The American College of Phlebology - Sclerosing = Solutions

From: Subject: The American College of Phlebology - Sclerosing Solutions Date: Sun, 14 Sep 2003 15:01:44 +0300 MIME-Version: 1.0 Content-Type: multipart/related; boundary="----=_NextPart_000_0000_01C37AD1.1C7E5220"; type="text/html" X-MimeOLE: Produced By Microsoft MimeOLE V6.00.2800.1165 This is a multi-part message in MIME format. ------=_NextPart_000_0000_01C37AD1.1C7E5220 Content-Type: text/html; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.phlebology.org/docmechanism.htm The American College of Phlebology - Sclerosing = Solutions

=20

SCLEROSING=20 SOLUTIONS

Craig F. Feied, MD, FACEP, FAAEM

Back to=20 Primer Table of Contents

=20

Part One

=20

Goals of Sclerotherapy=20

When we treat varicosities and telangiectasias, we want = to remove=20 or obliterate the abnormal vessels that carry retrograde = flow,=20 without damaging adjacent or connected vessels that carry = normal=20 antegrade flow. Obliterating a vessel is not easy: a small = amount of=20 damage will produce intravascular thrombus, but thrombosis = alone=20 usually does not result in obliteration of the vessel. = Intact=20 endothelium aggressively lyses thrombus, and a thrombosed = vessel=20 with intact endothelium will not be sclerosed.=20

Recanalization = of=20 thrombosed vessels

Vascular fibrosis and obliteration only occurs in = response to=20 irreversible endothelial cellular destruction and exposure = of the=20 underlying subendothelial cell layer. If an injected = sclerosant is=20 too weak, there may be no endothelial injury at all. If the=20 sclerosant is a little stronger, the varicose vessel is = damaged, but=20 recanalization occurs and an incompetent pathway for = retrograde=20 blood flow persists. If the injected sclerosant is too = strong, the=20 varicose vessel endothelium is destroyed, but the sclerosant = also=20 flows into adjacent normal vessels and causes damage there = as well.=20 The key goal is to deliver a minimum volume and = concentration=20 of sclerosant that will cause irreversible damage to the = endothelium=20 of the abnormal vessel to be sclerosed, while leaving = adjacent=20 normal vessels untouched. It is important to protect normal=20 superficial vessels, and it is critically important to avoid = injuring the endothelium of deep veins, because deep vein = thrombosis=20 places patients at risk of death from thromboembolism, as = well as=20 causing permanent disability from chronic deep venous = valvular=20 insufficiency. The rational treatment of varicosities and=20 telangiectasias by chemical sclerosis depends upon our = ability to=20 produce vascular endothelial damage that is irreversible in = the area=20 under treatment, but that does not extend to adjacent normal = vessels.=20

To limit endothelial injury to a controlled area, we = exploit=20 differences in flow dynamics between the abnormal veins = being=20 perfused with sclerosant and the adjacent normal vessels = that should=20 not be sclerosed. A thorough understanding of the mechanism = of=20 action of the principal sclerosing agents is essential, as = is a firm=20 grasp of the biophysical principles underlying the = techniques of=20 sclerotherapy.=20

Volume Dilution and Patient Positioning=20

Sclerosant is diluted with blood as it diffuses away from = the=20 site of injection. Thus, if a strong sclerosant is injected, = there=20 will be three zones of action. In zone 1, vascular = endothelium is=20 irreversibly injured: the vessel will be fully sclerosed and = eventually will be completely replaced by a fibrous tissue. = In zone=20 2, vascular endothelium is injured, and the vessel will be = partially=20 or completely thrombosed but will eventually recanalize. In = zone 3=20 the sclerosant will be diluted below its injurious = concentration,=20 and there will be no endothelial injury.=20

Dilution by = diffusion=20 from the injection site

Dilution by Diffusion from the Injection Site=20

Because dilution of the sclerosant with blood occurs = immediately=20 upon injection, the original injected concentration is of no = real=20 importance. What is important is the diluted concentration = of=20 sclerosant at the surface of the endothelium. An injected=20 concentration that is perfectly effective in a spider vein = (where=20 sclerosant displaces blood rather than mixing with it) may = be=20 ineffective in a reticular feeding vein or a truncal varix = simply=20 because dilution reduces the final concentration so low that = there=20 will be no endothelial injury whatsoever (no zone I or zone = II). If=20 the injected concentration is too high, dilution will leave = the=20 final concentration so high that endothelial damage will = occur where=20 it is not wanted (zone I and zone II are too large). If the = injected=20 concentration is just right, dilution will leave a final=20 concentration that is sufficient to injure the local = varicose=20 endothelium, but not high enough to damage normal = superficial or=20 deep veins (most of the varicose vessel falls into zone I, a = small=20 amount falls into zone II, and all normal vessels fall into = zone=20 III).=20

When we select a particular volume and concentration of a = chemical agent with which to sclerose a vessel, we are = explicitly or=20 implicitly adjusting the injected concentration and volume = to take=20 into account the dilution that will occur when the = sclerosant is=20 mixed with blood immediately after injection. We also must = take into=20 account the further dilution that will occur as the = sclerosant flows=20 or diffuses away from the site of injection. The importance = of=20 patient positioning in determining dilutional volume often = is not=20 properly appreciated by the novice in phlebology.=20

Because of the cylindrical geometry of blood vessels, the = volume=20 contained in a vessel depends on the square of the vesel = radius: the=20 volume of any cylinder is calculated as (pi)(r2)(L) (where r = is the=20 radius and L is the length of the vessel). Vessels collapse = to a=20 smaller radius when the legs are elevated, thus the volume = contained=20 is reduced dramatically. For this reason, the position of = the=20 patient has a very powerful effect on the final diluted=20 concentration of sclerosant at the surface of the vessel=20 endothelium.=20

