Burn Wound Infections (R. Mitri)

Burn Wound Sepsis

Updates in Identification and Management

Dr. Rita MITRI Journee Anesthesie – Chirurgie MSF- Paris 30th November 2013

Introduction

• Morbidity and mortality due to fire and flames has declined in the past decades mostly in the developed countries

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• Nowadays, 90% of burn deaths occur in Low to Middle Income Countries, because of lack of prevention programs and inconsistent quality of acute care

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• Burns are a major global public health problem

• Nosocomial infections • Emerging multi-drug-resistant strains of bacteria • Fungi

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• Infection and septicemia became the leading causes of mortality • Severe burn (>20 % total body surface area) predispose to development of burn wound sepsis:

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Introduction

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Why are burn patients prone to infections?

• Begins within five days of a major burn injury and persists for as long as one year • The increase in metabolic rate is directly proportional to the burn size – increase of 1.5 to 3 folds the basal metabolic rate from the Harris- Benedict equations • causes the loss of lean body mass, the loss of bone density, muscle weakness, and poor wound healing

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• Sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion which initiate the cascade of events leading to the acute hypermetabolic response

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Hypermetabolic Response

Hypermetabolic Response - Characteristics

• Characterized by:

increased heart rate marked myocardial depression (TBSA > 80%) increased body temperature increased oxygen and glucose consumption (anaerobic glycolysis) increased CO2 production

• Catabolic response:

• increased glycogenolysis • increased lipolysis • increased proteolysis ( for gluconeogenesis) leading to nitrogen loss and a potentially lethal depletion of essential protein and amino acid stores

• Immune system responses:

• high levels of proinflammatory cell mediator increase stress hormones and protein catabolism • Accumulation of these factors at the site of injury results in “spillover” into the systemic circulation, giving rise to immunosuppression

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• • • • •

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• Hyperdynamic circulatory response:

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Hyperdynamic circulatory response Massive protein and lipid catabolism Total body protein loss, muscle wasting Peripheral insulin resistance Increased resting energy expenditure Increased body temperature Increased infection risks Synthesis of acute phase proteins ( CRP, Procalcitonin)

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• • • • • • • •

Hypermetabolic Response

Inflammatory Response

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•Starts immediately after trauma and persists for almost 5 weeks postburn •Initially, Local inflammatory response to promote wound healing •burns of sufficient extent can incite a systemic inflammatory response •Innate and adaptive immune system mediate both of these phases

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A- Proinflamatory:

Inflammatory Response

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•Begins few days after burn injury •Anti-inflammatory in an effort to maintain homeostasis and restore normal physiology •T lymphocytes number fall in proportion to injury severity during the first week after injury •the burn patient is immunosupressed by a week after his injury •loss in Lean Body Mass contributes with further significant increases in infection rate and marked delays in wound healing

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B- Anti-inflamatory

• Burn patient have systemic inflammatory response which makes traditional indicators of sepsis both insensitive and nonspecific

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• Baseline temperature of 38.5*C, tachycardia, tachypnea, leukocytosis are routinely found in patients with extensive burns

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Hypermetabolism V/S Spesis

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Chronologic appearance of organisms

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• The burn itself consists of avascular necrotic tissue that provides a protein-rich environment favorable to microbial colonization and proliferation

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Microbial invasion of burn wound

Chronology and characteristics

Gram positive result in early colonization of burns

- Streptococcus and Staphylococcus species primarily

Gram-negative species dominant >5 days

- Source: upper respiratory tract, - 2 to 4 days post-burn sweat gland and hair follicules

- Source: Patient skin, upper respiratory tract, gastrointestinal tract, and hospital environment - P. aeruginoasa, Acinetobacter baumannii, E. Coli, Klebsiella

pneumoniae, Enterobacter cloacae.

yeast appear If gram-negative cover is initiated - Yeast and fungi colonization follows antibiotic treatment - Mainly Candida species (oropharynx), other fungi are increasing in frequency

Resistant bacteria and fungi invade the wound - MRSA, VRE, multi-drugresistant Pseudomonas and Acinetobacter species, and fungi - secondary to inadequate host response or therapeutic measures (excision burn, topical and systemic antibiotics) - Transition from colonization to invasion

CLASSIFICATION OF BURN WOUND INFECTIONS

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• Pathologic concentrations of bacteria per gram of tissue • Burn wound changes • Clinical manifestations

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• Burn wound infections are classified by:

Bacterial colonization : • <105 bacteria/gram tissue cultured • absence of clinical or microscopic evidence of infection Noninvasive bacterial infection: • erythema, pain, purulent exudate, and edema surrounding the wound • No systemic findings • >105 bacteria per gram of tissue (wound or eschar) Burn-related surgical wound infection: • in the excised burn as well as donor sites that is not yet reepithelialized • purulent exudate, loss of synthetic or biologic covering, wound hyperemia and erythema of uninjured surrounding skin Burn wound cellulitis: • erythema involving unburned skin greater than expected for the burn injury itself • Localised symptoms: progressive swelling and erythema Burn wound impetigo: • loss of epithelium due to an infection at a previously reepithelialized surface Invasive burn wound infection: • In an unexcised deep partial-thickness or full-thickness burn wound and adjacent unburned tissue • Risk of bacteremia and burn wound sepsis

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Risk Factors : •patient age (very young and very old) •impaired immune status ( within 1 week of the burn injury) •extent of burn injury (>20 percent total body surface area) •depth of the initial burn (deeper than superficial) •Smoking •Alcoholism increase the risk of bacterial translocation from the GI tract •Diabetes mellitus •Infections in perennial area •Wounds colonized with resistant germs

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Burn infections – Risk Factors

