Burn Wound Sepsis

Burn Wound Sepsis -

Little attention has been focused on the local burn wound environment, even though burn wound sepsis is a common cause of death in the burn victim. To characterize the effect of the local burn wound environment on neutrophil function and metabolism, the opsonic activity of blister fluid specimens against Pseudomonas aeruginosa was measured as was the effect of blister fluid on control neutrophil oxygen consumption using preopsonized zymosan and f-met-leu-phe (FMLP) as stimuli. Blister fluid did not support the killing of P. aeruginosa by normal neutrophils as well as normal serum. Additionally, blister fluid inhibited zymosan-stimulated, but not FMLP-stimulated, neutrophil oxygen consumption. The inhibitory effect of blister fluid on zymosan-stimulated oxygen consumption correlated with the extent of complement activation, measured as C3d or C3AI (p less than 0.01). That blister fluid did not inhibit the FMLP-mediated respiratory burst supports the concept that the blister fluid inhibitory effect on the zymosan-mediated respiratory burst was mediated through the complement receptor. These findings that blister fluid can affect the bactericidal and metabolic activity of normal neutrophils support the concept that cellular function can be altered by the microenvironment in which the cells are bathed. This potential impairment of host defenses within the burn wound could predispose the burn victim to burn wound sepsis.

Background: Infection remains the leading cause of death among patients who are hospitalized for burns. The risk of burn wound infection is directly correlated to the extent of the burn and is related to impaired resistance resulting from disruption of the skin's mechanical integrity and generalized immune suppression.

Burn wounds may be classified as wound cellulitis, which involves the unburned skin at the margin of the burn, or as an invasive wound infection, which is characterized by microbial invasion of viable tissue beneath the burn wound eschar. Bacterial burn wound infections and mortality from burn wound sepsis decrease with rapid burn debridement and wound closure and the use of effective topical and systemic antimicrobial chemotherapies. Unfortunately, the number of invasive fungal burn wound infections has risen significantly, likely because of excessive antimicrobial use. Overall mortality rates from burn wound sepsis remain high.

Management of severe burn wounds is aimed at preventing the progression of injury by maintaining adequate tissue oxygenation through aggressive volume repletion and early removal of necrotic tissue followed by wound closure. Effective topical antimicrobial therapy and daily wound inspection are necessary to monitor for infection, which may cause conversion of partial-thickness burns to full-thickness injuries.

Pathophysiology: Burn injury causes mechanical disruption to the skin, which allows environmental microbes to invade the deeper tissues. The usual skin barrier to microbes is replaced by a moist, protein-rich, avascular eschar that fosters microbial growth. The avascularity of the eschar prevents migration of immune cells and restricts the distribution of systemically administered antibiotics. Furthermore, toxic intermediaries released by the eschar can impede the immune response.

The burn wound surface is sterile immediately following injury; however, it is repopulated quickly with gram-positive organisms from hair follicles, skin appendages, and the environment during the first 48 hours. More virulent gram-negative organisms replace the gram-positive organisms after 5-7 days. Gram-negative organisms have greater motility, possess many antibiotic resistance mechanisms, and have the ability to secrete collagenases, proteases, lipases, and elastases, enabling them to proliferate and penetrate into the subeschar space. If host defenses are inadequate, invasion of viable tissue occurs.

Thermal injury has a severe impact on the host's cellular and humoral immune systems. The degree of immune suppression is proportional to the duration and temperature of thermal exposure. The injury produces a loss of skin and subjacent tissue, resulting in an area of irreversible central coagulation necrosis surrounded by an area of pronounced inflammation and hyperemia. The presence of major thermal injury impairs all circulating and stationary phagocytic cells, as well as bactericidal activity. Reduction of T-cell activity, decreases in inflammatory cytokine levels, and decreases in complement levels result in global impairment of host defenses.

Although advances in local burn therapies, including the judicious use of antimicrobials, undoubtedly has reduced infectious complications from large burns, secondary opportunistic infections with fungal pathogens have been noted in recent years. This especially is prevalent in patients sustaining larger burns (>40% total body surface area [TBSA]) who receive multiple doses of broad-spectrum perioperative antibiotics during wound debridement and/or antibiotics for infections at other sites.

