Dr. Blais link on capsules..again

[Guest guest]

I was just looking through the links to find Shari's new one that

Ilena put up for us (didn't find it yet...), and found this great

article. Thought I would repost it. We have alot of good links

actually!

This one is by Dr.Pierre Blais. The info about the capsules is what

caught my attention:

http://implants.clic.net/tony/Blais/020.html

INJURY FROM SALINE INFLATABLE BREAST IMPLANTS

Where Implants Go Wrong:

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.

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, other 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.

Where the Surgery Goes Wrong:

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.

Importance of the Patient's History:

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.

Capsule-Implant Relationships:

The capsules which form around the prostheses are 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.

Slow 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

seventies and the basic product designs have become worse with time,

reaching their nadir in the early -eighties. 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. The mechanisms of injury may appear

to 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 reaction information.

Injury Mechanisms:

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 degrade and the debris may include 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 interactions leading to tissue

degeneration or denaturation to produce host tissue- derived

antigens that elicit antagonistic host-directed antibodies

(autoimmune disturbances); (6) pathologic effects induced through

bacterial, viral or fungal colonization of the capsule space leading

to low grade chronic infections and toxic phenomena from

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.

The Role of Capsules in Implant-Related Diseases:

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 produce 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.

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.

The silicone elastomers also contain silica.

The Role of Silica:

Implant studies document long term biodegradation and bio-erosion of

shell materials. The effect is particularly notable for saline

inflatables and multi-lumen prostheses filled with aqueous

solutions. The deterioration processes results in embrittlement of

the material, erosion of the polymer as well as spallation of silica

fillers particles 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 aluminum oxide are also encountered as fillers

and opacifiers in some brands of implants.

The resulting biodegraded silica agglomerates are coarse, bioactive

structures 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.

Capsule Calcification:

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

contaminated by 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 the 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 hematocrits 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.

Background and Problems with Saline-Containing Implants:

Breast implants consisting of containers filled partly or wholly

with aqueous fluids have been described in medico-surgical

publications and in patents for more than forty years. Numerous

variations exist. Several types were commercialized during the

sixties and seventies. Shell durability, aesthetic deficiencies and

filling port closure reliability emerged as problem areas from the

outset. The same problems remain without resolution today. Patient

dissatisfaction, replacements and adverse reactions has surrounded

the use of the products for at least 20 years.

Conceptually and predictably, the most serious problem of " saline-

inflatable " breast implants is their ability to sustain

microbiological activity within the saline-containing compartment;

the most widely cited problem is their susceptibility to rapidly

lose their saline filling charge because of valve or filling port

failure or late shell perforation as a result of material fatigue

and physico-chemical deterioration.

Most " inflatables " ultimately fail through classical fatigue-related

shell wall perforation, a process termed by industry as " benign late

spontaneous deflation of unknown aetiology " . When reviewed against a

background of microbiology, parasitology and infection control, late

shell integrity failures have a much more ominous prognosis. They

are the end stage of a sequence of events which begins by

inoculation of a warm, protected micro-environment which can later

receives nutrients at librium. This is followed by florid

colonization of the aqueous medium within the object. Chronic

release of secondary inoculae through faulty valves and shell

defects takes place concurrently. Ultimate deflation with release of

the fluid charge amounts to a direct high volume injection of viable

entities of mixed type including mycobacteria which are well suited

to survive the closed environment of a saline implant.

Contributing Factors to Saline Implant Misadventures:

Contrary to expectations, saline prostheses have water permeable

shells. Their permeability to larger molecules increases with dwell

time in vivo. For typical products made with conventional acid

catalyzed shells ( " RTV " ), ingress of extracellular solutes such as

amino acids and proteins becomes significant after about 5-7 years.

Gradual loss of volume then takes place and capsule contraction

forces the shells to involute and pleat on themselves. Continuous

movement from the user's daily occupation erode and fatigue the

material. The shell later perforates at pleats and pucker points.

