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Resident Orientation Manual

Produced by Galveston Shriners Burn Hospital and
The University of Texas Medical Branch Blocker Burn Unit.
Contributors:  Sally Abston MD, Patricia Blakeney PhD, Manubhai Desai MD,
Patricia Edgar RN, CIC,John P Heggers PhD, David N Herndon MD,
Marsha Hildreth RD, Ray J Nichols Jr. MD

 

POST-BURN INFECTION & SEPSIS

   Before embarking on the antimicrobial therapeutic approach in the treatment of burn wound sepsis, it is important to establish certain consistencies in terminology.

  Bacteremia:  The transient presence of bacteria or other microorganisms in the blood. (e.g. bacteria in the blood after brushing one's teeth)

  Septicemia:  The invasion of the blood stream by pathologic microbes from a focus of infection or a locus minoris resistentiae and an active proliferation of these microbes accompanied by hyperthermia, hypothermia and/or prostration.  Frequently, it is diagnosed clinically by the presence of any 3 of the cardinal signs:  obtundation, hyperventilation, ileus, thrombocytopenia, hyperglycemia, leucocytosis or leukopenia.

  Colonization:  The mere presence of bacteria, establishment of a colony;  bacterial counts of
105 bacteria/gm of tissue with no evidence of invasion into viable tissue.

   Infection is the most common and most serious complication of a major burn injury related to burn size.  Sepsis accounts for 50-60% of deaths in burn patients today despite improvements in antimicrobial therapies.  Sepsis in burns is commonly due to bronchopneumonia, pyelonephritis, thrombophlebitis, or invasive wound infection.  The burn wound is an ideal substrate for bacterial growth and provides a wide portal for microbial invasion.  Microbial colonization of the open burn wounds, primarily from an endogenous source, is usually established by the end of the first week.  Infection is promoted by loss of the epithelial barrier, by malnutrition induced by the hypermetabolic response to burn injury, and by a generalized post-burn immunosuppression due to release of immunoreactive agents from the burn wound.

   Burn injury leads to suppression of nearly all aspects of immune response.  Post-burn serum levels of immunoglobulins, fibronectin, and complement levels are reduced, as well as a diminished ability for opsonization.  Chemotaxis, phagocytosis, and killing function of neutrophils, monocytes, and macrophages are impaired.  Granulocytopenia is common following burn injury.  Cellular immune response is impaired, as evidenced by delayed allograft rejection, anergy to common antigens, impaired lymphocyte mitogenesis, and altered mixed lymphocyte responsiveness.  Burn injury results in reductions of interleukin-2 (Il-2) production, T-cell and NK cell cytotoxicity, and helper to suppressor T-cell ration (HSR).  Furthermore, infusion of serum from burned to normal patients or animals can transmit some of these immunosuppressive effects.
 

Control of Infection
   Although care of the burn wound is not the initial priority, subsequent survival depends upon it.  The avascular burn eschar is rapidly colonized by 5 days post-burn, despite the use of antimicrobial agents.  If the bacterial density exceeds the immune defenses of the host, then invasive burn sepsis may ensue.  When bacterial wound counts are >105 microorganisms per gram of tissue, risk of wound infection is great, skin graft survival is poor, and wound closure is delayed.

   The goals of local wound management are the prevention of dessication of viable tissue and the control of bacteria.  These are achieved by use of topical antimicrobial agents and/or biological dressings.  It is unrealistic to expect to keep a burn wound sterile.  Bacterial counts of less than 103 organisms/gm are not usually invasive and allow skin graft survival rates of >90%.

   Antimicrobial therapy is directed by bacterial surveillance through routine tri-weekly sputum, urine, and wound cultures.  In addition, punch biopsies for each 18% BSA of burn are obtained qMWF for wound monitoring until the wound is closed.  Quantitative wound biopsy is a better determinant of significant pathogens than qualitative surface swabs.  Organism identification and
in vivo sensitivities to antibiotics are obtained within 48 hours.  Agar diffusion assays can also be performed to test susceptibilities to topical antimicrobials.  If quantitative biopsies reveal microbial density of >103 organisms/gm, a change in topical therapy is indicated.  If bacterial counts are 105, wound infection should be suspected and rapid histologic analysis and gram stain should be performed to confirm this.  Wound infection is confirmed by histologic evidence of tissue invasion or clinical sepsis.  Systemic antibiotics must be instituted, and the wound excised.

