Impact of Breast Implants on Users:

A mammary prosthesis can injure a user in many ways. Some implants need not even suffer frank shell rupture or gross perforation to induce major health problems. Effusive loss of mobile impurities, errors in material formulation, incorrect sterilization, tissue-incompatible surface coatings, inappropriate shell designs and adverse interactive effects between implants and capsules can initiate or worsen serious diseases.

In addition, the physiologic consequences of inserting large, coarsely manufactured foreign bodies in a disease-prone part of the human body can lead to mechanical or physiologic damage such as deformity, discomfort, pain, neuro-sensorial changes, ischemia and other lasting problems.

In some cases, the problems are simply the result of forcibly fitting a device of a significant size in a space that was never meant to contain it. However, others adverse effects have more complex mechanisms that have to do with pharmacological, infective and immunological processes that take place within the space between the implant and its surrounding semipermeable tissue capsule.

Inappropriate implantation procedures and flawed surgery often create additional problems and exacerbate pre-existing diseases. The surgery which evolved in support of this technology was optimized for speed and early aesthetic gratification as opposed to lasting comfort or breast health. The environment where such surgery is carried out is frequently inappropriate. Many surgical suites are totally unsuited for implant procedures in terms of design, instrumentation, environment control, cleanliness and microbiological safety.

Sterility is important in any surgical context but it is a key consideration in procedures which involve implants. The surgical fields that receive "permanent" implants are susceptible to tenacious infective processes. Elaborate measures for control of sterility in the implant space are required to ensure even a modest success.

Extemporaneous office settings and improvised stand-alone surgeries are unsuited for this medical technology. Even with ideal implants, "improvised" surgical settings are subject to serious sterility pitfalls with lasting consequences for the patient. In retrospect, these factors account for much morbidity in cosmetic and reconstructive breast surgery.

There are important variations between patients which make some more vulnerable than others to deficient implants and marginal surgical practices, in particular deficiencies in implant design, material composition, implant site preparation and infection control.

The background of the implant user predetermines the" service life" of the surgical procedure and the severity of late implant problems. There are significant variations amongst different individuals ability to tolerate implants, in particular large surface area, debris releasing, low quality devices such as breast implants. Some of these variations may be traceable to genetic or disease history of the individual. Others relate to prior medico-surgical treatments.

The special vulnerability of albino, celtic, nordic and northern caucasian phenotypes (depigmented skin tone, "freckled", red or pale blond hair, gray or blue eyes) to tissue diseases and surgical complications is reflected in adverse reaction risks to implants and poor long term prognosis when complications set-in. Conversely, negroid phenotypes are generally recognized as prone to proliferative tissue and scarring phenomena; many present with intractable implant capsules and post-implant complications. Individuals subjected to thyroid and thymus gamma irradiation as children, treated with certain pharmaceuticals (novobiocin, chloromycetin, etc) also show selective problems which appear creditable to such treatments.

However, the breast surgery history of an implant user inevitably decides the long term outcome of a new implant procedure. Replacement of implants is commonplace and patients with records of five or more replacement surgeries are not rare. Failed implants also tend to leave long lasting local and systemic damages.

Most cosmetic and plastic surgeons try to replace unsatisfactory implants and patients feel compelled to accept replacement for fear of deformity. Regrettably, there are generally no lasting cosmetic benefits or remission of symptoms with simple implant replacement. The errors of past breast surgeries and earlier implant misadventures are generally cumulative. Replacement may provide a temporarily gratifying result but, after a brief remission, the problems return.

It is not uncommon to encounter implant-bearing patients with ongoing disease processes induced by failed implants removed many years before. This sometimes explains why recently implanted and nearly new prostheses are removed from symptomatic patients. Their problems may stem from prior prostheses while their current implants and the capsules maintain conditions suitable for ongoing disease processes.

The capsules which form around the prostheses are also difficult to assess. They are not "normal" connective tissue structures. They are often the decisive factors that complicate existing diseases or create new ones. Such capsules can contain large amounts of prosthetic debris and modified natural substances with scope for adverse effects. Typically, they incorporate prosthetic debris, oils, coarse mineral deposits and denatured tissue.

Deep colonization by atypical micro-organisms and embedded solid metabolites from the entities are also frequent. Granulomatous reaction products to foreign debris of synthetic or micro-biological origin generally co-exist with the tissues. Failure to retrieve this material at explantation delays healing. It can also have lasting adverse consequences.

Progress in Mammary Implant Technology:

Mammary prostheses have long been marginal products aimed at a professional community that has not habitually been concerned with product quality or long term safety and durability of implants. Furthermore, the implants themselves have mostly been common low cost items based on faulty scientific and engineering concepts. Manufactured in large volumes with minimal quality assurance and considerable variations from batch to batch, their marketability was dependent on aggressive promotion, protection from adverse reaction reporting and exaggeration of performance and benefit claims. It seems that the industry was driven primarily by the appeal of widespread cosmetic augmentations as opposed to post-cancer reconstruction procedures.

In spite of three decades of implantation and the production of more than 6 million units, the devices and the implantation techniques have not progressed significantly. Preferred quoted research focusses principally on favorable or trivial aspects of the art. Adverse results receive little attention. Well publicized but superficial epidemiological and psycho-behavioral surveys emphasize illusory benefits and infer the absence of adverse effects. Promotion by manufacturers and cosmetic surgery clinics continue in the U.S. and abroad. Official disclosure of serious long term problems to government agencies, clinicians and users were very rare.

In retrospect, the technology appears to have deteriorated since the 1970s and the basic product designs have become worse with time, reaching their nadir in the early 1980s. Clinical failures then became so common that they were perceived as "normal" or unimportant. Evidently the surgical community and the industry that supported it failed to learn from past failures and consistently disregarded well established biomedical principles in favor of speed, volume and profitability of a promotable cosmetic procedure.

By the late 1980s, adverse reactions encountered by users in great numbers were predictably the result of these factors in combination. Presently, the mechanisms of injury may vary from case to case but the pattern of failure and the type of implant-associated diseases are predictable and consistent with the accumulated adverse information, including the early work on free silicone oil injections to the breast and the face. The pattern becomes even more evident when the product type, the dwell time and the surgical factors are taken into consideration.

The insertion of ill-conceived implants in a disease prone area has potential for injury which rises with the dwell time of the product. It is well established that the implants cause major structural, physiological and biochemical changes in the breast environment. They also act as "time release systems" for pharmacologically active compounds.

Prosthetic injuries in breast implant users can be attributed to at least six major mechanisms: (1) surgical trauma and surgical misadventures resulting in damage to functional/sensorial parts of the chest and the muscle of 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 remodeling 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 (auto-immune disturbances); (6) pathologic effects induced through bacterial, viral or fungal colonization of the capsule space leading to low grade chronic infections and toxic phenomena associated with microbiological metabolites.

For most long term users, all of these effects are present to some degree concurrently. Their 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 for systemic adverse effects. Protected intracapsular infections that remain for a long time have the ability to enhance capsular fibrosis and 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 these toxins may account for disturbances noted in some long term prosthetic users.

Capsule problems are common in prosthetic patients in general. The literature makes reference to cases where incompletely removed capsules with prosthestic 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 chemical debris establishes a condition which produces bioactive mixtures of silicone compounds with dispersions of denatured proteins.

