Rupture Phenomena in Implants:

Loss of shell integrity resulting in frank failure of the shell through natural deterioration, material fatigue, traumatic events, iatrogenic accidents or other processes are expected for typical breast implants. Devices manufactured under poorly controlled conditions using inadequately purified reagents and processed haphazardly are particularly vulnerable and early failure is inevitable.

Well-fabricated breast prostheses of all types, whether they are of the gel, saline, gel/saline or double lumen, are also easily damaged. This is not surprising in view of the very thin enclosing structures used to contain the augmentation fluid. Design aspects of such prostheses greatly exacerbate their vulnerability as they allow many types of implants to ‘fold back’ on themselves, pleat, invaginate and somehow distort to pack in a breast pocket in a haphazard way. This causes a multiplicity of sharp creases and these sharp creases move with the user’s activity. Such a situation is ideally suited for fatigue failure and thus even under ideal conditions material fatigue is the normal end point for most commercial prostheses.

The uptake of interactive biological substances such as lipids by the shell elastomer adds additional factors which lead to losses in mechanical properties and increased susceptibility to natural failure of the shell. These processes are termed plasticization phenomena and frequently lead to major changes in size of shells and are accompanied by significant and progressive losses in mechanical properties. The problem was encountered first in the sixties in connection with silicone elastomer cardiac valve components.

Outright chemical changes can also take place in some classes of inappropriately formulated silicone elastomers. The incorporation of additives, in particular fillers such as silica, titanium dioxide and radio-opaque agents, further accelerate the process. Residual reactive sites left in the shell material provide further opportunity for reactions in vivo which may culminate in local changes in chemical structure of the elastomer where there are concentrations of such reactive entities. Reactions of this kind may affect parts of the siloxane backbone and/or the crosslinking sites depending on the exact formula. Most commercially manufactured elastomers incorporate such residual unsaturation (double bonds) and other reactive chemical groups which are induced through side reactions including oxidation of vulnerable parts of the molecule during thermal processing.

Parasitic or side reactions introduce defects in the molecular network for elastomers of all kinds. Silicones are no exception. Their chemical vulnerability is a function of overall formulation and processing conditions. Unlike elastomeric material used for consumer products such as vehicle tires and high temperature tubing (radiator hoses), the degree of control of the process was comparatively poor for most commercially manufactured breast implants. Vulnerable segments in the elastomer network are found in virtually all commercial products sold in significant quantities.

Anomalous pockets of chemical reactivity and unique sites of vulnerability in implant shells are readily visible in many explanted prostheses with dwell times exceeding 10 years. In some instances, the changes are so dramatic that they are visible to the eye unaided and the mechanical properties are so drastically altered that the material has lost much of its elastomeric attributes and may be embrittled to the point where it fractures on simple bending.

Repeated mechanical action or cyclic phenomena such as repeated muscle movement affecting the same area (arm, chest, dorsal and neck areas), superpose on focal chemical deterioration. Processes such as sharp bending and the induction of strain in elastomers has the ability to increase the reactivity of the site. These are well established mechano-chemical phenomena which have been studied since the fifties, in particular in connection with rubbers. Silicones as a class of elastomers are amongst the most vulnerable within the ‘rubber’ families. This is the result of their poor tear strength. Tear strength is a function of structure and formulation. It is one of the most sensitive parameters within the mechanical properties of this class of substances. Such elastomers suffer severe alterations of mechanical properties and in particular tear strength along crease lines and in areas subject to stresses and repetitious flexing and bending.

Material deformation is expected for common breast implants and is evidenced in nearly all specimens of explanted breast prostheses with significant dwell times in vivo. 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 vary according to the prosthesis type, size and position. The pleating pattern is related mathematically to the shape of the device and the ‘fullness’ of the filling substance. This phenomenon is predictable from existing engineering concepts which have been taught since the thirties. However, the equations are complex and detailed analyses of these patterns require sophisticated numerical control simulations. Empirically, the results are predictable and failure along such preferred pleating zones, in particular the equator or the margin of underfilled implants, are widely noted. Failures along stress concentration points such as patch edges and valve flanges are also widespread. 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. Mineralization of the space between the capsule and the implant is almost universal for users exceeding 10-12 years. The formation of semi-rigid, abrasive entities lining the prosthesis shell creates supplemental conditions conducive to late failure. From observations of mammographic records, calcified periprosthetic capsules are precursor signs of early failure along pleat lines through abrasive phenomena. Calcific entities excoriate the shell at prominent pleat points; this is notable for devices which are surrounded by large organized crystalline aggregates in the intracapsular space (cohesive concretions or plaque-like 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, the shell is clearly discontinuous and sometimes is simply held in the original position for a brief period by a contracted capsule. Minor trauma including that from daily occupations and medical diagnostic procedures is sufficient to complete the separation of the shell and initiate full rupture. Rupture ultimately develops even without trauma if sufficient time is given.