Cracking of the material with loss of particles then takes place .

Rapid deflation usually follow with release of the filling charge

and its acquired contaminants. These contaminants frequently include

a large bioburden of viable micro-organisms which colonized the

charge with the aid of nutrients that permeate the shell. This also

complies to multi-compartment systems such as double lumen implants

which have aqueous fluid. Such prostheses also share problems of

assembly and valve security.

Valves and filling ports are not secure. Whereas the early models

such as the Arion, the and the Birbaum designs achieve

irrevocable closure of the filling port by forcibly inserting a plug

into the orifice, the more recent versions use valves that leak.

Ideally, the leakage rate is low and takes place in response to

compression from contracture of the capsular tissue. This is

expected to achieve a kind of decompression. Even late versions of

the " " incorporate a valve plug that is easily avulsed from the

orifice. This feature appears to have been deliberately designed

into the product in order to justify the claims of `low capsular

contracture' even at a cost of product safety.

Saline prostheses obscure mammograms. Contrary to product claims and

often repeated opinions by proponents, silicone elastomer shell and

valves are radiodense. Mammograms of saline users clearly show the

prostheses and eclipse nearly as much information about possible

tumors as do gel filled devices. Thus they can significantly delay

or preclude meaningful tumor detection depending conventional

mammographic techniques. All presently used salines are markedly

radio-opaque and have radiographically visible fine structure which

greatly complicate the interpretation of radiographic projections.

In the late stages, most undergo severe calcification at the tissue

interface. These crystalline entities are in the same size range

as " micro-calcifications " used as criteria of malignancy by

radiographic oncologists. In tumor screening and post resection

cancer follow-up procedures, the implants have the ability to

obscure even large and dense proximal malignancies. They also

introduce complex artifacts which further confuse the results.

Such characteristics, independently and in combination have long

term safety implications. From studies on recovered implants and

medical records of their users, deflated implants, grossly leaky

valves, frangible and degraded shells, atypical periprosthetic

infections and their sequelae account for a large part of morbidity

in what ought to be a healthy segment of the population.

Paradoxically, these risks are not well explained to potential users

or else termed " remote " by promoters.

The diagnostic of saline implant-related diseases and the clinical

management of patients bearing saline inflatables present medical

and technical costs which far exceed the benefits that the devices

provide. For individuals who prefer to retain the devices in spite

of their obvious risks, the area requires additional study to

quantify the probable life of each shell type, the factors involved

in colonization, the identity and the population of organisms

present in the charge and the best treatment modalities for users of

implants that chronically release small quantities of inoculae into

the periprosthetic space.

Similar problems have been encountered with other classes of

implantable devices that harbor stagnant aqueous fluids such as

trans-cutaneous " port " drug administration devices (Hickman-type

catheter systems) and inflatable penile implants. Presently, saline-

filled devices are increasing in popularity 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.

There are numerous claims of long term success by proponents but

there is a paucity of credible data on properties and performance of

the devices. Results of preliminary studies performed on explants by

many centers are discordant with commercially distributed

information. Replacements and treatment for chronic sequelae from

the devices boost public costs associated with the use of this

technology

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. Some of these problems appeared as

official adverse reaction reports and a few articles on the topic

were printed in plastic surgery journals.

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 nineties 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.

Microbiological Issues and Pharmaceuticals in Saline-Containing

Implants

The instillation of pharmaceuticals to solutions in saline

inflatable implants and in the outer lumen of multi-compartment

prostheses started in the early seventies following a publication by

Perrin. By the late seventies, several influential authors in

plastic surgery of the breast were advocating the procedure and its

use became widespread. Other contemporary publications were

outlining serious adverse affects. The procedure was also meeting

with strong objections from pharmacologists and from the makers of

drugs used in connection with the claims.