Effect of = position on=20 varicose geometry

Effect of Position on Varicose Geometry=20

Standing=20

For a standing patient with a superficial varicosity of 2 = cm in=20 diameter, the final concentration at a distance from the = injection=20 site of 10 cm (4 inches) is 30 times lower than the initial=20 concentration. Doubling the initial concentration serves = only to=20 double the final concentration, which will still be 15 times = weaker=20 than the concentration in the syringe. In other words, if 1 = cc of a=20 3% solution is injected, the final concentration at the = endothelial=20 surface is 1% at a distance of 1 cm from the injection = point, 0.5%=20 at a distance of 2cm, 0.25% at a distance of 4 cm, and 0.2% = at a=20 distance of 5cm (2 inches) from the injection point. As we = shall=20 see, this means that it is very difficult to achieve = sclerosis of a=20 large vessel by injecting detergent sclerosants with the = patient in=20 a standing position: if the highest available concentration = is=20 injected, the dilution factor may still drop the final = concentration=20 below the threshold of effectiveness within 1.5 inches from = the=20 injection site.=20

Supine=20

What about the supine position? Varicose vessels that = bulge when=20 the patient is standing may collapse when the patient is = supine, but=20 duplex ultrasound readily demonstrates that the veins are = not empty=20 of blood. Both varicose and normal vessels contain a = significant=20 volume of blood with the legs extended in the supine = position. A=20 bulging varicosity that has a diameter of 2 cm in the = standing=20 position may have a diameter of 1 cm in the supine position = and of=20 0.5 cm or less when the legs are elevated as high as = possible. With=20 such a patient in the supine position, injection of 1 cc of = a 3%=20 solution leads to a final concentration of approximately = 1.7% at a=20 distance of 1 cm and a concentration of about 0.6% at a = distance of=20 5 cm (2 inches). This supine technique limits dilution = enough to=20 allow successful sclerosis of large vessels using detergent=20 solutions, so long as sufficient concentrations and volumes = of=20 sclerosants are injected. The only problem is that if an = injection=20 of sclerosant at a high initial concentration is made = directly into=20 a perforating vessel, so that sclerosant flows directly into = the=20 deep system, dilution within the deep vessel will still = permit zone=20 I and zone II endothelial injury for a short distance within = the=20 deep vein. This can lead to deep vein valve damage and = chronic=20 venous insufficiency, to deep vein thrombosis, and to=20 life-threatening pulmonary embolism.=20

Legs Elevated=20

In contrast to the standing and supine positions, when a = patient=20 lies supine and the legs are raised vertically so that they = are well=20 above the central circulation, most superficial varices = collapse to=20 the point where they no longer contain any significant = volume of=20 blood. Repeating the calculation above for a patient in this = position, injection of 1cc of a 3% solution leads to a final = concentration of 2.5% at a distance of 1 cm from the = injection, and=20 a final concentration of 1.6% at a distance of 5 cm (2 = inches). In=20 fact, the final concentration will still be above 1% at a = distance=20 of 10cm from the injection site. Because the superficial = varicosity=20 is collapsed, there is very little dilution with distance so = long as=20 the sclerosant stays within the floppy-walled varicosity.=20

Graph: = volume of=20 dilution vs distance from injection site =

What happens when sclerosant passes through into normal = vessels?=20 Although flow measurements reveal little or no spontaneous = flow=20 through varices and smaller superficial veins when the = patient is in=20 the leg-up position, a substantial intravenous volume and a=20 substantial rate of flow still persists in the deep veins = and in=20 normal larger superficial veins, which have less collapsible = walls.=20 This difference between the volumes contained in floppy = superficial=20 varicose veins and the volumes contained in normal surface = veins and=20 deep veins may be exploited to cause damage that is almost = perfectly=20 localized to superficial varices. If an elevated, empty = varicose=20 vessel is perfused with a concentration of sclerosant so = low=20 that even without dilution it is just barely sufficient to = cause=20 endothelial injury, then any further dilution will reduce = the=20 concentration below the threshold of injury. Because larger=20 superficial vessels and deep vessels continue to carry a = volume of=20 blood in the leg-up position, any sclerosant passing into = these=20 vessels will immediately be diluted to a safe and = noninjurious=20 concentration, sparing the endothelium of vessels that we = wish to=20 preserve. Injection of this 'threshold' concentration = directly into=20 a perforating vein (or even directly into a deep vein) will = not=20 cause any deep vein injury.=20

Types of Sclerosants=20

Virtually any foreign substance can be utilized to cause = venous=20 endothelial damage. Historical methods for producing venous=20 endothelial trauma have included 'a slender rod of = iron',=20 reportedly used by Hippocrates himself, absolute = alcohol,=20 introduced by Monteggio and by Leroy D'Etoilles in the = 1840s, and=20 ferric chloride, introduced by Charles-Gabriel Pravaz = in=20 1851. In 1910 it was noted that the injection of = antisyphilitic=20 mercurial drugs caused obliteration of antecubital veins, = and these=20 agents were adapted for use in sclerotherapy. There were = many other=20 drugs and techniques used for venous sclerosis during these = years,=20 but all of them suffered from one or another problem that = made them=20 unacceptable for modern use. Early sclerosing agents caused = many=20 deaths from sepsis and from pulmonary embolism, as well as a = high=20 incidence of allergic reactions, local tissue necrosis, = pain, and=20 failed sclerosis.=20

Sclerosing=20 Solutions, Part Two=20

Back to = Primer=20 Table of Contents=20

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