Frequency:

In the US: Burn wound infections are rare in partial-thickness wounds. The risk of invasive burn wound infection is directly related to the extent of the burn. Burn wound infections account for 3-7% of all infections in patients with burns and occur most frequently in children, followed by elderly patients.

Internationally: Burn wound infections occur more frequently in countries with overcrowded burn units, fewer infection control barriers, and less access to immediate wound debridement or antimicrobial therapies.

Mortality/Morbidity: Burn wound cellulitis usually is responsive to topical and systemic antibiotic therapy and rarely is associated with progression or death. Invasive burn wound infections occur most often in critically injured patients with severe burns. Invasive burn wound infections with extension of tissue injury and multisystem organ dysfunction are associated with a mortality rate as high as 75%.

Age: Burn wound infections occur most frequently in children, followed by elderly patients.

CLINICAL

Section 3 of 9

Author Information Introduction Clinical Workup Treatment Medication Follow-up Miscellaneous Bibliography

History: Burn wound infections are rare in partial-thickness burns unless they have been neglected or managed improperly. Invasive wound infections typically occur in patients with full-thickness burns involving more than 30% of their body. Risk of wound infection is increased in wounds that remain open because of a failure of the primary closure modality or because of comorbidities.

Burn wound cellulitis is characterized by worsening localized pain and erythema in the skin surrounding the burn.

Invasive infection occurs in patients with a significant full-thickness burn in which closure is delayed.

Physical:

Burn wound cellulitis

Inflammatory changes in the skin adjacent to the burn are typical of burn wounds. However, areas that have progressive erythema or become more painful indicate cellulitis.

Cellulitis may not be associated with fever, tachycardia, or leukocytosis.

Invasive infection

Gauging burn wound sepsis by clinical signs and symptoms is difficult.

Patients with extensive burn wounds generally manifest physiologic changes associated with hypermetabolism, including tachycardia, hypothermia or hyperthermia, tachypnea, ileus, glucose intolerance, and mental status changes.

The clinical diagnosis of an invasive burn wound infection is best made by careful serial evaluations of the wound.

Clinical signs suggestive of burn wound infection include the following:

Progression of partial-thickness to full-thickness injury

Change in wound color (focal areas of red, brown, or black discoloration)

Green discoloration of the subcutaneous fat

Violaceous discoloration and edema of wound margins

Subeschar hemorrhage

Rapid eschar separation

Causes:

Risk factors for the development of a burn wound infection

Burn covering more than 30% TBSA

Full-thickness burn

Extremes in patient age

Preexisting disease (eg, immune suppression, diabetes, vascular insufficiency)

Virulence and antibiotic resistance of colonizing organism

Failed skin graft

Prolonged open burn wounds

Improper initial burn wound care

Organisms most frequently isolated from burn wound biopsy specimens

Staphylococcus aureus

Pseudomonas aeruginosa

Enterobacter cloacae

Klebsiella pneumoniae

Enterococcus faecalis

Acinetobacter baumannii

Aspergillus species

Candida albicans

Organisms most frequently causing burn wound infection

Aspergillus species
Mucor species
Enterobacter cloacae
Aeromonas hydrophila
Enterococcus faecalis

WORKUP

Section 4 of 9

Author Information Introduction Clinical Workup Treatment Medication Follow-up Miscellaneous Bibliography

Lab Studies:

The diagnosis of a burn wound infection is suggested by the physical characteristics of the wound; confirmation rests with histological verification of microbial invasion of viable tissue.

The WBC count is of little specific value in the diagnosis of burn wound infection and may be elevated, within the reference range, or decreased (with or without a left shift).

Other Tests:

Wound surface cultures: Swabs of the wound surface cannot be used to differentiate microbial colonization from invasive tissue infection. Swab cultures are helpful to identify potential pathogens colonizing the wound, and they provide valuable information to guide prophylactic perioperative systemic antibiotic selection for wound debridement.

Procedures:

Burn wound infection is confirmed by obtaining a wound biopsy that distinguishes microbial colonization from invasive infection.

A 500-mg sample of tissue that includes viable tissue under the eschar is excised sharply from the wound. A portion of the biopsied material is sent for culture and antibiotic sensitivity determination, and the remaining portion is submitted for histologic examination.

Histologic samples can be processed rapidly by frozen section; a 4% false-negative rate is reported.