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 maintained, capsule wall lysis takes place. When capsule integrity is breached, accumulated denatured (lysed) tissue, prosthetic silicones and proteinaceous material from the bacterial and/or fungal colonies escapes.

This mixture has properties similar to Freund's complete adjuvant; mixed with denatured autogenous tissue, it can elicit the formation of antibodies against the denatured autogenous tissue proteins. Eventually, with time, sensitization to the protein itself becomes possible (autoimmunity). Clinically evident damages result when the titre of auto-antibodies rises to the point where the rate of destruction of natural tissue becomes greater than the rate of repair.

Silicone compounds of this class were investigated for possible commercial development as immuno-stimulants (modified Freund adjuvants for in-vivo and in-vitro applications). The work was performed by Dow Corning staff in the early seventies and some of the results appeared in confidential memoranda issued in 1974 (LeVier and Boley studies on adjuvant effects of silicone compounds and 1975; Lake and Redonovich studies on pharmacology of silicone derivatives, Bennett memoranda and proposals).

Studies on the pharmacological activity and the ability of low molecular weight silicone compounds to serve as synergistic potentiators for riot control agents, chemical warfare and agricultural pesticides were also explored and reported in part by the same group. The validity of the original immunologic studies was reconfirmed independently by Naim in 1991-93.

More recent 1992-93 studies by staff scientists at Dow Corning and others also supported the original discoveries and identified gel types with marked immuno-active properties. Concurrent work by Kossovski and associates on the serology of prosthetic patients characterized antibodies specific to silicones associated proteins. Such work performed on long term users of breast implants gives additional credence to Dow Corning's reseach the immuno-modulating properties of silicone-derived substances in humans.

There is a long standing consensus that many silicone-based compounds similar to those found in mammary implants are pharmacologically active. It is also well known within the chemical professions that many members of the silicones family can act as dispersants, emulsifiers, biological adjuvants and promoters of immune phenomena as well as facilitate the absorption of toxic chemical entities which would not otherwise enter living organisms.

Implant studies document long term biodegradation and bio-erosion of the shell materials used for saline and aqueous solution-filled multi-lumen prostheses. The deteriorative processes results in embrittlement of the material, erosion of the polymer matrix as well as exposure and spallation of silica fillers in the form of reactive agglomerates.

This bioactive silica originates from the silica reinforcing fillers incorporated in silicone elastomers. These compounds are an intrinsic component of most shells. They are present in the finished products at levels of 10-30%. Other types of fillers such as titanium dioxide and aluminium oxide are also encountered as fillers and opacifiers in some brands of implants.

The resulting biodegraded silica agglomerates are coarse, bioactive and co-exists with intracapsular calcific crystalline structures which further enhance the tissue interaction by abrading against the contiguous tissues. Silica in the form of natural aggregates of similar size has been recognized as an occupational hazard since the turn of the century. It is associated with tissue fibrosis and atypical auto-immune diseases when in prolonged contact with soft tissue and organs.

The use of thermal cautery and electrosurgery (Bovie dissection) for removal of tissue proximal to extravasated gel prostheses also generates silica in-situ through pyrolysis of silicones. This material is difficult to remove from the surgical site. It remains deeply embedded in tissues and is frequently found in capsular tissue of prosthesis users, in particular if they have a history of multiple implant misadventures .

The formation of mineralized tissue is commonplace in long term implant users and the process is often a decisive limitation on the ultimate service life of the device. This situation prevails for biologically derived implants such as animal tissue cardiac valve prostheses and stabilized tissue vascular prostheses. Totally synthetic implants can also induce the deposition of minerals in their surroundings. However, these situations are drastically different from what is routinely encountered in users of early breast prostheses.

Individuals with early style implants incorporating tissue fixation systems are very prone to the process. The very early Dow Corning devices fitted with large Dacron fabric backplates offer some of the most spectacular examples of gross atypical mineralization.

Many other devices without fixation systems also calcify abundantly in different ways after about 15-20 years in situ. Saline filled implants manufactured prior to the mid eighties are commonly found with grossly calcified shells where the mineralization process has penetrated deeply into the elastomer rendering it permeable and brittle.

More recently marketed items are also occasionally found with significant amounts of finely divided mineralization dispersed in the periprosthetic tissues. Anecdotal observations of such mineralization are numerous and many pathologists routinely describe the calcific entities as "dystrophic breast calcification".

Implant-related mineral deposits are evidence of catabolic activity and are unlike entities found in implant-free breasts which include small spheroidal calcific concretions (frequently seen in mammograms of normal breasts from older patients). They are also unlike spicular calcific microcrystals arranged in clustered or radiating patterns that are also encountered in breasts without implants but with aggressive tumors; their presence is regarded as reliable radiodiagnostic criteria for neoplastic anomalies.

The aetiology and the basic mechanism of formation for these "natural"structures are not the same as prosthetically induced mineralization but appear nevertheless related insofar that they are pathological and reflect ongoing tissue destruction. They are unlike true osseotropic phenomena such as bone mineralization which are primarily driven by epitaxial crystal deposition on specialized structural proteins.

The formation of periprosthetic, dystrophic and tumor-associated calcification are deemed to be sequelae of chronic tissue destruction and necrosis occurring over long time spans. The morphological differences between the entities formed are primarily creditable to the mechanism and the rate of catabolic processes and the differences in the environment where the tissue destroying activity is taking place.

Tissue destruction can result from mechanical (abrasion, disruption, comminution), chemical (toxicological, hypoxic, desiccative) and microbiological (lytic, proteolytic) damage to cell organelles and structural proteins. All of these conditions are met in the closed space around an implant. Unique physico-chemical, physiologic and biochemical environments develop early around such prostheses and eventually the intracapsular space becomes a specialized isolated compartment with a composition that deviates markedly from extracellular fluids, where non-equilibrium conditions prevail and where otherwise unfavored or forbidden biochemical processes take place. Its characteristics compare to that of an active wound site with foreign debris, synthetic oils and catalytic substances surrounded by a diffusion-controlling barrier membrane. In effect, these compartments become self-regulating environments with a capacity to form chemical and biological products that reflect local composition as opposed to normal tissue metabolites.

This favors aberrant anabolic and catabolic processes. After several years, the periprosthetic implant space becomes heavily contaminated by leached synthetic impurities released from the implant. Capsular tissues and extracellular products trapped in the zone also deteriorate to form metabolites. These entities would normally be removed from the site and eliminated or converted elsewhere via natural processes. Thus the damage would appear elsewhere if it were not for containment by the capsule wall.

As it matures, the capsule densifies and becomes progressively more impregnated with oils and shell debris; it is a diffusion controlling membrane which regulates the intracapsular environment. Later, the capsule becomes much less permeable and the environment becomes stagnant. The traumatic effects of sharp perforating crystalline inclusions in vascularized tissue causes periodic leakage of blood and blood proteins into the compartment thus increasing the diversity and the reactivity of the incubating mixture.

Eventually the integrity of the capsule membrane is lost through erosion, lysis and excoriation. The semi-fluid mixture of denatured proteins, fine calcific debris, cell and tissue fragments and grossly contaminated extracellular fluids escape into the breast and the regional lymph nodes. Shell particles and silicone oil emulsion adds to the diversity of the mixture, generally triggering systemic symptoms. Finally, the site becomes very uncomfortable from accumulated coarse solid calcific and prosthetic materials and the removal of the prosthetic debris becomes mandatory.