After approximately 4-7 years, implants develop shell flaws and most are severely compromised with reference to their mechanical properties. The more durable kinds of devices tend to be the ones manufactured from simple shell configurations which are fully filled. This type of structure does not easily pleat and assuming that gross chemical deterioration of the material has not taken place, perforations occur late and mostly through calcific excoriation. 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 line perforations" found on paper documents that have detachable portions where machine-made perforations facilitate precise tearing along dotted lines. Failure proceeds similarly along the established pleat zone at the earliest opportunity.

The Implant as an Exacerbating Factor for Tissue Injuries:

Users of mammary prostheses are subject to special modes of injury. Some risks issue directly from the release of inimical or outright toxic substances from the filling core or viable microbiological entities which have grown within the compartments of the implant over the dwell time. Other injuries result from the infiltration of the tissue by natural substances which undergo changes. Variations on these themes also include phenomena which are the outcome of drastically reduced flow of fluid in the prosthetic areas which affect the physiology of the site and encourage reactions between natural substances which would otherwise not take place. In summary, prosthetic areas in particular with poorly designed implants, have no ability to cleanse themselves of effluents as there is insufficient movement of fluid to ensure success of this natural process.

Another type of injury is the result of placing a foreign object below a comparatively thin skin cover. Anabolic processes under such conditions attempt to compensate for the loss of irrigation pathways by enlarging blood vessels, in some cases causing such vasculature to develop over the implant cover in a very unsightly fashion. In addition, a semi-rigid or even a flexible object under stress from contracture appears ‘solid’ much like an inflated vehicle tire. Such objects act in a similar way to ‘anvils’ by concentrating the force of external pressure and momentary traumatic events against the thin overlying tissue. The possibility of damage to tissue and vasculature and possibly to a grossly compromised prosthesis from trauma also exists but is overshadowed by what generally occurs to surrounding tissue. This is primarily a consequence of the strength of the capsular material which surrounds the tissue and the limited deformation that the shell can undergo even under strong compression; even impaired prostheses with frank fatigue-induced perforations do not easily undergo spreading of these rupture sites even on compression.

With widespread use of compression capsulotomy as a ‘therapy’ for contracture over the last two decades, one would expect more compression trauma-induced ruptures amongst retrieved specimens. Surprisingly, this is not the case. Even individuals with histories of multiple closed compression capsulotomies do not show a prevalence of frank compressive ruptures. Instead, they show deep tissue ingress of oil and gel which is a consequence of forcibly extruding material extravasated from long-ruptured prostheses into areas remote from the implant site. Accordingly, compression capsulotomy is deemed to be a highly hazardous procedure for the user but it does not contribute to frank shell rupture in an uncompromised prosthesis.

Iatrogenic Damage to Implants:

There are other mechanisms whereby shell integrity can be lost. They are also obvious. The thin wall is particularly vulnerable to penetration by surgical instruments such as scalpels, scissors, bone rongeurs and other instruments which may be part of the surgical tray for removal of such devices. Pinching from devices such as forceps and retractors also leads to frank perforations and frequently other more serious damage.

Curiously, instruments such as Bovie electrosurgery units which are widely used in plastic surgery of the breast do not injure prostheses unless there is a gross lack of care on the part of the surgeon; accordingly, damage from Bovie type probes is more frequently the result of mechanical perforation as opposed to the normal cutting action of such instruments which depend on electrical discharge (‘plasma torch’). This is the result of the mechanism of cutting for Bovie discharge systems; such devices require electrical conduction of substances that are to be ‘cut’ and breast prostheses are non-conductors. Consequently, electrical discharge instruments are ineffective in non-conductive fields and there is no mechanism to operate or to ‘cut’ a breast prosthesis shell or the thin layer of oil-infiltrated tissue which generally surround leaky implants using a Bovie probe.

Iatrogenic loss of shell integrity can also take place intentionally. A popular procedure which evolved in the mid-seventies, credited to Dr. John Hartley of Atlanta, recommends an hypodermic needle be inserted into the breast so as to intentionally perforate the outer shell thus allowing part of the fluid to ‘leak out’. This would reduce the pressure of the area due to excess volume. This procedure received wide popularization and was performed on numerous types of implants with aqueous fluids in their outer compartments. The consequences of such procedures are discussed separately under "Hartley Decompression Techniques".

