8 Burn and Thermal Injury

Steven J. Hermiz, Paul Diegidio, C. Scott Hultman

Abstract

This chapter addresses the critical issues resulting from injuries due to fire in its various manifestations. Included are discussions of burn management, airway management, resuscitation, wound care, and surgery. The pathophysiology of burns is detailed, along with procedures for accurately assessing the extent and damage due to burns. The multidisciplinary approaches to burn treatment are also reviewed and include topical antimicrobial therapy, nutrition and local injury guidance, anesthesia, infection, airway treatment, excision and grafting, and reconstruction. The chapter includes two clinical cases that apply the treatment procedures covered.

8 Burn and Thermal Injury

8.1 Goals and Objectives

  • Familiarize with the first steps of burn management, inclusive of airway management, resuscitative support, wound care, and surgery.

  • Understand effective resuscitation starting with accurate assessment of the extent and depth of the burn injury, followed by the application of the Parkland formula for fluid replacement, to ensure adequate end-organ perfusion, including skin.

  • Review the need for early enteral feeding, within the first 24 hours, in burn patients as it decreases the catabolic response, improves nitrogen balance, maintains gut mucosal integrity, and decreases hospital stay.

  • Learn the basics for successful surgical management of the burn patient: burn wound excision, topical antimicrobial therapies, and resurfacing with skin grafts are key to successful management.

  • Become cognizant of the multiple treatment modalities that can be offered to a patient with hypertrophic burn scars, including nonsurgical care (silicone sheets, pressure garments, and splinting) as well as several different types of laser therapies. Contractures and unstable wounds can be reconstructed with tissue rearrangements, flaps, or skin substitutes.

  • Familiarize with the different types of burns, including thermal injury, chemical burns, frostbite, electrical burns, and radiation burns.

8.2 Patient Presentation

8.2.1 History and Epidemiology

Since the discovery of fire, burn injuries have posed a threat to human wellbeing due to direct contact and scald. 1 The foundations of burn treatment can be traced back several thousands of years in time. However, the confluence of medical, surgical, and technological advancements since the mid-1900s has revolutionized burn care and have drastically improved patient outcomes. The major advances documented throughout history are listed in Table 8‑1. 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20

Table 8.1 Major advances in burn care

Author/Event

Year

Contribution

Ebers Papyrus

1500 BC

Earliest description: burns treated with oils, plant extracts, honey and animal tissues

Hippocrates

500 BC

Pig fat and resin to heal burns

Celsius

1st Century AD

Lotion of wine and myrtle to treat burns

Galen

2nd Century AD

Greek surgeon; vinegar and open-air exposure for wounds

Amboise Pare

16th Century AD

Onions to treat burns; early burn wound excision

Guihelmus Fabricius Hildanus

1607

1st systematic classification of burns/treatment of contractures (De Combustionibus)

Edward Kentish

1790

Pressure dressings to alleviate pain and blisters from burns

Marjolin

1790s

Squamous cell carcinoma in nonhealing burn wounds

Guillaume Dupuytren

Early 1800s

Occlusive dressing treatment, allowed development of burn depth classification

Topical antimicrobials

18th century

Sodium hypochlorite for infection control

Edinburgh Hospital

Mid-19th century

1st hospital to treat large burns surgically

Burn Education

Late 19th century

Textbook and reference books detailing medical and surgical management of burns

Nutrition

Early 20th century

High-calorie intake recommended

Wars/Industrial accidents

20th century

Disaster burn management development

World War I

1914

Surgical skin transplantation, scar reduction, and pain management were most effective burn management

William Monafo

1941

0.5% silver nitrate—Agent of choice

Boston’s Cocoanut Grove nightclub fire

1942

1st comprehensive description of inhalational injury

Improvements in topical antimicrobials

Shock resuscitation

Antibiotic use

Understanding the metabolic response after burn injury

Beginning of burn care facilities, public safety legislation

Truman G. Blocker Jr.

1947

Deadly ammonium nitrate fertilizer explosion; demonstrated value of multidisciplinary team approach for burn treatment

O. Cope, F.D. Moore

1940s

Quantified fluid amount needed for resuscitation

I.E. Evans

1952

Fluid requirements for resuscitation based on surface area burned and body mass (Parkland formula)

Douglas Jackson

1960

Excision and grafting up to 30% body surface area on day of injury

J.C. Tanner Jr.