The removal of implant remnants is, however, difficult. Resection of the thickly encapsulated devices and their the associated contaminated tissues, add to add to the implants' injuries and complicate the post explantation recovery. Conditions leading to injuries from prosthetic mineralization processes , are reconstructed as follows:

(1) Fixation accessories such as the large surface area open Dacron fabric "patches" or related structural irregularities on the posterior side of the device such as protruding valve stems, shell patches or "suture loops" initiate inflammation. (2) Fibrosis locks the item deeply into the chest wall. (3) A thick fibrotic zone of dense pannus develops on the posterior face of the implant and the area loses much of its vasculature and permeability. (4) Hyperplasia and contracture of capsule tissue then accelerates and diffusion limitations causes tissue hypoxia and necrosis to set in. (5) Denaturing of tissue and other aberrant biological processes continue for many years with and a gradual release of soluble minerals in the form of ions takes place. (6) Intracapsular fluid supersaturation and poor fluid exchange in the are causes precipitation of the salts and complexes as solid crystalline entities. (7)t The intracapsular space becomes filled with grossly atypical minerals in the form of large, densely clustered plaques or compacted concretions of microcrystalline debris. (8) Some of these crystals develop sharp edges and form cutting structures which cause additional tissue trauma on movement. (9) Intracapsular bleeding takes place resulting in for deposition of hemosiderin within the capsule; low haematocrits and abnormally elevated haemoglobin nay be noted. (10) Continuing osseotropic remodelling affect the thoracic area and cause pain or limitation in expanding and contracting the thoracic cage. (11) Anatomic and physiologic changes affect the area; deformity or drastic changes become evident in the mechanical characteristics of the upper chest area. (12) Eventually the accretion of sharp, rigid debris becomes radiographically evident or even palpable in the vicinity of the prostheses and motivates the patient to seek removal of the devices. (13) The explanting surgeon then encounters a major problem in resecting the offending implants; in view of the large amount of surrounding mineral inclusions which cannot be penetrated by Bovie or sharp instruments. As a result, improvisation is required and extemporaneous methods are used to explant the prostheses and their fixation appendages.

Ultimately, such patients may require staged surgery in order to regain a reasonable level of comfort. Secondary surgery may also become necessary to retrieve residual prosthetic debris and secondary mineralization products. Radiographic follow-up is sometimes necessary during the post-operative period to ensure appropriate healing and the absence of fluid-filled pockets with risks of their own.

Injuries from Superficially Undamaged Prostheses:

Mammary prostheses and their associated surgical procedures are associated with morbidity and health care costs. There is a wide spectrum of injuries ranging from the benign to the very serious. Some injuries are direct consequences prosthetic system failure resulting in release of tissue-incompatible substances . Others result from mechanical, physicochemical and microbiological processes which take place in the space between the implants and the surrounding tissue capsules. Still others are sequelae of surgical misadventures. Sometimes it is a combination of all factors and it is necessary to review medical files to understand the relative impact of each of the factors. There are important variations amongst patients which make some more vulnerable than others to this technology.

Apparent anomalies are also found. In some cases, prostheses are removed and, to the eye of the surgeon or the pathologist, the devices appear superficially "intact" or "unchanged". Detailed examination of such explants nevertheless show significant chemical changes with potential for major adverse health impact through classical toxicology mechanisms.

Breast prostheses are not made to the same level of quality as other long term implants. They are low cost products manufactured in large volumes and with considerable variations from batch to batch. The technology embodied in the products precludes uniformity. At any rate, the cosmetic surgery products industry has not historically been noted for sophistication in research and production techniques. As a result, this class of medical products lacks the durability, quality, safety and efficacy expected of modern health care devices.

Breast implants and related products habitually undergo deep changes. They also initiate changes in the surrounding tissue, sometimes by absorbing and converting natural biological substances from the host into modified products with adverse health implications to the user. This process takes place in the intracapsular space and within folds of the shell which entrap tissue and proteinaceous fluids.

Capsules which form around the prostheses are decisive factors in initiating and maintaining a disease condition. This is why surgical centers with experience of medical removal advise patients to have this tissue excised. Some surgeons elect not to perform this procedure or else do it only in part. It is frequent to have such patients with capsule residuals return for surgery within one to three years in order to retrieve this material and its associated debris in the hope of resolving continuing health problems. Patients who have undergone multiple replacement of implants or who have encountered immediate post-surgical problems are particularly vulnerable to such effects.

Many patients are in this situation and tend to be left puzzled as to what has affected them during the time they had the devices in place. There are numerous explanations for problems encountered by breast prosthetic patients. Some are the result of forcefitting a device of a significant size in a space that was never designed to contain it. Others are more complex and have to do with pharmacological and immunological effects that take place in the space between the implant and its surrounding artificIally-created tissue capsule.

Most patients who have been subjected to more than a few years of implant usage tend to be injured from a multiplicity of factors, some which relate directly to the implant but where most have suffered greater impact from capsule-related phenomena or mechano-anatomic dysfunction associated with interference of the large foreign object with essential functional structures in the vicinity of the upper chest.

Mechanisms Of Rupture; General Observations:

As shells expand, surface area is created and the devices become somewhat underfilled. Pleating, involution and invagination of the shell takes place with greater ease. Low profile items are specifically prone to the problem and their performance is much worse than the more puffy high profile versions which have less excess surface area.

Shell shows pleat patterns which are specific to shell styles and to the degree of filling. Severe pleating culminating in loss of shell integrity is encountered in most implants after about 7-10 years in vivo. Such pleats may have been less prominent shortly after implantation as the shell may have been less swollen and thus would have behaved as if I was more fully filled. surplus surface area.

Pleats and creases severely limit shell durability. Many implant styles incorporate unique design features that facilitate pleating. Others have semi-rigid features which create high stress pleats in vulnerable areas. Patches, filling ports and fixation appendages are strong contributions to the formation of destructive pleats and puckers which concentrate fatigue and focally strain the material beyond its elastic limits.

These features can greatly increase the risks of rupture and magnify injuries by insidiously releasing larger quantities of the filling substances with time thus dulling the user’s perception of problems . Intracapsular spaces gradually flood with oils and gel by-products and users do not perceive the changes in sensation dramatically. They are thus motivated to delay action until the problems become severe as the oil/gel infiltrated tissue masses become palpable or when systemic problems develop.

Why Implants Rupture; Etiology of Shell and Containment Failure:

Many shells consists of incorrectly formulated and poorly processed elastomer parts. Usually, the crosslink density is insufficient or non-uniform. Such shells are subject to plasticization primarily from low molecular reactive oils and degradation products released by the gel. The mixing of gel with aqueous substances in the presence of catalytic impurities leads to loss of crosslinks and reduction of molecular weight in certain formulations. Low molecular weight entities formed in most instances.

The shells of used implants are frequently found swollen and distended. Typically, about 10 % linear swelling is encountered. The phenomenon is visible on simple inspection. Patches and injection port boundaries, in particular for implant designs incorporating fabric reinforcement, show stress pleats radiating peripherally. This confirms significant changes in surface area of the shell as a result of physico-chemical alterations of the material as low molecular products interact with the elastomer.

Explanted prostheses, on average, show pleat failure that antedate the surgical removal by many years as evidenced by the extensive development of deep pleats with drastic local changes in elastomer properties and deep iol incorporation in tissue. Crazing on pleats and refractive index changes are almost always encountered in thick-shelled implants. Once crazed, the affected areas rapidly become porous allowing further leakage of low viscosity substances. There are concurrent reduction in mechanical properties of the shell which impact adversely on tear strength, elongation and tenacity.