Appearance of focal, multifocal, or generalized dark brown, black, or violaceous discoloration of the wound

Separation or discoloration of the eschar - Hemorrhagic discoloration of subeschar tissue

Presence of green pigment (pyocyanin) in subcutaneous fat

Erythema, edema, pain, warmth of surrounding skin

Edema and/or violaceous discoloration at the margin of the burn and unburned skin

ecthyma gangrenosa in adjacet unburned skin

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conversion from partial thickness to full thickness

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Burn infections and sepsis _ wound appearance:

• Abdominal distention • Residual volumes (two times the feeding rate in adults and >150 mL/hr in children) • Uncontrollable diarrhea (>2500 mL/day for adults and >400 mL/day for children)

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Clinical manifestations: • Hypo/ hyperthermia • Progressive tachycardia • Progressive tachypnea • Refractory hypotension (MAP in adults and 70 + Age/2 in pediatrics) with somenlence and signs of hypoperfusion • Irritation (children) • Inability to tolerate enteral feedings for more than 24 hours based upon:

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Burn infections – Clinical manifestation

•Blood or urine cultures — Isolation of a pathogen in blood or urine cultures in the absence of another identifiable source of infection is consistent with a burn sepsis

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•Leukocytosis, leukopenia •Platelet count <100,000/microL (adults) or < 2SD of normal age •Hypo/ hyperglycemia •Serum procalcitonin levels can be used as an early indicator of septic complication in patients with severe burn injury

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Burn infections – laboratory

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â&#x20AC;˘ Standardized definitions for sepsis and infection that are specifically applicable to the burn patient were developed in 2007 â&#x20AC;˘ Distinguishes the change in patient status as a result of a microbial infection from changes that occur secondary to the hypermetabolic response of the burn itself

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Burn wound sepsis - Criteria

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The American Burn Association (ABA) consensus criteria for the definition of sepsis and infection in burn patients includes at least three of the following parameters: 1.Temperature >39째C or < 36.5째C 2.Progressive tachycardia 3.Progressive tachypnea (adults >30 breathes per minute; children >2 SD above age specific normal values) 4.Refractory hypotension 5.Leukocytosis or leukocytopenia 6.Thrombocytopenia that occurs three days after resuscitation

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Standardized burn sepsis criteria I

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7. Hyperglycemia >110 mg/dL (6.1 mmol/L) in the absence of pre-existing DM 8. 8. Infection is confirmed on a culture (eg, wound, blood, urine) 9. 9. Pathologic tissue source is identified (>105 bacteria on quantitative wound tissue biopsy or microbial invasion on biopsy) 10. 10. A clinical response to antimicrobial administration is documented

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Standardized burn sepsis criteria II

• Abdominal distention • Residual volumes (two times the feeding rate in adults and >150 mL/hr in children) • Uncontrollable diarrhea (>2500 mL/day for adults and >400 mL/day for children)

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11. Inability to tolerate enteral feedings for more than 24 hours based upon:

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Standardized burn sepsis criteria III

• Heart rate ≥110 bpm, systolic blood pressure ≤100 mmHg, and intubation were the best predictors of early sepsis (within 10 days of burn)

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• In a retrospective chart review study published by the journal of Burn care and research, the ABA trigger for sepsis did not correlate strongly with bacteremia

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Standardized burn sepsis criteria

â&#x20AC;˘ A change from immersion hydrotherapy to showering hydrotherapy, the rate of burn wound infection appeared to decrease.

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â&#x20AC;˘ Early excision and skin grafting has been one of the greatest advancements in the treatment of patients with severe thermal injuries, and a mainstay of therapy

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Management of burn wound sepsis

Management of burn wound infections Anesthesia surgery day

• wounds cleansing • Debridement • Topical antimicrobial agents (silver sulfadiazine, combination antibiotics, chlorhexidine) • dressings (compresses, biosynthetics, biologics)

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• Topical agents:

Management of burn wound infections treatment by Excision

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•Systemic therapy — antibiotics and antifungals are reserved for patients demonstrating sepsis or septic shock •G+ and G- coverage should be started initialy and de- escalated after culture result

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Invasive Aspergillosis:

Viral infection of burn wound

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After 7 days of treatment with antiviral

Prevention – Envirmomental Factors

• handwashing • the use of personal protective equipment gloves, caps, masks and plastic impermeable aprons (rather than isolation gowns) for direct patient contact • All equipment in the isolation room must be regularly cleaned

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•Minimize the uneccessary traffic of health care workers and visitors •Contained spaces • Modern infection control practice - simplified barrier isolation protocol :

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A- control of nosocomial infections

Prevention- Factors related to the patient

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•Early and adequate nutritional support to restore protein synthesis and normal immune function •Pain management •Early mobilisation of the patient •Avoid hypotension with adequate hydration calculated by the Parkland Formula •Avoid wound ischemia by tight bandages •Avoid mechanical trauma to the wound during dressings C- Decrease colonisation •Topical antimicrobial and silver sulfadiazine help decrease colonization •Selective digestive tract decontamination •Prophylactic systemic antibiotherapy is NOT indicated

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B- Improve patient’s immunity

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â&#x20AC;˘ Morbidity and mortality in burned patients is burn size dependent is due to an increased hypermetabolic and inflammatory reaction, along with impaired cardiac function

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Conclusion

• The diagnosis require: • close attention to any acute change in the patient’s clinical parameters • rapid changes in the burn wound appearance • As well as fulfillment of one of the three required American Burn Association (ABA) consensus criteria

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• The recognition of early sign of sepsis is a mainstay in improving the survival rate of burn patients.

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Conclusion

Thank you Anesthesia surgery day

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Questions?