The use of assorted antibiotic and bacteriostatic pharmaceuticals

was predicated on the basis that they would prevent proliferation of

microorganisms inside or outside the shell. Anti-inflammatory

steroidal preparations and other drugs were believed to prevent or

mitigate capsular contracture by slowly diffusing out through the

leaky implant wall. Eventually the fashion was extended to gel

prostheses where the additives were sometimes injected as a bolus

through the shell wall.

The first commercially attractive saline inflatable designs are

credited to , Arion and Birnbaum. The derived multi-compartment

or double lumen implants are attributed to Hartley. All of these

products appeared in the early seventies. Early double lumen

products had large volume saline compartments and were

mostly `saline' as opposed to gel. They behaved like saline

inflatables. In their original form, they were designed to address

capsular contracture through optional deflation of the outer

compartment. This is made clear by Hartley in his patent on double

lumen implants entitled " A Deflatable Mammary Augmentation

Prosthesis " .

By the mid -seventies, another variation of the double lumen

appeared. It was specifically intended to convey pharmaceuticals to

the surrounding capsular tissue. The drugs were added to the saline

in the outer lumen at the time of implantation. Such special

variants of double lumen prostheses had very small saline volumes.

They were designed in response to demand created by advocates of the

drug-release procedures.

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 seventies, 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 or

saline inflatable devices. Other studies had documented the rapid

growth of microorganisms in the outer shell of double lumens and

salines. Several widely read journal had published articles on the

topic.

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 ought to

have been forecast that the instillation of pharmaceuticals designed

for other purposes would enhance the risk of microbiological

contamination of the compartment. This would magnify risks arising

from substances created by the deteriorating pharmaceuticals.

Therefore, even to an unsophisticated practitioner, the risks of the

procedure would have perceived.

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 the

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. There never was a

scientific basis for claimed benefits from the procedure.

Microbiological Risks for Saline-Containing Systems:

All saline-filled devices have been sold as sterile products since

the late-seventies. Saline chambers with small amounts of viable

micro-organisms occur occasionally and recalls take place. It

appears that improperly sterilized products have beset the industry

for many years and forced the introduction of specialized

sterilization technology in the eighties.

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 resterilization attempts following

unsanctioned device re-use or extemporaneous 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 are simple variants of unidirectional

flow control devices. They were developed for consumer applications

or 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.

Composition of Aqueous Solutions Within Used Breast Implants

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

endogenous 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. 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.

Valve Designs and their Problems:

Saline-filled mammary augmentation devices first appeared

commercially in France circa 1965. Made by Simaplast S.A., they

consisted of a silicone bag made by joining two half-shells and

forming a filling tube integrally by bonding a strip extending from

the perimeter of each half shell. Closure was achieved by knotting

this seamed tube or by inserting a solid Teflon™ plug in it. These

devices were credited to H. Arion, a French physician. These were

imported to the U.S. by Klein Associates Corporation which

later became the Mammatech Corporation.

The first true valved implant was the " " style inflatable made

commercially by the Heyer Schulte Corporation from about 1968. It

incorporates a diaphragm valve at the apex supplemented by a push-

plug. Other systems were introduced in the seventies by Klein,

3M/McGhan, Dow Corning, -Uphoff and the Medical Engineering

Corporation. Heyer Schulte adapted another style of valve used

originally on its hydrocephalus shunt; it used a flattened tube.

Most of these valves were used on saline inflatables as well as

bilumen implants.

The Heyer Schulte Corporation also released a number of unusual

implant designs. One variant consisted of a thick shelled

conventional gel-filled implant presented as a " variable " size

implant. The instructions for use were remarkable. They recommended

the direct injection of supplemental saline through the user's skin

and the shell wall in order to increase the implant size. To this

end, a volume of saline or other aqueous-based solution was

instilled into the gel mass and dispersed as a separate phase within

the silicone gel. This technique of `post-filling' implants spread

widely in plastic surgery of the breast.