Longer dwell times are generally needed for development of grossly visible shell rupture points, usually 1-3 years. Progression of fatigue-induced damage takes place at a rate related to the user's work habits and is affected by the relationship of the devices to the chest structure. For underfilled or swollen implants, compression is not a significant factor in the enlargement of perforations. Contrary to frequently expressed opinions from individuals not fluent with elastomeric material properties, such shell failures show unique characteristics. They are unrelated to trauma, impact or surgical mishandling. It terminal stages, the condition of the shells becomes so unstable that they cannot even sustain movement and stresses of explantation surgery without further propagation of failure lines.

Certain designs incorporating aqueous media compartments are notorious for releasing their low viscosity fluids over time. Saline inflatable implants, mixed gel-saline devices and multi-lumen prostheses gradually leak their aqueous additives. As a result, they lose part of their volume and become grossly underfilled. Pleating becomes more severe and crease fatigue rapidly lead to small shell perforations. Eventually the perforations enlarge to become gross rupture sites which progress with time and movement. Failures of this kind are typical of silicone elastomer shells manufactured according to processes which prevailed throughout the industry from the seventies to the nineties. Items manufactured in the early-eighties were particularly affected by the process. They account for more than 60 % failure rates in all such series.

Mechanical and dimensional effects such as device shape, nominal size, shell thickness, position of valves and patches interact. Typically, less compliant materials and thick shells are more prone to early fatigue failures at crease sites. They concentrate stresses and stains and buckle or pucker more easily than thin ones when deformed. Thick objects show increased stiffness and are much less tolerant of cyclic deformation than thin ones for the same reasons. This is well known in the electrical cable industry where large single conductors are avoided for applications subject to frequent bending and twisting movement. Multi-stranded or braided conductors or complex assemblies of thin foils and spiral tapes are preferred as the compliance and the durability of arrays of conductors can vary inversely with the fourth power of the thickness (or the diameter) of its constituent conductors.

Polymer-solute interactions such as swelling and degradative chemical phenomena are also involved. For example, the mixed gel-saline prostheses of the "Wood" type have an extremely poor record of durability and most show severe pleat and fatigue-induced ruptures with significant losses of gel/oil. This is primarily the result of changes in the shell ultrastructure aided by swelling from low molecular weight species.

Low viscosity oils are formed by aqueous degradation of siloxanes at pH exceeding 7-8. Grossly visible focal degradation of the elastomeric material at points of stress concentration is noted early and is evidenced by changes in refractive index and increase light scattering. Cyclic folding and rolling or displacement of the pleat line associated with normal in vivo usage is a dominant factor in accelerating the process.

Contracture of periprosthetic capsules contribute significantly to early ruptures as it increases compression on pleats. In most cases, the process rapidly leads to visible crazing at pleat sites, especially areas which show confluence points and cross-over of pleats and pucker zones. Creases which occasionally take place on seams and on patches are particularly destructive. They generally induce rapid failure of the structure at the thickest points. Delamination of patch laps and debonding of gel fill hole seals can also take place for devices that use marginal bonding processes or outdated adhesives. Formation of abrasive substances on the capsule wall accelerate the destructive processes.

Stress concentration in polymers increases the reactivity of elastomers at the stress sites. This is observable for all thermoplastics. Plasticized elastomers with high levels of impurity and irregular crosslinking introduced through secondary reactions (vulcanization), are strongly subject to the effect. Failures of this kind dominate breast implant studies.

Pleat-induced rupture and shell fatigue failure have been extensively studied. The processes are well known in select circles of plastic surgery insiders and within the breast implant industry. Complaints, litigation, product returns, patents and texbooks on polymer science as well as corporate business records spanning more than 25 years address these issues.

Injury from Trauma with Prostheses in Situ:

Users of mammary prostheses are subject to special modes of injury which result from the presence of a foreign object placed below a comparatively thin skin cover; this object acts in a similar way to an ‘anvil’ by concentrating the force of a traumatic event against the overlying tissue. The possibility of damage to an impaired prosthesis from trauma also exists but is overshadowed by what generally occurs to surrounding tissue. With widespread use of compression capsulotomy as a ‘therapy’ for contracture, iatrogenically-induced trauma to breast tissue is also a major part of the risks encountered by users of prostheses.

It is normal to expect injuries from traumatic events. It is also logical to expect the magnitude of the injuries to reflect the severity of trauma. Subjects with prosthetic systems in the upper chest area are not exempted from these rules. However, the mechanism of injury and the type of injury differ substantially from normal subjects. In addition, prosthetic damage which may result from the trauma is not what is expected on the basis of simple anatomic considerations. The intercalation of a large, soft and elastic device within a comparatively large mass of soft tissue drastically alters the biomechanical properties of the area and modifies the behavior of the mass to the point where new types of injuries must be considered.

Primary impact and crushing injuries to the upper chest area include mostly hard tissue damage, rupture of blood vessels leading to hematomas and seromas, glandular tissue injury leading to oedema, nerve damage culminating in late pain, cartilage trauma, and separation of muscle attachment points, muscle damage associated with overextension and deep trauma involving transmission of energy to more fragile internal organs, such as the liver. In many patients, this translates most frequently as rib cage injury such as fractures with associated secondary soft tissue damage. These are commonly encountered under trauma conditions and are expected by trauma centre clinicians who habitually treat accident victims. For subjects with prostheses, all of the above damages are possible.

Other types of less frequent injuries are often encountered as well. Surprisingly, frank damages to sound prostheses are encountered but are comparatively rare. Frequently, failed prostheses or severely aged devices which are already compromised lose their integrity and release their content. Simultaneously, the tissue-containment pocket (prosthetic capsule) is often ruptured. As a result, gross contamination of surrounding tissue by prosthetic debris is amongst the secondary sequelae. Such material can spread and extrude deeply within muscle planes and may reach well beyond the confines of the original prosthetic site. Extrusion to the axillae and the upper arm are reported as well as downward extravasation into the abdominal area. Prosthetic damage can be demonstrated to have pre-existed the traumatic events for most cases.

Prostheses in the traumatized area magnifies the injuries and complicates the emergency treatment. They may also create conditions where emergency care is not sufficient. There is need for prolonged follow up to forestall late complications and ensure appropriate management of late sequelae. The most frequent complication results from occult bleeding within the prosthetic space. Other complications include post-traumatic infections arising from release of accumulated micro-organisms within the prosthetic space (intracapsular colonization). Failure of compromised shells or valves in contaminated saline-filled prosthetic systems account for other forms of post-traumatic complications with late sequelae.

Failure of the prosthetic device is not a dominant preoccupation for comparatively new implants. Devices with less than 4-5 years of dwell time and of reasonable quality do not fail from traumatic events, least of all impact. Perforation damages are possible but these are rare. Yet there are numerous anecdotes claiming rupture of implants from trauma. The episodes appear largely inaccurate on detailed analysis. Implants claimed to have suffered failure as a result of trauma were, in all cases studied by this facility, either already ruptured and partly contained within the tissue capsule or else the shells were severely compromised through pleating, fatigue, abrasion or material deterioration.