1964

Meshed skin graft

Z. Janzekovic

1970

Tangential excision and grafting (large burns)

Engrav, Herndon

1980s

Early excision/tangential excision—decrease mortality, reduce hospitalization, reduce hypertrophic scarring

J. Wesley Alexander

1981

“Sandwich technique”—covering expanded autograft with cadaver skin

John Burke, Ioannis Yannas

1981

Artificial skin (Integra)

J.F. Hansbrough, S.T. Boyce

1989

Composite skin graft

D.N. Herndon

1989

Continuous enteral feeding recommended in burn care

Metabolic support, including anabolic steroids (oxandrolone)

Burns are the fourth most common type of trauma injury following traffic accidents, falls, and interpersonal violence. 21 In 2004, 11 million people globally experienced burns severe enough to require medical attention. 21 Each year, burn injuries and fires claim over 300,000 lives worldwide, despite the vast majority of burn injuries being nonfatal. 22 , 23 In low and middle-income countries, where over 90% of all burn deaths occur, infrastructure to prevent and treat acute burns is lacking, and the healthcare burden is particularly high. 22

However, even in the United States, burns are a sizable source of morbidity and mortality. According to the American Burn Association, approximately 450,000 patients receive treatment for burns in a hospital or emergency room setting each year in the United States. Of those acute burn injuries, roughly 3,400 result in mortality each year. According to the Centers for Disease Control and Prevention (CDC), males account for 64% of the $7.5 billion total medical cost and productivity loss burden from burn-related injuries per year in the United States. 24 Additional factors and information related to burn epidemiology are described in Table 8‑2. 21 , 22 , 23 , 24 , 25 , 26 , 27

Table 8.2 Burn epidemiology

Global health issue

11 Million people world-wide and 450,000 in the United States

Large healthcare burden

Low- and middle-income countries with highest mortality

Mortality rate 3,400/y

$7.5 billion total medical cost and productivity loss burden/y

Age discrepancy

Pediatric population more at risk, especially for scald burns (non-Caucasian children)

Risk factors and higher morbidity and mortality rates

Male sex

Impoverished socioeconomic status

Children

Elderly

Disabled

Military personnel

Incidence

50% reduction in fire and burn related deaths and hospitalizations for acute burn injury

Types of Burns

Scald (most common)

Fire and flame (most common to require hospitalization)

Geographic discrepancy

Increased incidence in Africa

Burn injuries are a leading cause of death in children living in developing countries. 28 Burns are physically, emotionally, and psychologically devastating to the patient, family members, and the provider. They are a common household injury as children explore new surroundings and objects. 29 , 30 , 31 , 32 , 33 , 34 Delgado et al determined that 77.5% of burn cases occurred in a patient’s home (67.8% in the kitchen) and 74% were due to scalding. In order to prevent this debilitating injury, the clinician must be cognizant of the risk factors and protective factors aimed at burn prevention (Table 8‑3). 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36

Table 8.3 Pediatric burns: risk factors and protective factors aimed at burn prevention

Risk factors

Protective factors

Age < 6 y old

Mother literacy

Girls

Education on risks for burns

Impoverished

Living rooms separate from kitchen

Disabled

Smoke detectors

Small kerosene stoves

Emergency response systems

Candles

Good quality healthcare

Volatile substances

Intervention programs (developing countries)

Low rate of literacy

Residential sprinklers

Overcrowded living areas

Child resistant/fire-safe lighters

No supervision

Laws regulating temperature of hot-water taps

History of burns (siblings)

No regulations on smoke detectors/building codes

No access to water

8.3 Pathophysiologic Basis of Clinical Presentation

Burn injury results in coagulation necrosis of the skin and possibly the underlying subcutaneous tissue. The tissue surrounding this central zone of coagulation necrosis sustains a moderate degree of vascular injury, which decreases tissue perfusion and is known as the zone of stasis. Local mediators produced from the burn wound, such as arachidonic acid, are able to propel this zone into a partial thickness or full-thickness injury. They also cause arterial/venous dilation and platelet aggregation, thereby decreasing flow and perpetuating stasis. Thromboxane A2 is found in high concentrations in the burn wound and increases neutrophil migration in addition to platelet aggregation. 37