Quantitative bacterial counts less than 105 cells per gram of tissue rarely indicate invasive infection. Counts exceeding 105 cells per gram are accurate in predicting invasive infection approximately 50% of the time.

Histologic Findings: Microorganisms are present in viable unburned tissue. Aspergillus hyphae are 2-4 mm wide with frequent septa and a characteristic 45° branching pattern. Vascular microbial invasion and small vessel thrombosis are observed. Ischemic necrosis of unburned tissue and hemorrhage in unburned tissue is observed.

Staging:

Stage I - Colonization of nonviable tissue

A - Superficial colonization, ie, microorganisms present on burn wound surface

B - Microbial penetration, ie, microorganisms present in variable thickness of eschar

C - Subeschar proliferation, ie, multiplication of microorganisms in the subeschar space

Stage II - Invasion of viable tissue

A - Microinvasion, ie, microscopic foci of microorganisms in unburned viable tissue immediately beneath the burn wound

B - Generalized invasion, ie, multifocal or diffuse penetration of microorganisms into viable subcutaneous tissue

C - Microvascular invasion, ie, microorganisms present in unburned small blood vessels and lymphatics

TREATMENT

Section 5 of 9

Author Information Introduction Clinical Workup Treatment Medication Follow-up Miscellaneous Bibliography

Medical Care:

Bacterial infection

Cellulitis: Apply topical mafenide acetate burn cream twice daily, and administer systemic antibiotic therapy until the infection resolves. Most cases of burn wound cellulitis are caused by group A beta-hemolytic streptococci, which can be treated with penicillin. If specific cultures and sensitivities are not known, a broad-spectrum beta-lactam antibiotic should be administered.

Colonization of nonviable tissue (stage IA to IC): The wound should be debrided, followed by the application of silver sulfadiazine cream every 12 hours. Wounds that are colonized more heavily or those that deteriorate should be treated with mafenide acetate. The topical creams should be removed daily, and the wound should be cleansed with a surgical detergent.

Invasion of viable tissue (stage IIA to IIC): The infected wound should be excised surgically. Antimicrobial coverage should be started prior to excision to prevent hematogenous spread and organ seeding.
- Gram-negative infections: Invasive infections caused by gram-negative organisms should be treated with topical mafenide acetate to ensure penetration of the burn eschar. Subeschar clysis with an antibiotic solution prior to surgical excision may be helpful. The antibiotic solution is injected below the eschar 6-12 hours before surgery and again immediately prior to the procedure.
- Gram-positive infections: Invasive gram-positive infections are characterized by suppurative foci in the burned tissue. These infections require administration of appropriate systemic antibiotics and debridement, followed by a topical application of mupirocin, mafenide acetate, or silver sulfadiazine.

Fungal infection

Colonization of nonviable tissue (stage IA to IC): Candidal species rarely invade tissue and, therefore, do not require surgical excision. Wounds colonized with candidal species are treated with a twice-daily application of a topical antifungal cream, such as clotrimazole or ciclopirox olamine. Alternatively, mafenide acetate mixed with nystatin powder is effective for topical treatment of superficial fungal infections.
Invasion of viable tissue (stage IIA to IIC): Filamentous fungi, including Aspergillus and the agents associated with mucormycosis, are responsible for most invasive fungal burn wound infections. The treatment of invasive fungal infection is analogous to invasive bacterial infection, ie, surgical excision of the infected burn wound followed by application of topical antimicrobial therapy (clotrimazole or ciclopirox olamine). Systemic dissemination or extensive tissue involvement necessitates administration of systemic amphotericin B.

Surgical Care:

Invasive bacterial or fungal burn wound infections are treated with surgical excision to the level of viable tissue.

Wounds that can be excised completely should be covered with an allograft or autograft.

If complete removal of the infected tissue is not possible, 5% mafenide acetate should be applied, and the wound should be reexamined in 24 hours for possible repeat excision.

With aggressive fungal infections, particularly mucormycosis, radical debridement of muscle, including limb amputation may be necessary to control infection.

Consultations: An ophthalmologic evaluation should be performed in patients with suspected or proven candidemia to exclude the possibility of metastatic Candida endophthalmitis.

Diet: The basal metabolic rate is increased 100% above the reference range in patients with burns of greater than 40% TBSA.