Implants, when new, are surprisingly hardy or "elastic". They remain that way for a certain period of time, usually about 4-5 years. Studies performed by Dow Corning in connection with the defense of product liability claims support this view. Dow Corning experts further claim (Turner v. Dow, Colorado, 1993) that prosthetic devices can sustain enormous pressures that far exceed any realistic impact or sustained compressive trauma. They further claim that the devices remain that way indefinitely. According to the Dow Corning defense position, there is no basis to fear failure of prostheses from pressures that may be generated by a vehicle accident or deliberately induced "therapeutic compression capsulotomy" that would not cause gross anatomic damage such as broken ribs.

Such a position has validity only in the first few years of dwell time for some types of new prostheses. Shortly after implantation, the properties of the shell begin to change and eventually after 5-10 years shell failure takes place even without significant externally-induced trauma. This is a material problem and is the result of aging, "coldworking" and fatigue along pleat lines. Aging and deterioration occur through chemical, physico-chemical and mechano-physical processes. The decisive factors arise from repetitious movements associated with daily occupations. Concurrently, the implant shell materials decay by loss of bonding between the filler particles (silica reinforcement additives).

Penetration of the shell elastomer by interactive biological substances such as lipids lead to losses in mechanical properties. This is termed "plasticization phenomena". The problem was encountered first in the sixties in connection with cardiac valve components. Outright chemical changes can also take place in some classes of formulated silicone elastomers; these affect parts of the siloxane backbone and/or the crosslink sites. Stuctures which incorporate residual unsaturation (double bonds) and reactive pendant chemical groups are most vulnerable.

Reactions introduce defects in the molecular network thus enhancing the chemical vulnerability. The formation of vulnerable segments in the elastomer network takes place concurrently with normal synthesis (polymerization) of the primary polymer components and during the crosslinking reactions that lead to the finished elastomers. These anomalous chemical sites can occur in large numbers under coarse industrial preparative conditions.

Mechanical phenomena superpose on chemical deterioration. Mechanical properties of the elastomers are severely changed along crease lines and in areas subject to repetitious flexing and bending. This kind of deformation is almost universally encountered in explanted breast prostheses. These items suffer the predictable result of having been haphazardly packed into a prosthetic space for a long period of time.

Specific geometric patterns of pleating that vary according to the prosthesis type, size and position are noted. The deployment of such devices within the breast pocket is particularly critical in that respect; contracted capsules around severely pleated implants tend to induce early failure. Calcified capsules are also precursor signs of early failure along pleat lines through abrasive phenomena.

Calcific entities tend to excoriate the shell at prominent pleat points; this is particularly notable for devices which form large organized crystalline aggregates in the intracapsular space (margin calcification). Devices surrounded by such debris inevitably culminate in shell failure by mixed abrasive and fatigue-inducing processes. They may not be grossly ruptured as long as the periprosthetic capsule is in place undisturbed. However, minor trauma including that from daily occupations, is sufficient to complete the damage to full ruptures in many instances. At any rate, rupture ultimately develops even without trauma.

After approximately 4-7 years, implants develop a significant number of flaws and most have severely compromised shells. The more durable kinds tend to be the ones manufactured from simple shell configurations which are fully filled. This type of structure does not pleat as easily and assuming that gross chemical deterioration of the shell material has not taken place, perforations occur late. Most, however, though not grossly perforated or frankly ruptured show microscopic damage zones which coincide with planes of weakening. These clusters of defects are mechanically equivalent to the "dotted perforations" found on paper documents that have detachable portions where machine-made perforations facilitate precise tearing along dotted lines.

Impact trauma associated with vehicle accidents and falls are habitually of much lesser importance than deterioration or slow compressive trauma. This has to do with the nature of the implant filling material. Silicone-based filling gels that are correctly engineered have marked viscoelastic properties. These materials, at high rates of deformation such as may be met during a severe impact, behave nearly as "solid" objects; they do not deform substantially on impact.

Instead, they transmit energy to the support structures, usually the rib cage. The result is rib fracture or other mechanical damage to the chest. Capsule damage then subsequently follows, usually resulting in a rupture involving the upper medial anterior zone, an area where the tissue wall is generally the thinnest. Within the next few seconds, deformation of the shell does indeed take place and may complete the apparent failure of an already ruptured or compromised shell with severe extrusion of the gel. However, for a sound shell, the impact will leave the prosthesis undamaged and only tissue damage is observed.

Slow compression with a very large deformation can occur in a collision where the occupant is compressed and immobilized for a substantial period of time within the crushed vehicle space. An equivalent situation would be met by someone constrained within an array of seatbelts for several minutes. These situations may cause sufficient deformation to rupture an already compromised implant. However, unless the applied pressure causes deformation such as total flattening of a prosthesis to a thickness of less than 1 cm, rupture will not take place. Instead, a "closed capsulotomy" of the surrounding tissue may result. This type of compression termed "closed capsulotomy" or "compression capsulotomy" was at one time habitually prescribed for implant users with "capsular contracture", a condition that may affect as many as two patients out of three after five years of dwell time. According to certain physicians, this traumatic rupture of the capsule through compression was thought to be a "beneficial result".

Vehicle accidents or other traumatic events which cause impact to the upper chest do not habitually result in prosthesis damage. Instead, the periprosthetic tissue and structures may be more damaged than expected and the damage may be subtly different from what is normally found in normal accident victims. The presence of the prosthesis can hide more serious damage or delay the onset of key diagnostic symptoms. Hidden or delayed injuries include subtle rib fractures, the formation of intracapsular hematomas, muscle and cartilage detachment from the skeletal structure, rupture of blood vessels, impact damage transmitted to the more fragile internal organs (liver trauma) and other tissue damages that can be induced through large scale deformation. Adhesions between the capsule tissue, breast structure and chest muscles can add other injuries. However, events that do not lead to severe and prolonged compression or penetrating chest injury rarely have damaging effects on the prostheses.

The type of vehicle or event-induced trauma is also a key factor. Prosthetic damage can be expected for old devices, in particular if there is a large and sustained deformation such as may be expected when an accident leads to a vehicle compartment that is drastically crushed. Such a situation habitually leads to prolonged compression of the chest between the instrument panel or the steering assembly and the vehicle seat. A prosthetic rupture, however, requires enormous crushing loads maintained for significant periods of time, in effect a situation where the occupant is trapped in the vehicle.

Elastomers of the type used for breast prostheses have the ability to sustain large deformations when correctly manufactured. These deformations can be more than five to tenfold the original linear dimension of the material. For an average prosthesis, this means that the diameter of the device can be expanded by at least three to four times by compressing it. This is rarely possible without massive concurrent anatomic injury. Perforating trauma can occur from protruding objects which break the skin. These events can lead to frank tears or "shell rupture" through a combination of perforation, cutting, tear initiation and tear propagation but these are rare and are more typical of "anti-personnel" or "assault and battery" trauma.

Introduction:

One of the most remarkable characteristic of "saline-inflatable" breast implants is their ability to sustain microbiological activity within the saline-containing compartment. Another is their susceptibility to rapidly lose their saline filling charge because of valve failure or shell deterioration. Most fail through classical fatigue-related shell wall perforation, usually follow. The devices are also radio-opaque.

Such characteristics, independently and in combination have long term safety implications. On the basis of recovered implants and patient records, atypical infections and their sequelae account for a significant part of the morbidity and the public costs associated with the use of this technology.