Numerous surgeons attempted to increase the volume of conventional

gel-filled implants by transcutaneously injecting aqueous-based

solutions into previously implanted devices. The system did not

work. The hypodermic syringe perforations did not heal and aqueous

fluids leaked out. Damages created by the hypodermic syringe also

led to initiation points from which ruptures later developed. The

concept was abandoned and no explanation was provided to the

clinical community. Yet, the concept was superficially attractive.

At first, the shell was reinforced with fabric to forestall

propagating tears. Later, shell formulations were changed to

include `gel-like' sandwich layers which were designed to self-heal.

However, such structures were stiff and it was impractical to

incorporate into the whole implant surface.

Variations on the self-seal `patch concept' appeared at Dow Corning

and later at the Medical Engineering Corporation. Both distributed

saline inflatable implants which used small self-seal ports. These

were thick, fabric-reinforced elastomer/gel laminates which were

supposed to resist leakage after puncture by hypodermic needles used

for fluid filling. This concept is analogous to injectable vial

closures which have been in use since the late-forties.

Dow Corning Saline Inflatable Systems - The Varifil™ Series:

Following the early commercial success of the Arion-Simaplast saline-

filled prostheses imported from France, Dow Corning became involved

with saline-filled implants. Their early versions were made in the

seventies. Some included knotted tube filling systems. Others had

self-seal patches. The later versions became known as the Dow

Corning Varifil™ or Series 200 Saline Inflatable Mammary Prostheses.

These devices used a large volume grease seal system. It was

assembled from elastomer sheeting and had a space to accept a

viscous substance that would prevent leakage through the channel

once filling was complete. Critical portions of the shell and the

valve assembly were delegated to outside contractors.

By 1977, parts of the 200 Series, as well as components of a

structurally similar combination gel-saline, Series 300 implant,

were fabricated extramurally. A competitor was chosen for the work.

The items were fabricated by Uphoff Corporation of Santa

Barbara, California, then a new and small offspring corporation

founded by former employees of Heyer Schulte who had previously

worked for Dow Corning.

The Uphoff valve technology used discoid parts and slit-like

openings to minimize leakage of the occlusive grease away from the

sealing channel. The item remained on Dow Corning products until the

early-eighties. Uphoff also used this valve on their own saline

filled products. Later, Dow Corning developed its own simplified

version of the grease seal valve using exclusively die-cut sheet

parts.

Klein and Simaplast Systems:

Saline filled devices from Klein and Simaplast used mostly knotted

or plugged filling tubes. Several variations were made and some

continued to be sold through other distributorships into the mid-

seventies. The devices were also employed extemporaneously

as `tissue expanders'. This was done by severing part of the filling

tube and coupling the stem to silicone tubes sometimes externalized

through an opening for post-operative filling. Hickman-type

percutaneous catheters or Port-a-Cath™ chronic drug infusion ports

as well as PIC catheters designed for percutaneous drug delivery

were also used. Such ports would be buried in tissue at sites remote

from the implant (axillae, abdomen).

The concept was borrowed by corporations such as Heyer Schulte and

Surgitek and semi-commercial versions of devices with remote ports

were made. These products were designed for post implantation

filling using percutaneous injection ports. In some quarters, the

products were presented as variable volume prostheses which gave the

patient the ability to change her breast volume post-operatively.

The approach was not successful and morbidity resulted in

significant quantities, primarily through infection. However, the

concept of remote port filling was retained for applications

requiring gradual expansion of tissue. Commercial products of this

kind were widely sold and reached peak popularity in the late-

eighties. Numerous versions are still in commerce both from U.S.-

based manufacturers as well as offshore producers.

Remote Fluid-Filling Ports and Other Complex Fluid Filling Systems:

Tissue expanders and percutaneous drug-delivery catheters such as

Port-a-Caths and Hickman style catheters produce tough, convoluted

capsules that are infection and inflammation-prone. They are often

more than 5 mm in thickness and incorporate debris from multiple

prior failed prostheses, bacterial entities, suture remnants in

addition to granulomatous tissue formed from leakage of oil-based

contaminants such as gel.