Enteral feeding of a high-caloric diet through a nasogastric tube should be instituted within the first 12 hours after injury. The feedings should include a high-protein component (2 g/kg/d) and 3-10 times the recommended daily allowance of vitamins and minerals, particularly zinc (7 mg/d).

In severely injured patients, supplementation with omega-3 fatty acids and arginine has been shown to decrease sepsis.

Activity: Patients may be as active as they can tolerate. Aggressive physical therapy of extremity injuries is paramount.

The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.

Drug Category: Antibiotics -- Applied after injury to limit bacterial colonization. Established infection requires use of topical agents that can penetrate the eschar to reduce microbial counts and prevent systemic dissemination.

Systemic agents are instituted for cellulitic wound infections, gram-positive suppurative infections, extensive fungal invasion, or systemic spread.

Drug Name	Silver nitrate -- Silver ion has broad-spectrum antibacterial activity but does not penetrate burn wound eschar; therefore, it is most effective when applied early.
Adult Dose	Apply topically to wound to a thickness of approximately 1.5 mm qd or bid as moistened dressings
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; broken skin or cuts
Interactions	Decreases effects of sulfacetamide preparations
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Not for internal use; can cause sodium, potassium, chloride, and calcium leaching from wound

Drug Name	Mafenide (Sulfamylon) -- Topical sulfonamide. Diffuses freely into the eschar and is highly effective against gram-negative organisms, including Pseudomonas species.
Adult Dose	Apply cream to open wounds bid/tid
Pediatric Dose	Apply as in adults
Contraindications	Documented hypersensitivity; renal impairment
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Pain or burning may occur upon application; metabolized to a carbonic anhydrase inhibitor (p- carboxybenzenesulfonamide), which may result in metabolic acidosis

Drug Name	Mupirocin (Bactroban) -- Active against a wide variety of gram-positive bacteria, including methicillin-resistant Staphylococcus aureus. Also active against certain gram-negative bacteria. Exerts activity by binding to bacterial isoleucyl transfer RNA-synthetase.
Adult Dose	Apply to affected areas tid and cover with gauze dressing
Pediatric Dose	Apply as in adults
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Prolonged use may result in growth of nonsusceptible organisms; do not use on very large wounds where polyethylene glycol absorption is possible (especially in patients with moderate renal failure)

Drug Name	Silver sulfadiazine (Silvadene) -- Useful in prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria, including yeast.
Adult Dose	Apply to open wounds bid/tid
Pediatric Dose	<3 months: Not recommended >3 months: Apply as in adults
Contraindications	Documented hypersensitivity; women who are pregnant or breastfeeding (possibility of kernicterus in infant)
Interactions	Effect of proteolytic enzymes (eg, collagenase, papain, sutilains) is reduced when used concomitantly
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in patients with G-6-PD deficiency and renal insufficiency; may induce neutropenia as a result of direct bone marrow suppression

Drug Name	Penicillin G (Pfizerpen) -- Inhibits biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached and most effective during the stage of active multiplication. Inadequate concentrations produce only bacteriostatic effects.
Adult Dose	12-18 million U/d IV divided q4h
Pediatric Dose	25,000-50,000 U/kg/d IV divided q6h
Contraindications	Documented hypersensitivity
Interactions	Probenecid may increase serum levels by decreasing clearance; tetracyclines are bacteriostatic, causing a decrease in the effectiveness of penicillins when administered concurrently
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution in patients with renal impairment

Drug Category: Antifungals -- Mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis or altering the permeability of the cell membrane (polyenes) of the fungal cell.

Drug Name	Amphotericin B (Amphocin, Fungizone) -- Useful for many serious systemic fungal infections. Produced by a strain of Streptomyces nodosus. Can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in fungal cell membrane, causing intracellular components to leak, with subsequent fungal cell death.
Adult Dose	0.5-1 mg/kg/d IV (range is 0.25-1.5 mg/kg/d); not to exceed 1.5 mg/kg/d
Pediatric Dose	0.25 mg/kg IV over 6 h with frequent observation during the first several hours of the infusion; if no reaction with initial dose, a full maintenance dose may be administered Maintenance: 0.5 mg/kg IV (range is 0.25-1 mg/kg/d)
Contraindications	Documented hypersensitivity; hypokalemia and/or hypomagnesemia
Interactions	Concurrent use with loop diuretics (eg, furosemide, bumetanide, ethacrynic acid), corticosteroids or corticotropin, ACTH, cisplatin, or carbonic anhydrase inhibitors can cause additive hypokalemia due to renal potassium wasting; hypokalemia can potentiate cardiac toxicity of cardiac glycosides (eg, digoxin) and dofetilide; hypokalemia can enhance curariform effect of neuromuscular blockers (eg, tubocurarine)
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Monitor renal function, serum electrolytes (eg, magnesium, potassium), liver function, CBCs, and hemoglobin concentrations; resume therapy at lowest level (eg, 0.25 mg/kg) when interrupted for more than 7 d; hypoxemia, acute dyspnea, and interstitial infiltrates may occur in patients with neutropenia who are receiving leukocyte transfusions (separate time of amphotericin infusion from time of leukocyte transfusion)