The diagnostic of the condition and the clinical management of such patients present many challenges. The area requires additional study to establish the magnitude of the problems and the optimum treatment options. Similar consideration extends to certain other classes of trans-cutaneous "port" drug administration devices such as Hickman-type catheter systems. Inflatable penile implants and porous wall (textured) mammary implants are other devices that can incur microbiological colonization with elevated bioburdens.

The devices are still widely used and anecdotes of misadventures abound. Yet complications surrounding the use of saline filled devices appear drastically under-reported and the literature on the topic seems incomplete or possibly manipulated.

Finally, contrary to often repeated claims, all these devices are markedly radio-opaque. In tumor screening and post resection cancer follow-up procedures, the implants have the ability to obscure even large and dense proximal malignacies.

In summary, there is a worrisome paucity of meaningful data on the properties and performance of the devices. Moreover, the results of preliminary studies are discordant with information circulated by the proponents of such devices.

Historical Overview of Saline Implant Technology:

Saline mammary implants were introduced commercially in the mid-sixties. Early models were simple and robust. All were sold non-sterile. They required individual hospital sterilization as well as meticulously clean intraoperative procedures. Many gave excellent service for more than two decades and a few are still in use in original patients.

As demand grew, the quality diminished and many unsatisfactory designs were introduced. Most were promoted on the basis of lower prices, faster surgical implantation and more gratifying immediate appearance. By the late-seventies, the quality and performance had degraded to the point where seasoned clinicians avoided their use. Implants were deflating after several months and most perforated within 1-2 years following implantation.

Worse still, many were being explanted in grossly contaminated states with assorted viable and non-viable entities, sometimes visible to the naked eye. Intraoperative errors, manufacturing problems and inappropriate sterilization procedures were generally credited with the problem but its etiology and clinical significance were not widely recognized.

Many clinicians abandoned the products by 1980. Some successfully sued the manufacturers for loss of wages and damage to their reputation. The products then nearly vanished from the marketplace until their "renaissance" in the 1990s following a successful bid by the U.S. Food and Drug Administration to regulate the popular but problem-plagued gel-filled implants and other abuses surrounding silicone-based cosmetic surgery practices.

The instillation of pharmaceuticals added extemporaneously to solutions in the outer lumen of multi- compartment prostheses or to saline devices started in the early-70s. By the late-70s, several publications were advocating the procedure, notably that of Perrin. Other contemporary publications were outlining serious adverse affects. Initially promoted by plastic surgeons, the procedures met with strong objections from the pharmacologists and later fell into disfavor.

The use of assorted antibiotic and bacteriostatic pharmaceuticals was predicated on the basis that they would prevent proliferation of micro-organisms inside or outside the shell. Anti-inflammatories and other entities were expected to mitigate capsular contracture by slowly diffusing out through the leaky implant wall. Eventually the fad was extended to gel prostheses where the additive was sometimes injected through the shell wall.

The first commercial double lumen implants appeared in the early seventies. The design wa noting more than a conventional saline inflatable prosthesis which contained a smaller conventional gel-filled implant. Early products had large volume saline compartments. They were designed to address capsular contracture through optional deflation of the outer compartment.

By the mid-70s, another variation of the double lumen appeared. It was intended for pharmaceutical "doping" of the saline of the outer lumen by selected extemporaneous pharmaceuticals. Special variants of double lumen prostheses with very small saline volumes were designed in response to demand from proponents of the procedure.

Such devices with low outer (saline) volume were manufactured by most of the firms at the time. They initially promoted the technique but evidently met with objections from the pharmaceutical manufacturers whose products had been extemporaneously diverted for these applications. As a result, implant makers were later compelled to modify their product inserts to reflect that the inclusion of pharmaceuticals was an initiative of the surgeon.

By the late-70s, any individual skilled in the art would have been knowledgeable regarding the risks of contamination and the possibility of leakage of the outer compartment in double lumen and saline inflatable devices. Other studies had documented the rapid growth of micro-organisms in the outer shell of double lumens and salines. Publications to that effect had also appeared.

It is noteworthy that the surgical community as a whole always feared infection and growth of bacteria or fungi inside liquid-filled implants; this was a frequently-noted phenomenon. It follows that the instillation of pharmaceuticals designed for other purposes would have enhanced the risk of microbiological contamination and would present unknown supplemental risks arising from the deteriorating pharmaceuticals. Therefore, the state of the art at the time would have compelled clinicians and manufacturers to avoid the procedure.

The existence and continuing promotion of the low outer volume double lumen prostheses by manufacturers is by itself contradictory. In the light of published risks and failures to perform according to claims, the product would logically have been abandoned. At any rate, its use would appear, a priori, contrary to established standards of care surrounding the use of implants with aqueous media . The implant shells and their filling valves were generally known to allow the passage of chemical and even microbiological entities. Yet, these properties were exploited clinically by the very use of extemporaneously added pharmaceuticals (anti-inflammatories, antibiotics, cytotoxic agents, bacteriostats, etc).

These procedures fell into disuse when it was learned that all these products interacted and degraded quickly to toxicologically uncharacterized substances, some of which damaged the shells. Others such as steroidal anti-inflammatories were ineffective and were shown to entail significant health risks. At any rate, their use for these purposes was not well seen by manufacturers of the drugs. Device makers also objected to the practice in the later part of the episode. There never was a scientific basis for claimed benefits from the procedure.

Specific Risk Factors for Saline-Containing Systems:

All devices have been sold as sterile products since the late-seventies. Saline chambers with small amounts of viable micro-organisms occur occasionally. They may be improperly sterilized products. This problem beset the industry for many years and forced the introduction of specialized sterilization technology in the 1980s.

Because of the closed internal configuration of these devices, the validity of current sterilization techniques is still a contentious issue. Non-sterile compartments also reflect contaminated devices. Contamination can take the form of

surgically introduced pathogens during in situ filling as opposed to sterile field filling. Given the non-sterile character of the mammary gland, the introduction of viable entities from contact with extracellular fluids and breast tissue is very probable.

Additional pitfalls include re-sterilization attempts following unsanctioned device re-use or habitual filling with non-sterile substances. Deviations from established filling recommendations were commonplace in the recent past. Some of these procedures have been published and were once very popular. A few remain in use by some surgeons to this day.

Such procedures typically include filling with non-parenteral grades of electrolytes or colloids and extemporaneously prepared solutions of oral pharmaceuticals such as anti-infectives and anti-inflammatory steroids. The long term fate of these degraded mixtures in a closed environment is also worthy of consideration as "nutrients" to late arriving micro-organisms and in the context of chemically-mediated adverse reactions after shell rupture.

An inoculated prosthesis may remain in a biologically dormant state until the viable entities are provided with nutrients. If the filling substance contains no nutrient, no biological activity will take place. Alternately, the inocula may die spontaneously.

However, on balance of probability, some proteinaceous matter will eventually enter the compartment through valves, shell defects or late perforations. Paradoxically, very few valve designs demonstrate concern about this issue. Very few are secure even when new and definitive "plugs", cement seals and valve caps are rarely used even when available.

Most valves of the 1980s are simply variants of unidirectional flow control devices. They were developed for hydrocephalus drainage shunts. They allow inward flow and can be made to function as pumps that transfer liquid from the capsular space to the fluid compartment by manipulating the prosthesis-capsule assembly. There are therefore no reliable means of preventing nutrients from reaching an inoculum in these systems.