   Diagnosis of sepsis in burn patients can be difficult to distinguish from the usual hyperdynamic, hyperthermic, hypermetabolic post-burn state.  Blood cultures are commonly negative.  Fever spikes are not proportional to degree of infection.

   Clinical diagnosis of sepsis is made by meeting at least 3 of the following criteria:

1)  burn wound infection (>105 organisms/gm tissue) with histologic or clinical evidence of invasion
2)  thrombocytopenia (<50,000) or falling rapidly
3)  leukocytosis or -penia (>20,000 or <3,000)
4)  unexplained hypoxia, acidosis or hyper/hypoglycemia
5)  prolonged paralytic ileus
6)  hyper/hypothermia (>39C or <36.5C),
7)  positive blood cultures
8)  documented catheter or pulmonary infection
9)  altered mental status
10)  progressive renal failure or pulmonary dysfunction

   Local evidence of invasive wound infection includes:

black or brown patches of wound discoloration
rapid eschar separation
conversion of wounds to full-thickness
spreading peri-wound erythema
punctuate hemorrhagic sub-eschar lesions
violaceous or black lesions in unburned tissue (ecthyma gangrenosum)

   Appropriate systemic antibiotics are administered as indicated.  The appropriate use of antibiotics should be based on the following definitions:

  Prophylaxis - A preventative or precautionary measure designed to preserve health and prevent the spread of disease.

  Perioperative - This may also be considered prophylaxis.  It is the administration of systemic antibiotics as a protective measure for any type of surgical intervention.  The time frame for administration should be short-lived and is limited to 1 to 3 doses, depending on the operative procedure.

  Therapeutic - This is the administration of antibiotics for the treatment of infection.  Depending on the infection, therapy may continue for several days.
   Systemic antibiotic treatment for burn wound sepsis is continued for at least 72 hours after evidence of sepsis has resolved.  If the wounds appear clean, other sources such as the lungs, the kidney, and peripheral veins should be suspected.  In the absence of a confirmed organism or site, antibiotic selection should be based on routine surveillance cultures.  Empiric antibiotic choice should also be based on sensitivities of the burn facility's endogenous organisms.  We use Vancomycin, Imipenem, Timentin or Ceftazidime for coverage against the usual strains of Staph. aureus and Pseudomonas aeruginosa prevalent in our unit.  Routine perioperative antibiotics should also take ward-endogenous organisms into account.  Post-operative antibiotics are continued until quantitative excisional wound biopsies from surgery are identified.

  Blood Cultures - Blood cultures are essential in determining septic episodes.  The best time to collect the specimen is before the temperature spikes.  A temperature above 39.5 is the body's method for cleansing the blood stream of bacteria.  Most bacteria do not survive at prolonged temperature above 39.5.  Care must be taken not to contaminate the blood culture bottle.  Site selection for collecting the specimen must be meticulously and aseptically cleansed prior to specimen collection.  If the site is through a contaminated area, appropriate comments should be made on the request slip.

  Ova and Parasites - All burn patients arriving from Mexico, Central America, and South America should receive mebendazole on arrival for 3 days.  (The risk of treatment is low, so stool cultures are no longer performed.)  Remember, most parasitic cycles occur every 2 weeks.  Treat family members as well.

  Urinary Tract Infection (U.T.I.) - If a U.T.I. is suspected as the cause of sepsis, urine must be collected aseptically.  Appropriate comments should be made on the request slip.
(e.g.  Temp. 39.8, clean catch, catheterized, etc.)

  Upper Respiratory Infection (U.R.I.) - If a U.R.I. is suspected or evident from clinical signs, an x-ray, sputum, and bronchial washings are essential in order to identify the etiologic agent or infection.  However, based on recent mortality studies, the organism isolated from lung abscesses most closely correlated with organisms from the wound, rather than what organisms were isolated from sputum specimens.  Spittle is an unacceptable specimen.
 

Topical Antimicrobials
   Currently, a number of topical agents are available to assist in microbial control of the burn wound, including silver sulfadiazine, mefenide acetate, 0.5% silver nitrate, bacitracin/polymyxin B, mupirocin, and Mycostatin.  No single agent is totally effective and each has advantages and disadvantages.  Almost all agents will affect wound healing and increase metabolic rate.

