemic arterial blood pressure and cardiac output were also measured at the same time.
Figure 1 shows the changes in lower limb circulation in patient 1. In patient 1, IABP was started preoperatively in the intensive care unit for a low cardiac output. Immediately after the placement of the IABP, the blood flow velocity of the right dorsalis pedis artery decreased markedly while the right hallux skin temperature decreased by 3.1°C compared with the left lower limb. Early in the postoperative time in the intensive care unit, the right dorsalis pedis flow failed to be detected. A few minutes after the intraarterial administration of PGE1 was started at a dose of 2 ng · kg-1 · min-1 (the standard intravenous dosage is 10 to 100 ng · kg-1 · min-1), the right dorsalis pedis flow increased and the lower limb skin temperature gradually increased on both sides with no laterality. The recovery of the peripheral circulation in the right lower limb was maintained during PGE1 administration until the catheter was removed. Throughout this period, the systemic arterial blood pressure and cardiac output showed no significant changes.
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Fig 1. Changes in the blood flow velocity of the dorsalis pedis artery and in the temperature of the hallux skin after intraaortic balloon pump (IABP) insertion. Immediately after the IABP insertion, blood flow velocity in the right dorsalis pedis artery (RDPA) markedly decreased, and it could not be detected 2 hours after the operation. After the administration of prostaglandin E1 (PGE1), the RDPA flow increased and continued as long as PGE1 was infused. (LDPA = left dorsalis pedis artery.)
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The other patients showed almost the same hemodynamic recovery of the right lower limb from which the intraaortic balloon catheter was inserted by the continuous intraaortic drip infusion of PGE1 at a dose of 0.5 to 3.0 ng · kg-1 · min-1 from the tip of the intraaortic balloon catheter. Nitroglycerin was administered intravenously as a vasodilator in all patients at a dose of 0.5 to 2.0 µg · kg-1 · min-1, which could be decreased during IABP insertion, and no vasoconstrictor was used throughout this period.
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Comment
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Various efforts have been made to reduce the incidence of lower limb ischemia associated with IABP, including refinements in the catheter design such as a development of a smaller catheter, a side-holed sheath, and a sheathless catheter [2]. These catheter improvements have indeed decreased the incidence of complications; however, in some patients with severe lower limb ischemia, either catheter removal, a thromboembolectomy, an adjunctive femorofemoral bypass, or other types of surgical treatment are still required.
Prostaglandin E1 is known to be a potent vasodilator that mainly dilates arterioles and has been successfully used in the treatment of peripheral arterial occlusive disease by intraarterial administration with minimal systemic hemodynamic effects [3]. Moreover, PGE1 also has other advantageous physiologic properties such as inducing antiplatelet aggregation, improving red blood cell deformity, inhibiting superoxide production, and conferring a protective effect on the liver and kidney. The administration of PGE1 into the descending aorta has several merits. One is that the intraaortic administration requires a lower dose of PGE1 to have the same effects compared with an intravenous infusion because PGE1 is inactivated by 60% to 90% by the first lung passage. Another merit is that the accurate effective dose of PGE1 has been clearly established. Furthermore, based on our clinical experience, the peripheral vasodilatation induced by the intraaortic administration of a lower dose of PGE1 seems to be more remarkable than that induced by the intravenous administration of PGE1.
The site of the intraarterial infusion of PGE1 is also a matter of concern when treating lower limb ischemia associated with intraaortic balloon catheter insertion. We previously attempted to administer PGE1 into the femoral artery through the sheath of the catheter in several patients; however, this method failed to improve the distal limb circulation in all patients. We therefore changed the site of the administration of PGE1 to the tip of the intraaortic balloon catheter, and this method was able to achieve the satisfactory effect described herein. One possible mechanism may account for the fact that PGE1 improved the lower limb circulation distal to the insertion site of the intraaortic balloon catheter only when administered from the tip of the catheter. It is the ability of PGE1 to dilate the collateral arteries that bridge the site of the catheter insertion. In previous studies using an acute femoral artery occlusion model in animals, a decrease in the microvascular resistance distal to the ligation and an enlargement of the collateral arteries were observed almost immediately after a femoral ligation [4, 5]. The same collateral adaptation may occur after femoral artery obstruction with an intraaortic balloon catheter; however, in clinical situations after open heart operations using hypothermia and cardiopulmonary bypass, many factors including the use of catecholamine, a low cardiac output, and perivascular edema formation may also contribute to constriction of these collateral vessels. When PGE1 is administered from the tip of an intraaortic balloon catheter into the descending aorta in such patients, it enhances this compensatory enlargement of the arteriolar collateral vessels and, moreover, it might also relieve the spasm of the femoral artery induced by the catheter insertion. On the other hand, when PGE1 is administered from the sheath of the catheter into the femoral artery distal to the site of the catheter insertion, it does not have any such effect on either the collateral vessels or on the spasm of the femoral artery. Prostaglandin E1 should therefore be administered from the tip of the intraaortic balloon catheter to improve the lower limb ischemia associated with IABP.
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References
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- Funk M., Ford C.F., Foell D.W., et al. Frequency of long-term lower limb ischemia associated with intraaortic balloon pump use. Am J Cardiol 1992;70:1195-1199.[Medline]
- Tatar H., Çiçek S., Demirk
lç U., et al. Vascular complications of intraaortic balloon pumping: unsheathed versus sheathed insertion. Ann Thorac Surg 1993;55:1518-1521.[Abstract]
- Creuzig A., Creuzig H., Alexander K. Effects of intra-arterial prostaglandin E1 in patients with peripheral arterial occlusive disease. Eur J Clin Invest 1986;16:480-485.[Medline]
- Unthank J.L., Nixon J.C., Lash J.M. Early adaptations in collateral and microvascular resistances after ligation of the rat femoral artery. J Appl Physiol 1995;79:73-82.[Abstract/Free Full Text]
- Rosenthal S.L., Guyton A.C. Hemodynamics of collateral vasodilatation following femoral artery occlusion in anesthetized dogs. Cir Res 1968;23:239-248.[Abstract/Free Full Text]
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Abstract
Introduction