The Prosthesis as a Fermentation Reactor:

Inoculated devices with nutrients may not present an overt risk until the biological processes involve sufficient mass transfer to produce significant amounts of pathogenic material. In the early post-surgical period, the processes may be no more than survival of the most hardy entities and may not be sufficient to cause problems. However, with faulty valves and late perforations, conditions for proliferative colonization of the compartment will be met.

Even if sterile at the onset, leaky saline compartments constitute nearly idealized incubation zones for adventitious pathogens in the capsular space. Adjuvant-like impurities from leaky gel cores further complicate the chemistry of these pockets. They add to the denatured proteins, decaying tissue, fermenting pharmaceuticals and active micro-organisms. Scar tissue also re-form and can act as temporary plugs for the perforations, thus further improving the environment for less competitive micro-organisms such as anaerobes.

The cul-de-sac or "blind pocket" geometry of the area forbids irrigation by physiologic fluids or administered antibiotics. The limited oxygen permeability of the silicone wall favors anaerobic processes. Egress of this contamination eventually takes place in response to movement and pressure applied to the breast area. Dispersion of this material may periodically invade the prosthetic capsular space and may establish secondary colonies outside of the prosthesis. Symptoms of infection should appear at this stage but may resolve temporarily.

The composition materials placed in the interior of breast implants is not constant with time. Observations on silicone gel and saline-filled implants removed after in vivo dwell times of a few weeks show measurable amounts of particles evidently dislodged from the shells as well as uptake of water, ions, amino-acids, proteins, lipids and other substances originating from the host. Even "solid" silicone elastomer implants absorb and sometime reprecipitate endogeneous materials. After several months of use, the amounts are often visible to the eye unaided.

This is in contrasts to the behavior of most substances used for long term implants which include metals, inorganic glasses and other plastics widely used in medicine (Dacron™, Prolene™ etc). These materials have no detectable uptake of biological solutes even after many years of use.

Silicones of the type used here are permeable. They also incorporate large amounts of leacheables. They are compounded mixtures of large and small molecules that include unbound oils and mineral fillers. When made into shell membranes, they are very water and gas permeable from the outset.

As implants age shell permeability increases. Frank perforations ultimately develop when fatigue leads to fine crevices that propagates across the full thickness of the shell. The physical properties of the shells further change as soluble components leach out causing embrittlement and leaving microscopic sites of porosity. Bonding between filler particle and the polymer also weakens through interaction with water and lipids as more porosity develops.

Biological solutes absorb, dissolve and penetrate the shell materials on the outside of the implant. They reappear on the inside with added impurities leached from the implant shell. Thus, shells of breast prostheses are imperfectly closed semi-permeable membranes that allow bi-directional transport of most low molecular weight substances encountered in biological systems. They also add their own impurities to the fluid on the interior via leaching, disaggregation and extraction of plasticizing oils, filler particles, degraded polymer debris and incidental fabrication impurities.

1. Mammary implants are heterogeneous articles of commerce of poor design and low quality. Their use has been surrounded by adverse reaction reports since their introduction more than 40 years ago. Even in recent times and in spite of increasing usage and mounting problems of safety and durability, the destructive potential of these implants was not generally recognized by the clinical community until the late eighties. To this day, obvious and serious medical risks from breast implants are still disclaimed as rare or benign. This is in contrast to the attitude of most other clinical specialties who fear such misadventures and take elaborate step to avoid their occurrence. Yet protected infections around plastic surgery implants and their low-grade and debilitating sequelae are so common that they are regarded in some quarters as "normal". The problem is partly rooted in how the implants are made and the way they have been are used.

2. Physical characteristics and design peculiarities of widely encountered in breast implants of all sources make them difficult to disinfect and sterilize reliably without further compromising their brief service life and increasing the risk of early shell failure.

3. Implants containing aqueous solutions ("saline inflatables", multi-lumens, etc ) are particularly easy to contaminate because of unprotected valves, shell assembly flaws, leakage and faulty solution filling protocols.

4. Production facilities engaged in the manufacturing of cosmetic surgery products have been largely displaced from the U.S. Some U.S. based factories have resurfaced under new names in countries such as Germany, Ireland and Brazil with lackluster product safety records.

5. Plastic, aesthetic and cosmetic surgery of the breast deviate markedly from other medical disciplines. It promotes and performs more marginal procedures that use low quality implants than all other surgical areas. It also has the most elevated proportion of "redo" surgery.

6. Many implant users are affected by classical post-operative infection at the prosthetic site. Deficient operative techniques, site contamination and unsatisfactory medico-surgical consumables appear to be the main causes.

7. Even more implant users suffer long term chronic low grade infective processes. Faulty implant designs and closed "incubator-like" environments created by periprosthetic implant capsules can explain the observations.

8. With intracapsular colonization by microorganisms, the prognosis for implant "salvage" is poor even when only "benign flora" are involved. The devices require early removal with exhaustive debridement of the site.

9. Atypical microorganisms prevail in aqueous implant filling mixtures. They include hardy anaerobic and thermophilic entities with low metabolic rates. These entities are unlike classical nosocomial microorganisms and are often missed on fast routine laboratory culture tests.

10. Aqueous media in implants recovered at explantation almost always show evidence of internal microbiological activity. In some cases, grossly visible activity can be ascertained. Occasionally, several grams of bacterial and fungal debris are obtained from the interior .

12. Because of slow leakage of contaminated fluid, colonization of the capsule which formed about the implant also takes place. This occurs even without frank rupture of the implant shell. The periprosthetic capsule further provides a protective heaven for released inoculae.

13. The probability of intracapsular colonization increases with the dwell time of implants. The problem also extends to capsules surrounding gel-filled devices but it takes longer.

14. Even asymptomatic individuals with colonized implants and capsules are deemed to have potential for transmitting viable entities, their toxins and their metabolites. Breast engorgement and manipulations during breast feeding can traumatize the tissue about the capsule and thus cause release of debris that would otherwise have remained captive.

15. Many users suffer marked compression atrophy of the breast parenchyma after about 3-5 years. This reduces fluid irrigation at the site which further compounds contamination problem.

16. Common gel and "solid" elastomer implants, in time degrade, acquire porosity; they release debris and effuse reactive substances. Prosthetic by-products which include impure dispersible oils and silica-contaning particles are not retained within capsules nor are they easily excreted.

16. Implants which performed well at first as they started out with clean, thin-wall and permeable prosthetic capsules become progressively less satisfactory with onset of pain and deformity as the capsules mature. Problems rapidly escalate as capsules later colonize.

17. Some users present with early chronic problems that resist definitive treatments. Symptoms return upon discontinuation of therapeutic regimens such as antibiotics, anti-malarials, globulins or anti-inflammatories.

18. On average, a latency of about 6-12 years is required for the onset of frank symptoms. This can also affect gel-filled breast implants and "solid" silicone elastomer prostheses (malar, chin, Swanson finger joints, etc).

BREAST FEEDING WITH PROSTHESES IN SITU 

Breast prostheses have been implanted in large numbers for nearly forty years. Users have ranged from late adolescence to individuals of advanced age. The socio-economic profile of this cohort is tilted towards individuals of the upper income bracket and with a median age close to 35-38. Fertility and lactation for such a group would not normally be an important factor. The small fraction of users undergoing reconstruction after tumor resection or fibrocystic mastectomies is not concerned with breast feeding. On average, users are in the late fertility phase, are parous and few plan additional pregnancies. However, there is a younger sub-group consisting of women who hope to remain fertile for several years post-implantation and many expect later pregnancies. The concerns with breast feeding applies primarily to this sub-group.