   Silver sulfadiazine (e.g. Silvadene or SSD) is the most commonly used topical antimicrobial agent in burns.  Its antimicrobial properties are derived from the dual mechanisms of its silver and sulfa moieties (functional parts), and has a broad spectrum of antimicrobial coverage including gram positive bacteria, most gram negative bacteria, and some yeast forms.  Some gram negative organisms (e.g. some Pseudomonas species), do possess a plasmid mediated resistance.  Unlike mafenide or silver nitrate, silver sulfadiazine does not hinder epithelialization, although it does hamper contraction of fibroblasts.  Furthermore, silver sulfadiazine is painless on application, has high patient acceptance, and is easy to use with or without dressing.  Although true allergic sensitivities are rare, many patients will develop a transient leukopenia 3 to 5 days following its continued use secondary to margination of circulating white blood cells.  This leukopenia is generally harmless and merits observation, but not cessation of treatment.  However, if the white blood cell count drops below 3000, the medication is sometimes withheld until the WBC count returns to >4000-5000.  Mafenide acetate 11.2% cream (e.g. Sulfamylon) is one of the oldest effective topical antimicrobial agents.  Mafenide has a broad spectrum of antimicrobial activity, including silver sulfadiazine-resistant Pseudomonas and enterococci, but reduced antifungal properties.  Its exact mechanism of action is not clear, but thought to be related to its water-soluble sulfa moiety.  Mafenide cream is toxic to epithelial cells and fibroblasts. Unlike other topical agents, mafenide has good penetration through the eschar.  For this reason mafenide is commonly used on dirty or infected burn wounds, or electrical burns, and on burned ears to prevent chondritis.  Following its application, mafenide produces a manful sensation for several minutes, thereby earning its nickname of 'white lightning'.  Mafenide can cause an allergic skin rash.  Through carbonic anhydrase inhibition, mafenide can also cause bicarbonate wasting in the kidneys, hyperchloremia, systemic metabolic acidosis and compensatory hyperventilation.  To protect against such metabolic abnormalities one can sequentially follow serum electrolyte levels and treat abnormal values with appropriate intravenous replacement therapy.  Alternatively, applications of mafenide cream can be limited to no more than 20% of the BSA at any one time.  The sites of mafenide applications can then be rotated every 2 hours until the entire burn has been treated.  We will often alternate mafenide and silver sulfadiazine creams on seriously contaminated wounds as a form of 'pulse therapy'.

   Silver nitrate 0.5% solution is a broad spectrum, non-penetrating, painless antimicrobial agent.  It requires multiple daily applications on burn dressings and is messy and staining.  The solution is hypotonic; so electrolyte leeching, hyponatremia, and hypokalemia are common side-effects.  A rare complication of silver nitrate use is methemoglobinemia.  Silver nitrate dressings are used in treatment of toxic epidermal necrolysis syndrome and in rare patients allergic to silver sulfadiazine or mafenide.

   Petroleum-based antimicrobial ointments such as bacitracin and/or polymyxin B are clear on application, painless, and allow for easy wound observation.  These agents are commonly used for treatment of facial burns, graft sites, healing donor sites, and small partial-thickness burns.  Povidone iodine ointment has a broad antimicrobial activity, including bacteria, fungi, and some viral forms.  Mupirocin (e.g. Bactroban) has improved activity against gram positive bacteria, especially methicillin resistant Staph. aureus (MRSA) and selected enteric bacteria.  Gentamicin ointment will select for resistant organisms and diminish effectiveness of its parenteral form, but may be useful in selected cases.

   In severely burned patients (>40% BSA), the combination of Mycostatin ointment or powder with other topical agents reduces the incidence of fungal superinfection and improves antimicrobial action.  Mycostatin should not be combined with mafenide, however, because both become inactivated.  In addition, Mycostatin 5-15 ml given orally 3 times daily reduces alimentary fungal overgrowth.  This regimen has markedly decreased the incidence of candida septicemia in our patients.

   Topical antimicrobial creams are usually used with closed dressings.  This provides for greater patient comfort and less dessication than the open technique.  The creams are spread on fine mesh gauze, applied on the wounds, then covered with bulky protective gauze dressing and an elastic compressive wrap.  Dressing changes are performed every 8 to 12 hours.  At each dressing change, wounds are gently cleaned prior to re-application.  In contaminated or suspicious areas, the wounds are washed with an antimicrobial soap or phosphate buffered 0.25% hypochlorite solution (dilute Dakin's solution).  This antimicrobial irrigation reduces septic episodes and hypermetabolic sequelae, and improves subsequent skin graft survival.
 

