COMPLICATIONS AND PROBLEMS FROM FOAM-COATED IMPLANTS

Prosthetic injuries in breast implant users can be attributed to at least six major mechanisms:

(1) "Normal" surgical trauma and surgical misadventures resulting in damage to functional/sensorial parts of the chest and the upper limbs;

(2) Biomechanical effects induced by the presence of large foreign objects that cause compressive trauma, excoriation, distention, atrophy and restrictive adhesion of tissues or compressive/occlusive ischemia of the vasculature within the pectoral-axillary area;

(3) Locally injurious biochemical effects from reactive dispersible substances that induce fibrotic, inflammatory or destructive tissue changes;

(4) Long term tissue remodelling and deviant repair processes leading to hyperplasia, densification, mineralization and dehydration of the implant site;

(5) Implant-capsule-oil adjuvant interactions leading to tissue degeneration or denaturation to produce host tissue-derived antigens that elicit antagonistic host-directed antibodies (autoimmune disturbances);

(6) Pathologic effects from bacterial, viral or fungal colonization of the capsule space leading to low grade chronic infections and toxic phenomena from microbiological metabolites. Users of foam coated and saline-containing implants are specifically subject to such problems.

For most long term users, all of these effects are present to some degree concurrently and the severity generally increases over the period of use. However, the early occurrence of intracapsular infection, seromas and hematomas appears to be a strong accelerating and intensifying factor for implant adverse reactions and related diseases. Atypical infection may be a primary factor leading to systemic effects. Implant-specific defects can add and magnify these factors. Foam coated implants are particularly illustrative of the problems.

Users with degradable foam-coated implants are exposed to all of these risks in addition to new ones which include intractable periprosthetic infections. In turn, the rough surface with deep microscopic channels offers a nearly ideal environment for proliferation of micro-organisms of all types. Predictably, infective sequelae are difficult to control without explantation and exhaustive removal of the debris-contaminated tissue.

Protected intracapsular infections remaining for a substantial period of time have the ability to enhance capsular fibrosis. Such micro-organisms in protected compartments tend to resist antibiotics. Over the long term and with large colonies, the formation of pharmacologically significant quantities of toxins becomes possible. Health effects associated with chronic low grade infections and microbiological metabolites such as toxins may account for some of the disturbances noted in long term users. Capsule problems are common in prosthetic patients in general. The literature makes reference to cases where incompletely removed capsules with prosthetic debris led to continuing disease processes even after removal of the implant.

It is most probable that the early encapsulation of an implant that can leak oil and related chemical debris establishes a condition which produces bioactive mixtures of degradation products and silicone compounds with dispersions of denatured proteins. Furthermore, the site often attracts bacterial contamination and the oil ensures long term survival of the viable entities even in the presence of systemic antibiotics.

If the infection is allowed to remain within the capsule space, the capsule integrity is eventually lost, and the material escapes. Eventually the number of antibodies directed against such autogenous tissue antigens rises to the point where it can create rheumatoid-like and other degenerative tissue disease symptoms.

The process was investigated by Dow Corning in the early seventies and appeared in confidential reports issued in 1974 (LeVier and Boley studies on adjuvant effects of silicone compounds and 1975 (Lake and Redonovich studies on pharmacology of silicone derivatives).

Impact of Manufacturing Techniques and Design on Foam-Coated Product Risks:

Late issue foam coated implants produced in the 1980-91 period were not of consistent composition and quality. Several suppliers and numerous processes were used to manufacture the various prostheses which were sold during that period. In the latter years of production, the manufacturing site was also changed several times. Items manufactured after 1989 were significantly different from earlier versions. The processes and the materials were also prone to induce point-to-point variations in the product. There are therefore uncertainties in composition, predictability and safety of such products which cannot addressed generically and item-to-item variations are to be expected.

Technical, ethical and clinical problems surround these implants and their marketing. The most obvious is that the foam coating itself was incompatible with long term medical implantation. Its chemical constitution made it a likely candidate for the production of toxic substances. The manufacturing process failed to control the level of impurity of this material at time of release. Furthermore, the material deteriorated on the shelf and led to increasing levels of contamination with time, thus making the evaluation of the product dependent on the delay between manufacturing and use. The most obvious feature of the product was the rapid loss of adhesion and detachment of the foam from the core in-vivo. Once detached, the material broke up further leaving microscopic debris which remained in patients' tissues for a variable period of time during which cytotoxic metabolites appeared in breast milk, blood and urine.

Specific manufacturing problems impart additional risks and magnify existing ones. For example, the Replicons and the Memes made in the 1984-89 period were filled with gel via a puncture made at the center of the posterior shell patch. The puncture was not consistently sealed. It depended on adventitious application of RTV-based foam adhesive to occlude the hole. More than 70 % of explanted items from this period show open gel fill holes and leak oil and gel grossly into the chest nuscle area.

