CASE REPORT

TOXIC SHOCK SYNDROME AS A COMPLICATION OF BREAST PROTHESES.

MANY WOMEN WITH THIS TERRIBLE RESULT!

PIERRE BLAIS SAID: MANY WOMEN LOST ONE OR TWO POUNDS

"TISSU" AND A LOST OF " ARM, LEG…."

"SALIN BREAST IMPLANT"

Infections involving breast prostheses are uncommun. The reported incidence is 2 to 3 percent for augmentation mammaplasty and slightly higher after reconstructive breast surgery. Infection manifests itself as localized erythema, pain, swelling, and drainage from the operative site occurring between 6 days and 6 weeks postoperatively. We report a case of postoperative infection after augmentation mammaplasty with severe systemic manifestations but minimal local signs of inflammation consistent with toxic shock syndrome.

Toxic shock syndrome is maintly associated with menstruation and the use of tampons, but the incidence of nonmenstrual toxic shock syndrome is increasing. It was first describeb in 1978 and has risen from 4 percent of toxic shokc syndrome cases in 1979 to 13 percent in 1981. By 1986, Gaventa et al. Reported an incidence of 45 percent nonmenstrual toxic shock syndrome using active surveillance for cases in a defined geographic aera. Of increasing concern is the manifestation of toxic shock syndrome in a variety of new clinical settings notably postopérative wound infections, whick now account for 16 percent of the reported cases of nonmenstrual toxic shock syndrome is associated with a higher mortality rate. To our knowledge, four cases of toxic shock syndrome associated with breast prostheses have been reported previously. Our case illustrates the presentation of toxic shock syndrome in the postoperative setting and serves to remind the clinician of this potentially devastating complication.

CASE REPORT

3 women are victims of saline breast implants in Québec.

Patients are great victims by "saline breast implants" All with nausea, lethargy, and a rash. One "breast amputated and death, one, fingers and legs, and the other one breast and fingers amputated and secret name.

DISCUSSION

Toxic shock syndrome was first described in a group of seven children who presented with high fever, headache, confusion, a rash, vomiting, diarrhea, and multiple organ failure (shock, renal failure, hépatic abnormalites. And disseminated intravascular coagulation). The association with menstruating women using tampons gained a high profile in the media durant the early 1980s. Nonmenstrual toxic shock syndrome has been describeb in various clinical settings: soft-tissue staphylococcal infections, childbirth or abortion, vaginal infections and postoperative infections. The procedures implicated include herniorrhaphy, tubal ligation, arthroscopy, ureterolithotomy, pleurectomy, shoulder repair, spinal fusion and cystenucleation. Recently, as more cases of nonmenstrual toxic shock syndrome have been reported, the clinical setting has diversified to include trauma, burns, insect bites, influenza, sinusitis, tracheitis, pneumonia, arthritis, and osteomyelitis. Use of the contraceptive sponge and diaphragm also has been associated with nomenstrual toxic shock syndrome. Among plastic surgical procedures, it has been noted after nasal surgery, chemical peel, and augmentation and reduction mammaplasty.

Toxic shock syndrome is a clinical diagnosis based on a constellation of signs and symptoms and the exclusion of other diseases and etiologies that could cause a septic shocklike state. Both menstrual and nonmenstrual toxic shock syndrome share the same clinical profile, although nonmenstrual toxic shock syndrome as greater central nervous system involvement, less musculoskeletal symptomatology, a more severe anemia, and a greater delay in symptom onset. Toxic shock syndrome exotoxin 1 production is more prevalent in menstrual toxic shock syndrome with more than 90 percent of the S. aureus isolates producing toxic shock syndrome exotoxin 1, while only 40 t0 60 percent of nonmenstrual toxic shock syndrome staphylococcal isolates produced this toxin. Sixty percent of theses isolates also produced enterotoxins. The mortality rate for infection with toxic shock syndrome exotoxin 1-negative strains is 50 percent, compared to 10 percent with toxic shock syndrome exotoxin 1-positive strains.

Althrough toxic shock syndrome is in many ways similar to septic shock, there are two distinguishing features: (1) the predominance of gastrointestinal symptoms, namely, vomiting and diarrhea, in the initial phase and (2) the dermatologic manifestatins, including macular erythorderma of the trunk and extremities in the initial setting and during the convalescent phase, desquamation of the palms and soles.