Such capsules are ideally suited for complications that include

tenacious infections, painful abscesses, seromas and other local

problems. Ultimately, they calcify and many degenerate into infected

abscesses if not attended to in a timely fashion. Generally,

clinicians who encounter the capsules upon removal of the devices

will resect the surrounding tissue in order to ensure closure of the

wound site.

Port-like devices, does not lend itself to easy capsule resection.

The Becker Tissue Expander is particularly hazardous because its use

is predicated on its easy conversion from its " expander mode " to

its " permanent implant mode " by simply " removing " the port. This is

done habitually from a small incision which allows extracting the

percutaneous port and its attached filling tube by exerting traction

on the fixture. This allows the sleeve valve at the main prosthesis

to release the filling tube which slides conveniently through the

capsule " tunnel " and thus the accessory exits in toto from the small

incision. A priory, this may be an attractive option. However, on

closer examination, the procedure has obvious risks and contravenes

basic concepts of surgery. Extracting the tube causes the gel-coated

item to drag along the encapsulating tissue leaving most of the gel

and oils in the tunnel. The port site incision is then closed off

with an appropriate suture.

Unfortunately, Beckers as well as most percutaneous port devices,

have colonized capsule spaces which are often the primary cause of

local and systemic problems. To attempt the extraction of the

filling tube assembly spreads the micro-organisms present within the

saline or the ones harbored within the main implant capsule. As a

result, the capsule formerly occupied by the port, becomes

innoculated; closure later takes place at both ends thus ensuring an

ideal protected micro-environment for the contaminants and the

organisms.

Mentor Saline Implants:

In 1984, the Mentor Corporation acquired the product line originally

developed by Heyer Schulte and American Heyer Schulte in addition to

associated firms such as Polyplastic and Schulte Medical. A small

amount of intellectual property was also acquired at the same time

and included technology for tissue expanders and saline inflatable

prostheses. Mentor continued to manufacture saline-filled implants

originally developed by the Heyer Schulte Corporation. They included

the early Style 1600, round, with anterior valve and its oval

counterpart. Posterior leaf valve implants were also made under

product numbers 1800M and 1900M respectively for round and oval

styles. However, these latter two were not derivatives of the

original Heyer Schulte designs which bear the same code. The

original items had Schulte leaf valves. The Mentor versions included

instead a modified broad leaf valve dependent on a grease-like

sealant; this feature was copied from other manufacturers,

specifically 3M/McGhan who had employed this style of valve since

the mid-seventies on its own versions of salines and double lumen

implants. Uphoff was also using a similar style of valve

closure.

Mentor also introduced changes in the shell design. Textured Siltex™

variations were introduced for all of the products circa 1987-88.

These variants were of substantially the same styles known as the

Style 2600 (round, anterior valve), Style 2800 (round, posterior

valve), Style 1700T, (modified smooth wall oval), Style 1800M

(posterior leaf valve), and Style 1900MT (oval with posterior leaf

valve).

The most widely sold items were the Style 1600 and its more recent

derivatives incorporating the anterior valve system with a small

cap. These implants are colloquially known as " " designs and

are essentially the same as when they were first released in 1968.

Only the apex valve was changed; it introduced major undesirable

features such as deflation and new long term health risks because of

its tendency to expel the valve cap, leak part of the filling fluid

and recontaminate with viable organisms.

The product is widely copied. It is also frequently encountered as

an explanted device. The quality of the devices and their

performance are very variable. Failures taking place within a few

months of implantation occur in significant numbers. Conversely,

reports of more than 25 years of continuous use are not rare.

Durability problems stem largely from the composition of the shell

and the quality of the valve parts. Processing conditions for the

shell and valve assembly techniques impact on durability and

resistance to leakage. After long dwell times, the shell walls

deteriorate, become brittle and fragments of silica-laden degraded

polymer spallate and disperse in the vicinity of the implants to

become embedded in capsular tissue; adverse reactions are known to

occur from dissemination of such materials into the lymph nodes.