The Replicons used an internal and external patch system. About 10 % of recovered items show delaminated or debonded internal patches, leaving only the thin outer patch to maintain shell integrity. Some internal patches appear to never have bonded.

More than 20% exhibit gross delamination of the RTV from the shell surface. This produces a large amount of solid inflammatory debris in the adjacent tissue. The effect is particularly strong at the equator. It appears that many of the items were not adequately degreased prior to the application of the adhesive or the adhesive formulae were not suited for the application. Overall the product reflect a poor understanding of basic manufacturing principles that apply to elastomer products.

Special Gel Compositions in Foam Implants:

Silicone gels used in plastic surgery products are proprietary formulae which can vary in composition from brand to brand and even within items of the same type. All are multi-component mixtures with potential for migration and adverse reaction. Their biocompatibility characteristics are much worse than that of "medical" silicone oils typically used to lubricate syringe barrels or "solid" silicone rubbers included in many other classes of medical implants. However, the type of gel used in products associated with the Natural-Y technology differs grossly from many other contemporary types. There is no satisfactory explanation for this observation. Possibilities include errors in formulation, contamination of the batches, incorrect vulcanization or possibly deviations from recorded formulae. Many items from these production series are noted to have gels that are "brittle" and decant spontaneously to very fluid oils and comparatively coherent "lumps". The toxicological implications of such deviations are not researched; testing on gels was always conducted on "standard" formulae.

The uptake of gel components by tissues can contribute to fibrosis and affect the healing of the implant site. Residues from damaged gel prostheses can disperse into mobile bioabsorbable entities if there is a long delay between rupture and removal. Hyperplasia, adhesions and/or periprosthetic contracture generally worsen in the presence of oil contamination originating from leaky prostheses. Burst prostheses left in-situ for long periods correlate with systemic adverse effects in many patients.

Prolonged use of leaky devices increases the risk of systemic diseases in proportion to the time that the devices are worn and the rate of ingress of foreign material into tissue. The presence of foam debris and adhesive fragments exacerbate these effects. They stimulate phagocytotic activity in the area. All of these factors appear to be at their optimum for adverse reactions from foam prostheses. This may explain the rapid deterioration of some patients who have a history of multiple implants and where the last implant is a foam device.

Use of "Outdated" Foam Implants:

Foam implants effuse oil during the storage period; the foam progressively absorbs oil, reaching levels in some cases in excess of 30% of the foam’s dry weight. During the post-implantation period the foam absorbs quickly leaving behind an inflammatory, finely dispersed adulterated silicone oil in the immature capsule. The use of a foam implant from 1-3 years after its production amounts to injecting a bolus of impure silicone oil of about 1-3 gm.

Interaction of Foam and Tissue:

The fate of the very fine foam fragments over the long term is still the object of kinetic studies in several laboratories. What is known is that the very fine debris is long lasting. However, it represents from 2 to 20% of the original mass of foam. The resorption rate is strongly affected by the simultaneous presence of silicone oils, adhesive (RTV) and gel which act as protective coatings against degradation of the foam. The adhesive layer used to bond the foam to the shell is also vulnerable to erosion, comminution and biodegradation. Its terminal condition consists of very fine fibrosis-inducing fragments which are readily carried away from the implant site and which elicit macrophage activity. In summary, the scavenging of spallated debris from devices of this kind is a long and uncertain task with attendant risks which increase, in particular with the use of Bovie and thermal cautery.

Surgical Removal of Foam Coated Implants:

Foam covered implants are difficult to remove conservatively. In the light of present knowledge, exhaustive scavenging of such implants and their debris is necessary. This may be achieved optimally by removal of the implants, the foam coating residuals and part of the surrounding capsular tissue as a monolithic unit via extracapsular capsulectomy with the device still in situ. Alternately, enucleation and removal of the implant core (silicone shell and gel-filling) followed by dissection of the polyurethane debris contaminated capsule may be practical if the silicone shell is still intact and if the capsule tissue has matured to a reasonably coherent substance . Such variations of ablative capsulectomy are more laborious and more prone to contaminating the surgical field with prosthetic debris.

Pre-surgical radiologic studies (xeromammography, MRI) generally facilitate the delineation of contaminated tissue, silicone exudate and solid debris that surround the prosthesis and are valuable in cases involving ruptured and extravasated devices. The feasibility of a punctual capsulectomy procedure varies with the age of the implant and the original insertion technique. The shell coating usually remains coherent for several days after the implantation and removal during that period may be practical.