Features that distinguish toxic shock syndrome from the usual postoperative wound infection include its short incubation, rapid onset of profound hypotension requiring massive fluid resuscitation and cardiotomic agents, development of multiple organ failure, and the dermatologic manifestations describeb above. The median interval between surgery and onset of symptoms is 2 days. In the five patients reported after augmentation mammaplasty, onset of symptoms averaged 3 days; our patient presented 6 days after implantation.

The virulence of S aureus as a pathagen can be attributed to the physical and biochemical properties of its cell wall (including the presence of protem A), the production of extracellular enzymes and the elaboration of numerous toxins, including "staphylococcus" enterotoxins A,B and C., Shock can be produced by this pathogen through several different mecanisms (1) extensive local infection and hypiovolemia and activation of the complement and kinin pathways, and (4) toxigenic shock production. The genesis of the ful clinical spectrum of toxic shock syndrome is centerred on the last mechanism.

The manner in witch the full clinical spectrum of toxic shock syndrome arises is still unclear, although various mechanisms have been proposed. A direct toxigenic effect on host tissue by the exoproteins elavorated by the colonizing S aureus has been postulated. It aslo has been proposed that toxic shock syndrome exotoxin 1 enhances the susceptibility of the organism to endotoxin and that the two toxins act synergistically with one another. Given the similarity of toxic shock syndrome to septic shock and the multipe organ failure syndrome secondary endogenous mediators also have been implicated in the development of toxic shock syndrome and include interleukin 1, tumor necrosis factor, interferon-y and interleukin 2. In inducing these metabolites, staphylocoocal toxins (enterotoxins, exfoliative tozin, and toxic shock syndrome exotoxin 1) and streptococcal pyrogen exotoxins are referred to as superantigens, which at low concentrations stimulate proliferation of T cells and cause an alteration in the immune system homeostasis, clinically manifested as shock and multiple organ failure. Arachidonic acid metabolities, activation of the complement and kinin system, and platelet factors also have been implicated in the pathophysiologiy of this syndrome. Colonization by S. aureus is the primaty event; exoprotein (toxic shock syndrome exotoxin 1 or enterotoxin) release follows with consequent toxic insult to the host tissue and mediator release resulting in the multisystem injury.

In 1988, Nordstrôm et al. Mentioned a case of Serratia marcescens infection of a tissue expander used for postmastectomy breast reconstruction. As in our patient, bacteria were cultured from both the periprosthetic fluid and the saline within the implant.

The ability of bacteria to traverse the membrane elastomer appears to hod the key to understanging these pathologic process. The permeability of silicone implant to substances on organisms occurs by means of two proposed mechanisms. Either a substance can diffuse directly through the menbrane elastomer (as with ether, lidocaine, iodine, steroids and certain antibiotics), or it must leak through holes in the membrane or fill ports. Only one group has studied the passage of bacteria were unable to cross an intact membrane but could easily penetrate the implant if the fill ports had been punctured for access.

Once across the membrane, bacterial growth depends on an adequate milieu for organism survival. Further study is necessary to determine of the diffusion of tissue products accors the membrane and into the saline can produce an environment favorable to bacterial growth.

The presentation of the patient reported here is quite similar to that of the patients describek previously. All cases have been notable for a paucity of local signs of infections. Our patient was toxic shock syndrome exotoxin 1-négative and staphylococcal enterotoxin B-positive and her disease course appaears to be the most severe, save for the one fatality reported. Of the four previously reported cases of toxic shock syndrome secondary to breast prostheses, there were two patients who suffered severe multipe organ failure, but the toxin elaborated as toxic shock syndrome exotoxin 1-positive, were comparably less severe. Although toxic shock syndrome exotoxin 1-negative strain infections have been noted to have a higher mortality rate, it remains to be proven whether staphylococcal enterotoxin B-associated toxic syndrome is more severe variant of the syndrome and whether if has true progostic significance on morbidity or mortality. The present toxic shock syndrome laboratory panel tests for both toxic shock syndrome exotoxin 1 and staphylococcal enterotoxin B. Although our patient survived, the severity of her residual disbility must serve as a reminder to clinicians to be watchful for this rare but devastating complication.