Capping and valving failures are also commonplace. These lead to

early deflation. Underfilling of the saline shells is associated

with early shell failure due to pleating and puckering. It

culminates in frank perforations and spontaneous deflation. The

problem is particularly acute for the thick shell Siltex™ which has

a poor compliance and a low tear strength. Overfilling is habitually

done by experienced physicians in order to delay the phenomenon.

Perversely, the valve does not seal for many production items and

the excess volume leads to early avulsion of the cap with slow valve

leakage. The partly deflated implants pleat more readily and

perforations ensue. Colonization of the filling fluid ensues either

from retrograde flow of extracellular fluid with adventitious micro-

organisms and proteinaceous matter from the user or from residual

surviving inoculae. Serious problems with such devices remain and

are widely encountered but official reporting is comparatively rare,

perhaps for fear of attracting adverse public attention or FDA

scrutiny.

McGhan, 3M/McGhan and McGhan/Inamed Systems:

Several variations of saline inflatable prostheses were manufactured

by McGhan and 3M/McGhan. Some of these concepts were later continued

by successor and affiliated companies such as Uphoff and Inamed.

Early devices appeared in the mid-seventies. Unlike contemporary

products from other manufacturers, they had very thin shells and

several types were manufactured using shells made from platinum

catalysed, thermally cured elastomer as opposed to the older acetoxy-

based technologies. Some were round, others oval.

Two styles of valve were used: the small bore apex diaphragm valve

similar to other products of the same era and the classical McGhan

leaf valve. The Style 90 had anterior (apex) and posterior leaf

valve variants. Anterior valve versions had multiple patches,

usually the main patch being on the posterior side with subsidiary

patch and valve flanges on the anterior side. Valves and patches

were centrally located. The shells had thin, highly stressed and

failure-susceptible areas.

Saline implants of this kind were intended for `small incision'

surgery; they were be inserted in the deflated state and filled to

their optimum size during the surgery. The instructions for use

emphasized in-situ inflation with later (`blind') extraction of the

filling tube. The posterior valve variant was preferred for surgery

involving infra-mammary access; the apex valve variants were favored

for periareolar surgery. Style 90 valves were fragile. The diaphragm

valves frequently did not retain the obturators (`push-cap') and the

diaphragm was subject to displacement during the filling operation.

The leaf valve types had similar filling systems to that of double

lumen products such as Styles 76, 77 and 78. The valves were little

more than flattened tubes with grease seals, sometimes without the

added grease sealant. Plugs and obturators were not used on leaf

valve filling systems. In addition, the filling tube used to fill

the device stressed the shell during surgical manipulations and the

shell/valve assembly was often damaged incidental to filling

procedures.

This predisposed the shells to early tears and deflation, in

particular for the anterior (apex) valve implants. The items were

widely sold. During the late-seventies, they failed in large numbers

and were replaced repeatedly by most users.

The shells were so failure-prone and deflation was so common that

even surgeons complained publicly about complications. The product

was withdrawn by the manufacturer and as a result, saline implants

from all sources became unpopular. By 1984, the saline-filled

devices had nearly vanished from commerce. Litigation from

dissatisfied patients and embarrassed surgeons had risen

dramatically. Several manufacturers discontinued salines outright.

Others sold them only as custom made items.

Curiously, the salines reappeared in the late-eighties following the

FDA moratorium on gel-filled breast implants. Newer models of

implants using similar valves were reintroduced. Some were textured.

At present, the leaf valve implants are recovered with leaky valves

depleted of sealant and with ruptured shells. The few that remain

with fluid in the saline compartment are generally colonized with

micro-organisms that may have invaded the valve along with tissue

fragments and extracellular fluids. Atypical micro-organisms are

normally present in significant amounts and nosocomial entities are

sometime found in such fluids. With leaky valves, the organisms can

spread through the capsule and beyond to colonize tissue. Patients

report discomfort, pain, low grade fevers and other unusual

disturbances that motivate requests for removal. Others tolerate the

symptoms until severe forms of disease become apparent.