Drug Name	Ciclopirox (Loprox) -- Interferes with synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.
Adult Dose	Apply to affected area bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Avoid contact with eyes and other internal routes

Drug Name	Clotrimazole (Lotrimin) -- Broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing death of fungal cells.
Adult Dose	Apply to affected area bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Not for treatment of systemic fungal infections; avoid contact with eyes; if irritation or sensitivity develops, discontinue use and institute appropriate therapy

FOLLOW-UP

Section 7 of 9

Author Information Introduction Clinical Workup Treatment Medication Follow-up Miscellaneous Bibliography

Deterrence/Prevention:

Early removal of full-thickness burned tissue in addition to early definitive wound closure and strict enforcement of infection control procedures

Complications:

Systemic spread and seeding of distant organs or invasion of muscle may occur; limb amputation may be required.

Sepsis can contribute to multisystem organ failure and death.

Methicillin-resistant S aureus infection

Methicillin-resistant S aureus (MRSA) infection is a serious and increasingly common cause of nosocomial infection in patients with large burn wounds.

The incidence of MRSA colonization and subsequent infection has increased dramatically in the last decade, primarily because of antibiotic selective pressure in critically ill hospitalized patients.

Risk factors that have been associated with MRSA colonization or infection include age, coma, invasive procedures, and extended hospitalization.

MRSA colonization/infection rates may be reduced by early eschar excision, wound closure, bacterial wound surveillance, and strict enforcement of infection control procedures.

Systemic vancomycin therapy and topical application of mupirocin cream are indicated for burn wounds infected with MRSA.

Hospital personnel who have been demonstrated to harbor MRSA should receive mupirocin nasal ointment until surveillance culture results are negative.

Prognosis:

Infections leading to mucormycosis are the most difficult to eradicate. Amputation is required in 35% of patients, and an associated mortality rate exceeding 40% can be expected.

Burn Wound Sepsis Burn Scar Treatment - Topical Care

BIOSKINCARE™ has a two fold effect: (1) Degrades debris, damaged, abnormal and necrotic tissues & decongests the skin as it helps to dissolve all damaged structures into their amino-acid and other components by the action of enzymes. (2) Favors tissue regeneration.

It leaves your skin smooth, refreshed, soft and with use over a period of time it reduces contractures and takes away keloid, hypertrophic and all types of scars and blemishes: acne, scars, keratosis bumps, razor nicks and burns, actinic keratosis lesions, roughness, dryness, ezcema, dermatitis, the effects on the skin of radiotherapy for cancer, blisters, scrapes, cuts, and the list can go on and on... It clears and enhances the complexion.

Made in the USA. 50 grams = 1.76 oz

Save at least 20% off price & save on shipping costs
when you order more than one jar

Regular Price for One Bottle: $59.98

Discount Price Two Bottles: $47.98 each

Ultra exfoliate rough scars and dull skin with BIOSKINEXFOL

Home microdermabrasion cream. Contains the same natural ingredients in BIOSKINCARE but infused with micro-crystals so that you may rub it with your finger tips to remove old, hard, and tough scars or stretch marks by a physical breakdown of the scar tissues. Best also for oily skin and aged skin, actinic keratosis scales and pitted acne scars. Not for keloids and not if your skin is still fragile (use BIOSKINCARE for a few months first to strengthen your skin). The compounded action of the physical abrasion and the enzymes in the cream liquefy damaged proteins more thoroughly helping to release amino-acids to aid in rebuilding damaged tissues quickly. Results are not only immediate, but compound over time and do not trigger inflamm-aging of delicate skin tissues.