However, degradation of the foam is rapid. With an "immature" implant in the early post operative phase, the original foam layer softens and peels off the shell core spontaneously in vivo; the foam also looses most of its tensile strength within a month or two. Tissue may then grow into the weakened porous material and eventually consolidate it, but this composite layer of plastic, foam and tissue may not be initially strong or coherent enough for complete removal. As a result, early explantation with extemporaneous scavenging of this immature capsular material may be a difficult and uncertain task with marginal benefits. Removal appears easier after about 18-24 months have elapsed.

There are supplemental risks in removing partly decomposed foam earlier than about 18 months post-implantation. They arise from possibility of infection from surgery and the difficulty in treating patients with foam fragments that have become infected. Many patients have experienced post-surgical infection; the damage it causes can be greater than what could result from leaving an asymptomatic device in place until the natural end of its service life.

Ablative capsulectomy with implanted foam prostheses left in situ for a brief period are difficult because the hyalinized portion of the capsule generally remains friable; an obvious cleavage plane does not appear between such capsules and the surrounding tissue. The boundary is frequently made even more irregular by embedded fragments of partly digested foam.. If an attempt is made to remove the foam layer that has detached from the surface of the prosthesis, it can remain partly attached to the immature capsule, thus making the capsule even more difficult to resect neatly.

Traction applied to the residual foam causes it to shred and much of it can stay within the capsule tissue. This weak tissue must then be removed separately with sharp dissection. Electrodissection (Bovie cutting) cannot be safely used because of toxic pyrolysis products from the foam-tissue composite.

At that stage, the foam is still full of small pores that can protect bacteria if it ever got infected for any reason. After about 18-24 months, the foam usually opens up and dissolves partly. It leaves nonporous debris behind which, in principle, should be easier to treat if somehow got infected. Waiting, on the other hand, exposes the patient to a greater amount of soluble toxic degradation products. However most of the covering seem to degrade and come out as soluble products in the first 2-3 years. The release rate of degradation products then diminishes to the point that the implants behave similarly to conventional prostheses without foam.

Except for the Meme ME (Natural-Y/Aesthetech) prostheses, which are particularly weak and leaky from the outset, this class of prosthesis has a envelope (shell) life expectancy of about 5-7 years for an average user. An athletic patient with the implant underneath the muscle should expect somewhat less. The main risk then is gross leakage of the filling gel through small perforations or outright rupture of the silicone inner shell.

Contrary to the manufacturer's repeated claims, severe contracture can also take place with polyurethane implants and thus the patient may also have to consider removal to regain aesthetics and/or comfort.

In summary the device, once in place for about a month, an immature implant-capsule composite cannot be taken out without enhanced risks of supplemental complications for 12-24 months. The alternative may be to leave the prosthesis in place as long as it is not burst (normally about 4-5 years). Concurrently, the condition of the shell should be evaluated through mammography every year for the first 3-4 years and every 6-8 months after that.

Removal is a specialized task. Unlike implantations, ablative procedures involving foam prostheses can rarely be satisfactorily performed in improvised private surgeries. They have greater risks of post surgical problems such as hematomas and seromas and may require more extended convalescence. They can lead to a significantly greater reduction of breast volume with corresponding loss of aesthetic effect than their smooth wall analogs .

Electrosurgery and Foam Prostheses:

The use of electrosurgical procedures such as electro-dissection and electrocautery, two procedures believed essential for the safe removal of breast prostheses with mature capsules, lead to the formation of significant amounts of injurious substances. The pyrolysis of polyurethane debris and silicone-based material results in toxic, mutagenic and immunogenic substances such as amine-oxides, amines, carbamates, silica, as well as other combustion products suspected of adverse bioactive effects.

Risks from Unresected Foam and Adhesive Residuals:

Foam and adhesive debris cannot be removed exhaustively without elaborate extracapsular capsulectomy procedures. In situations involving ruptures and avulsion of the foam coating into disorganized clusters, extracapsular debris may also be present. This debris takes the form of conplex tissue-foam-adhesive composites and may be remote from the main periprosthetic capsule.

The insertion of prostheses though axillary incisions are particularly prone to this problem. Infra areolar implantions share the problem but to a lesser degree. Such deposits of foreign material are discernable under radiology, MRI and sonography. Predictably, their resection leads to supplemental loss of tissue. Risks contamination of the surgical site is also more severe for these patients and adds to the risks of removing the implants.

Leaving the encapsulated debris in situ is not a logical alternative. These ‘pockets’ of bioreactive debris and poorly irrigated tissue create an environment which is propitious for aberrant biochemical and biophysical processes and are associated with lasting inflammatory diseases. If they formed as sequelae to implant ruptures or were created through compression capsulotomy procedures, they may pose major infection risks and radiological interpretation difficulties.

The clinical management protocols for patients with this profile have not yet been developed. Consequently, additional risks and costs arising from necessary human experimentation aimed at developing corrective protocols may compound the adverse effects from the prostheses themselves.