Biological Dressing
   All topical antimicrobial agents adversely affect wound healing, alter metabolic rate, and require re-application and daily maintenance.  Biological dressings have no direct toxins or antimicrobial properties.  However, they create a wound environment that prevents dessication, diminishes bacterial proliferation, reduces loss of heat, water, protein and red blood cells, and promotes more rapid wound healing.  Biological dressings also reduce burn wound pain.  These materials may be organic or synthetic in origin, but good wound adherence is key to function.  Organic materials include skin allograft from donors, pigskin (xenograft), and human amnion.  Examples of synthetic covers include Biobrane Op-site and Omiderm.

   Fresh skin allograft (also called homograft) has become the 'gold standard' for temporary coverage of the clean open burn wound.  Allograft achieves an environmental 'seal' of the burn wound at the graft-wound interface and improves host immune defenses.  Allogenous human skin graft can be obtained from fresh cadavers within 18 hours of death or from living relatives to assure that skin cells within the graft are viable.  The graft can re-vascularize once adhered to the wound.  Allograft provides the best temporary closure of the excised burn wound.  However, the Langerhans cells in the transplanted epidermis retain their antigenicity, and the skin allograft will undergo rejection in 7 to 14 days in normal patients.  Immunosuppression of major burn patients increases tolerance of the allograft for up to several weeks, allowing prolonged temporary wound closure awaiting permanent skin autograft.  Allograft promotes angiogenesis and maturation in underlying granulation tissue.  Healing of subsequent skin autograft can be anticipated in areas of good allograft 'take'.

   However, fresh skin allograft has a high price tag, a limited supply, a short shelf life (2-3 weeks), and a need for refrigerated storage.  Although shelf life may be improved by freezing or lyophilization, these processes diminish cell viability, graft adherence, and protective functions of the altered allograft.  Fresh skin allograft should only be used on clean wounds where graft 'take' is anticipated.

   Amnion is readily available from the delivery suite and is inexpensive.  However, it adheres poorly to the wound and must be covered by an occlusive dressing.  Although amnionic coverage can promote angiogenesis and increased wound capillary density, its use in burns has become disfavored.

   Porcine xerograph (heterograft) is nonviable, adheres less than allograft, and does not undergo re-vascularization by the recipient bed.  Xenograft (pigskin) undergoes progressive degenerative necrosis rather than classic rejection.  Also, xenograft does not provide the same level of protection from infection as allograft, so pigskin is often embedded with salts of antimicrobial agents to increase its bacteriostatic potential.  Febrile responses can be caused by reaction to the treated pigskin or to hidden wound infections, and a fever requires at least temporary xenograft removal.

   However, pigskin is well-suited for temporary coverage of full and partial-thickness burn wounds.  Pigskin is cheaper and more available than allograft.  Its recommended uses include protective coverage of partial-thickness wounds to allow spontaneous healing, temporary coverage of clean granulating wound beds between autografting procedures, and to serve as a 'test graft' to decide suitability for autograft closure.  Pigskin should not be used on densely contaminated or
non-viable wound surfaces.  On deep dermal defects, pigskin should be changed every 3-4 days to prevent infection.

   Synthetic biological dressings also provide wound protection from dessication and contamination, increase the rate of wound healing, and reduce patient discomfort.  Good wound adherence is needed for success as intervening necrotic tissue or serum results in infection.  Diligence in application is essential.  When used to cover clean partial-thickness wounds, the dressing detaches as re-epithelialization and keratinization occurs underneath.

   Biobrane is a synthetic, bilaminate membrane with an outer semi-permeable silicone layer bonded to an inner collagen nylon matrix.  In-growth of granulation tissue into the inner Biobrane layer increases its adherence.  Its elasticity and transparency allows easy drape ability, fuller range of movement and easy wound inspection.  Biobrane is suited for use on donor sites, superficial partial-thickness burns, and clean/excised wounds prior to grafting.  Biobrane gloves on
partial-thickness hand burns reduce discomfort and increase motion, allowing earlier aggressive physiotherapy.  Biobrane can also be used to cover meshed skin grafts to prevent slipping and dessication.  The major problems with Biobrane are its expense and its lack of inherent antimicrobial properties.  Wound infections are not uncommon.

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