The Style 90 and other variants of the 3M/McGhan saline implants

were the object of discussions at the FDA Classification Panels in

the late-seventies. Issues surrounding frequent failures, unreliable

valves, distorted claims and the need to forewarn users regarding

the brief life cycle of the products were discussed extensively.

Similar discussions took place abroad where the Style 90 was also

used with particularly poor outcome. No formal advisory regarding

the long term risks of this product was ever issued.

By the late-eighties, there appears to have been very few users of

the Style 90 with surviving non-perforated implants. However, many

users appear to have retained the products in the ruptured or

deflated condition on the premise that they presented no risk. This

is not a correct perception. Perforated saline inflatable products

of this kind are associated with severe and lasting adverse

reactions, primarily because of their ability to colonize within the

residual aqueous fluid and because of the propensity of shell to

degrade to solid silica-rich material with highly inflammatory

properties. The filler for the elastomeric material ultimately

reappears in its original agglomerated form within surrounding

tissue. Material of this kind is deemed to be scleroderma-inducing.

All users of devices of this series will ultimately require

explantation and many will demonstrate severe and difficultly

manageable sequelae, in particular individuals who sustained early

deflations but did not have the collapsed prosthesis removed. Late

users and surviving asymptomatic patients with yet non-perforated

but colonized implants are subject to late deflation with leakage of

contaminated saline. Such patients have potential for severe but

preventable complications including septicemia.

Saline Inflatable Products From Late-Eighties Corporations:

Several items were made commercially by other firms. Most were

copies of existing prostheses. Examples include saline inflatables

resembling Heyer Schulte designs by Les Laboratoires Sebbin of

France, NovaMed (US and Germany), Silimed (Brazil), Uphoff,

Uphoff International and the Bioplasty Corporation of Minnesota.

These firms manufactured a wide range of breast surgery products

including saline-inflatables and gel-filled, smooth wall silicone

implants. Later, textured surface implants with claims of reduced

capsular contracture were marketed. All shared the same problems of

the existing salines as the valve designs were similar or in some

cases identical. Habitually, elastomer quality was unpredictable and

early failures are also reported widely. Uphoff is currently

known as the CUI Division of Inamed.

Leaf Valves Problems:

These valves are variations of the hydrocephalus cerebrospinal fluid

drainage valves patented by Heyer Schulte in the sixties. The

original device was a flattened tube which could open from a

unidirectional increase of pressure. It had been successfully used

on implants for drainage of fluid from the cranial cavity. Other

variations of this valve used two flat sheets of silicone with the

space filled with grease that ensured adhesions of the two halves

with filling of the spaces. The original versions required the

insertion of a cap into the throat of the valve in order to provide

a secure fluid occlusion. Later versions made that optional.

These devices are recovered from explantation with deformed, kinked,

expanded, swollen and disassembled valves. Most are missing caps and

show gross leakage. Tissue ingrowth in the form of fibrous pannus is

frequently found within the orifice and retains the valve in the

open position. Contamination extends to the interior and tissue is

frequently found within saline inflatables and double lumen devices

fitted with the same types of valves. Colonization and evidence of

large quantities of microbiological metabolites are also widely

encountered.

This style of valve, which became commercial in the early-seventies,

has the ability to transport fluid from the intracapsular space to

the interior of the device. The mechanism is similar to that in

peristaltic pumps and depends on differential cyclic pressures

pulses which arise from the user's movements. Accordingly, movement

causes compression of the capsule and leads to a momentary increase

in the periprosthetic pressure. The second part of the cycle relaxes

this pressure and a brief differential is created when small amounts

of fluid are driven across the valve orifice. This mechanism

provides both the innoculae and the nutrient necessary for florid

colonization of the saline solution over time.