Implant Damage and Injury from Trauma:

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 generally expected by clinicians who habitually treat accident victims. For subjects with prostheses, all of the above damages are possible.

Other types of 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. Curiously, prosthetic damage can be demonstrated to have pre-existed the traumatic events for most cases studied to date.

Predictably, the presence of prostheses in the traumatized area magnifies the injuries and complicates the emergency treatment. They may also create conditions where emergency care is not sufficient. Instead, policies advising a more prolonged follow up to forestall late complications and ensure appropriate clinical management of late sequelae may be necessary. 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).

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 enormous 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".

In summary, 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. In addition, 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, the breast structure and the chest muscles can often add other dimensions to such injuries. However, events that do not lead to severe and prolonged compression or penetrating chest injury rarely have permanent 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 cuts" through a combination of perforation, cutting, tear initiation and tear propagation but these are rare and are more typical of "antipersonnel" or "assault and battery" trauma.

Hartley Decompression Technique - Illogical and Hazardous Practice:

An early product brochure for the "Hartley" double lumen implant reprinted by Heyer Schulte describes the "Hartley decompression procedure" and provides an illustration. The procedure was later described with minor modifications in the text of product inserts from American Heyer Schulte. It disappeared from Heyer Schulte product literature circa 1979-81. No other manufacturer made explicit reference to the procedure but all firms with similar products evidently were aware of the technique and had reprinted information available indicating suitability of the "Hartley decompression" for their double lumen implants.

The "Hartley decompression procedure" was widespread and was applied to numerous styles of double lumen implants. Users of this style of prosthesis in the mid-seventies and eighties were frequently subjected to this procedure as a means of resolving pain and capsular contracture.

Its philosophy required perforating and draining the aqueous fluid from the outer lumen, thus causing it to collapse against the inner shell. The device was then left in situ as a silicone gel-filled core surrounded by a deflated membrane with one or more perforations in its wall. The procedure was illogical and it is difficult to credit anyone using it without expecting recurrence of contracture as the capsular tissue conformed to the new reduced volume. It is also difficult to believe that proponents did not foresee severe long term adverse reactions. Firstly, these implants would have an open tract between the tissue and the compartment where the saline solution originally was. This would allow ingress of biological fluids, proteins and adventitious micro-organisms which would mix with prosthetic oils and debris and later incubate to form complex mixtures of potentially injurious substances.

From knowledge of the time, it was easy to forecast that such a pocket would ultimately become filled with denatured proteinaceous material and would become colonized early. The continuous release of debris and decaying autogenous products from such a space had predictable immunological and infection control applications. On balance of probability, no one performed studies on the impact of the procedure. Numerous case histories confirm that contracture would nevertheless recur within a few months of performing the decompression thus invalidating any useful effect.

The product inserts made specific reference to the procedure. They identified Dr. John Hartley as the author and illustrated the insertion of large gauge needles percutaneously through the breast into the implant’s outer compartment. All parties appeared unconcerned about the nearly inevitable perforation of the inner shell with the hypodermic syringe and its implication with respect to shell failure from a propagating tear originating at the site of accidental shell perforation. They also seemed unconcerned with possible infection of the pericapsular space incidental to the procedure.

In the light of the knowledge of the time, the procedure is even more surprising. Investigations had already confirmed chronic sub-clinical pericapsular infection with micro-organisms and inflammatory gel/oil effusion into tissue as the primary causes of contracture. The "Hartley decompression" did not address either of these problems.

Such a practice would have been expected to further exacerbate leakage of gel-derived products from perforation of the core shell or worsen infective processes by introducing new inoculae into the intracapsular space. Yet, for many years, perforating decompression was fashionable and numerous users of double lumen implants were subjected to it, in some cases with compression capsulotomy.

This habitually led to gross expulsion of captive biological material in the outer lumen and rupture of the gel core with dissemination of gel derivatives. The processes were often repeated until adverse reactions became so severe that device explantation, site debridement and prolonged antibiotic treatment were the only alternative.

Adverse reactions from "Hartley decompression" was a common side issue in many serious double lumen implant misadventures. It was also a concern for numerous clinicians who had responsibility for treatment of patients injured incidental to breast prostheses failures. In retrospect, perforating decompression of a double lumen implant breached fundamental aspects of surgery, cleanliness and common sense, even in the eyes of a layman.