Microdermabrasion Benefits

Made in the USA. Two to Three Month's supply 120 grams = 4.23 oz

120 Gram Bottle: $79

Get rid of hiperpigmentation of scar areas and tissues and sun & age spots while reviving and protecting the skin from the effects of free radicals with BIO SKIN REJUVENATION

A deeply moisturizing natural skin care cream that replenishes the lipid barrier of the skin and triggers the repair of cells damaged by UV radiation and Free Radicals. Also gets rid of brown, sun and age spots, actinic keratosis scales and all types of skin blemishes. The same ingredients in BIOSKINCARE with an added natural substance that reduces melanin hyperpigmentation and a biomimetic peptide that inhibits the accumulation of melanin pigments.

Skin Rejuvenation Benefits

One Month's Supply 1.76 oz., 50 Gram Bottle: $69.98

Toll Free USA & Canada

phone BIO SKIN REVIVAL

Certified Seller Safe, Honest, & Guaranteed

The Biological Skin Treatment Serum

Our products contain a biological serum created by a living creature to (a) take care of its own skin everyday and keep it moisturized, and healthy, (b) neutralize free radical oxidation and the damaging effects of excessive solar radiation and (c) keep microbes in check by the action of antimicrobial peptides secreted on the skin, (d) repair and regenerate its skin. It even regenerates some of its organs whenever damaged.

It keeps the skin moisturized, prevents skin infection, repairs wounds, promotes scar less healing, and renews the skin.

The collection of the biological ingredient in our products is done by using a humanely method that inflicts no damage upon the little creatures.

Skin Treatment Products

BIOSKINCARE™
A natural skin care cream that triggers the regeneration of damaged cells and replenishes the lipid barrier of the skin while preventing and removing scars from accidental injuries and post surgery; stretch marks; hypertrophic and keloid scars; keratois pilaris, actinic keratosis, dermatitis, psoriasis scales and all types of skin blemishes. 50 gram jar = $59.98 and for two or more 20% discount.

BIO STRETCH MARK CREAM™
Prevents stretch marks, strengthens fragile skin, firms sagging breasts and body areas and reduces cellulite. It also works for newly formed stretch marks and scars, while BIOSKINEXFOL works best for old, rough and raised marks. The base cream is the same as in BIOSKINCARE, in a more economical container, with 6 oz. but for use only on the body, not on the face, because it contains a slightly higher proportion of the biological complex which results in an invisible film that retains in moisture by occluding the area where it is applied but may feel a little tacky on the face. 6 oz (180g) tottle = $119.00

BIO SKIN REJUVENATION™

Same cream base and enzymes as in BIOSKINCARE to "digest" or dissolve blemishes, speed skin turnover and tighten skin, and two added ingredients: one is a human growth factor peptide, derived from the melanocyte-stimulating-hormone. Blocks melanin synthesis, and reduces the formation of unwanted pigmentation, allowing control over skin tone and brown spots. The other is a natural plant extract that takes away dark pigmentation. Leaves skin bright and refreshed! 50 gram jar = $69.98.

BIOSKINCLEAR™

An oil free moisturizer gel for acne, rosacea and facial scars. Heals lesions to the cells lining the hair follicles which is the root cause of inflammatory acne. Removes dead cells, unclogs sebum canals and dissolves scar tissues by enzymatic hydrolysis, without peeling. Promotes the proliferation of antimicrobials that control acne bacteria. Boosts reproduction of glycosaminoglycans, the molecules that retain water, thus truly moisturizing the skin from within. Tells the body it is being taken care off and can moderate an otherwise extreme inflammatory reaction that may end up destroying healthy skin cells and creating crater like scarring and not only the acne bacteria. 50 gram (1.76 oz) airless pump bottle $49 and 20% off for two or more.

BIOSKINEXFOL™
A home microdermabrasion cream with micro-crystals that breakdown hard, rough and old scar tissues, and allow for a deeper penetration of our natural skin moisturizing and regeneration complex contained in the microdermarasion cream. 120 gram (4 oz) jar = $79

The articles you may access from the menu below provide information from different sources about burn care, wounds, Burn Wound Sepsis, scars and other related subjects of interest. We are working to update all of them and when they are ready this message will no longer be here.

Other Links Related to Burn Wound Sepsis