The origin of current beliefs suggesting that breast feeding is possible and safe for implant users is not known. What is known is that in the early-sixties and seventies, breast feeding was not deemed desirable. Some physiologists did not regard it as generally possible. Their views were based on biomechanical, biochemical and physiologic considerations. The prostheses incorporated mechanically damaging features such as fibrosis-inducing appendages which were expected to modify the breast and eventually damage the vasculature and the lactation apparatus over the long term. The high impurity levels, in particular the oils similar to what had been used before in connection with silicone-injected breasts, were also factors deemed to impact adversely on lactation for toxicological reasons. At any rate, the experience of oil-injected patients had produced sufficient pathological information to support the view. In the years that followed, the issue remained dormant and no major investigation was performed. Instead, a combination of hearsay and fiction enveloped the area and it gradually became accepted amongst the lay public and some general practitioners that cosmetically augmented patients would routinely be able to breast feed without problems.

This optimistic outlook is not shared by individuals close to the field. The emergence of foam-coated implants in the seventies further reinforced the basis for contra-indications. The dissent came from members of the mainstream medical community fluent with breast prosthetics technology and included pioneer plastic surgeons. However, their views were not widely publicized. The aggressive promotion of cosmetic augmentation started in the late seventies submerged conservative opinions based on pathology studies. Chemical debris from filling materials and unstable coatings of unknown composition, as well as the frequent infections around implants, were the dominant factors supporting the opinions.

Fertility and lactation studies were never conducted systematically by opponents or proponents. In retrospect, this is not surprising because the work seemed unnecessary. Collapse of the lactation system was a logical clinical expectation from gross contamination of the breast by dispersible reactive debris. Similar results were also expected from the introduction of implants that exerted continuous pressure on the breast gland, the vasculature and, in addition, caused uncontrollable fibrosis. Other concerns focussed on fibrosis and the impact of fixation appendages. These accessories altered the breast and removed much of their elasticity. This would have induced severe discomfort upon engorgement prior to lactation.

Fertility and lactation studies were never conducted systematically. In retrospect, this is not surprising because the work would have been deemed unnecessary. Collapse of the lactation system was a logical clinical expectation from gross contamination of the breast by dispersible reactive debris. Similar results were also expected from the introduction of implants that exerted continuous pressure on the breast gland, the vasculature and, in addition, caused uncontrollable fibrosis. Other concerns focussed on fibrosis and the impact of fixation appendages. These accessories altered the breast and removed much of their elasticity. This would have induced severe discomfort upon engorgement prior to lactation.

In the late-seventies, the popularity of the procedure increased significantly and large numbers of low quality prostheses were being implanted. Adverse reactions, failures and compatibility problems were widely encountered by the plastic surgeons and the industry but the information remained within that community. The mainstream medical community believed that complications amongst implant users were rare because publications reflected only favorable results. Poor inter-professional communication gave further credibility to the misconceptions. Adverse reactions were being encountered and many of the problems had clear impact on the ability of implant users to breast feed safely and without risk to the infants.

European publications of the seventies contra-indicated breast feeding. Their views were based on empirical data gathered from users of the previous decade as well as less prominently cited research from a few centers, in particular Switzerland. Contra-indications to breast feeding focused on retention of desirable cosmetic results (avoidance of post-lactation ptosis and tissue distention), comfort and absence of pain in the augmented breast (stretching and pressure in the breast structure during lactation), microbiological colonization of the implant area (intracapsular mastitis) and toxicological considerations from implant materials.

Biomechanical and physiologic considerations of the prosthetically modified breast clearly demonstrate why breast feeding is impractical and frequently destructive. The use of a retromammary implant eventually causes pressure atrophy of the breast gland and collapse of the ducts which convey fluid to the nipple. It is very rare when atrophy is not present in surgically augmented breasts after implants have been in site for 2-4 years. Microvascularization within the critical area is drastically reduced and prominent veins have appeared in the periphery of the breast implant close to the skin. In some cases, compression also causes focal ischemia and oxygen depletion. These factors militate towards failure of the milk producing system.

Assuming a successful pregnancy takes place and the breasts engorge in preparation for breast feeding, additional compression results and in some instances pain will be noted, thus making the process uncomfortable and unpleasant. Upon cessation of breast feeding, the breast returns to its initial augmented volume but tissues and ligaments are stretched and the patient re-encounters ptosis. Thus, the cosmetic benefits may be lost thus invalidating the rationale for the implantation. Re-do surgery often takes place following difficult lactation.

Breast prostheses are not conventional medical products; they lack many of the attributes of other classes of implants. Many were little more than novelty items. Throughout the years they have been a heterogeneous mixture of generally low quality products with high levels of impurities and features which made their users vulnerable to chronic infective processes. Like most implants, they could induce infections that would remain dormant for many years but still produce destructive local effects and high quantities of microbiological metabolites. The capsule around the implant rarely sealed the compartment. It only delayed the onset of release. Capsules deteriorated and remodelled with time. They eventually opened to release their content some time in the 4th-8th year of post-implantation or after trauma to the chest. Even common contracture treatments fostered infective complications.

Processes such as compression capsulotomies and intentional percutaneous perforation of the outer envelope on double lumen implants (two widely used procedures in breast augmentation practices) encouraged colonization and release of microbiological material to the lactation apparatus. The procedures would release large amounts of impurities with unknown biological effects. Chemical impurities included important quantities of substances that varied from brand to brand and frequently from batch to batch of the same brand. The impurities were not limited to silicone oils; they included substances as diverse as platinum organometallics (alkylating agents) as well as residual solvents, reactive silicone intermediates, silica filler, in addition to biologics and denatured tissue arising from biological and microbiological activity within the capsular area. Sub-mammary implant locations gave direct access of the breast gland to prosthetic impurities and contaminants.

Implantations in the sub-muscular position were no better. The continuous mastication of the devices by muscle movement accelerated the release of debris from the implants and led to comparable levels of contamination within the general upper chest area. Evidence of necrosis and tissue degeneration surrounding implants is found in nearly all users with implant dwell times exceeding three years. Graphic evidence of this is seen from mammographic studies showing large quantities of calcific debris associated with tissue deterioration and fat necrosis.

Multi-lumen and saline implants were potentially much worse. The multi-lumen devices were more prone to contaminating the breast with micro-organisms and their metabolites. They also dispersed finely divided silicone oil emulsions and silicone related by-products within the saline compartment. Saline-filled devices had unstable shells which degraded rapidly to expose the silica filler; this material spallated and invaded tissue. It had an ability to stimulate the production of deviant biologics from the patient's own proteins and tissues. The saline charge in these devices could not be maintained sterile. The compartments habitually contaminated early with innoculae of atypical organisms. They in turn added their toxins to the already substantial list of implant-related debris which had access to the breast compartment.

Paradoxically, national and international parenthood and breast feeding promotion organizations maintained that lactation in implanted mothers was feasible, practical and safe. Today there are still organizations who support the practice on the strength of opinions devoid of clinical, physiologic and biochemical basis. To this day, there is no scientific basis to assume safety for the lactating mothers with implants or their offspring. On the contrary, established thinking based on the physiology of the breast strongly supports an elevated probability of adverse effects. Preliminary studies conducted on small samples of children from implanted mothers note adverse effects and should be a strong deterrent to breast feeding for any individual who either has or who has had a breast prosthesis in her lifetime.