There are multiple cytokines involved in burn injury (Table 8‑4) and their actions are responsible for both the local and systemic effects seen in burn patients. 34 Burn wound colonization and bacterial translocation (Table 8‑5) are the nidus for endotoxin production and its effects. 37

Table 8.4 Cytokines involved in burn injury and their actions

Cytokines

Action

TNF-Alpha

Neutrophil sequestration (microvascular injury/burn size extension into zone of stasis)

IL-1, IL-2, IL-4, IL-6, IL-8, IL-12, INF-gamma

Active other classes of inflammatory mediators (potentiating their actions)

Alterations in hypothalamic control of temperature and metabolism

Potentiate organ failure progression

Abbreviations: TNF, tumor necrosis factor; IL, interleukin; INF, interferon.

Table 8.5 Burn wound inflammatory response

Bacterial colonization and dermal necrosis

Associated actions

Endotoxins (translocation)

Activates neutrophils and macrophages: inflammation/tissue damage

Inflammatory response

Activates Proapoptotic signaling pathway

Proinflammatory mediators and neutrophils

SIRS response

Abbreviation: SIRS: systemic inflammatory response syndrome.

The extent of damage done by a burn is not limited to the body surface area involved. 38 The insult of a burn disrupts hemodynamic, respiratory, and metabolic systems. 37 Burn injury releases inflammatory mediators that are responsible for the downstream cascade of events that ultimately results in burn shock, specifically hypovolemic and distributive shock (Fig. 8‑1). 38 , 39 , 40 Distributive shock is the result of total body fluid expansion resulting from third spacing to include the intravascular, intracellular, and interstitial spaces. Hypovolemic shock ensues from massive interstitial fluid sequestration, and fluid is lost from the wound, resulting in decreased circulating plasma volume, and consequently, preload and cardiac output are decreased. 38 , 39 , 40 Demling et al concluded that edema continues and reaches a maximum level of 24 hours after injury and begins to resolve 1 to 2 days after the injury. 38 , 39

Fig. 8.1 Burn pathophysiology flow chart.

The degree of metabolic derangement is related to the extent of the burn injury. The first phase is referred to as the “Ebb phase,” which is characterized by a decrease in cardiac output and metabolic rate. After adequate fluid resuscitation, the cardiac output increases and there is an increase in resting energy expenditure. Cytokines activate other inflammatory mediators, which cause alterations in the hypothalamic control of temperature and metabolism resulting in fever and hypermetabolism. 41 The thermoregulatory set point increases 5 to 15 days postburn and remains elevated for up to 2 months. 41 The metabolic rate in burn patients is estimated to be twice normal. 41 Cortisol, glucagon, and catecholamines are elevated in the burn patient. Cortisol is responsible for a catabolic state and creates a negative nitrogen and calcium balance. It stimulates gluconeogenesis and proteolysis. Catecholamines stimulate glycogenolysis, hepatic gluconeogenesis, and lipolysis and also create peripheral insulin resistance. Therefore, as a result of elevated glucagon levels, both glucose and insulin levels are elevated. Muscle protein catabolism leads to high concentrations of amino acids and decreased protein anabolism as a result of decreased levels of growth hormone and insulin-like growth factor. 41

In the postburn patient, increased levels of catecholamines and catabolic hormones lead to a global hypermetabolism syndrome. This is evident by tachycardia, fever, hepatic protein synthesis derangement, and muscle protein catabolism. A heightened response leads to immunodeficiency, impaired wound healing, loss of lean body mass, cardiac ischemia, and sepsis. 37

Complications from this disruption may lead to acute lung injury, systemic inflammatory response syndrome (SIRS)/sepsis, immunosuppression, acute respiratory distress syndrome (ARDS), and multisystem organ failure (MSOF), potentially culminating in death. 37

8.4 Preparation for Surgery

8.4.1 Initial Evaluation and Treatment

The first step in effective resuscitation is accurate assessment of the extent and depth of the burn injury. The second step is to determine if smoke inhalation injury is present. Smoke inhalation is suspected with facial burns, carbonaceous sputum, or a history of being in a closed space. 41 The goal of fluid resuscitation is to support the patient through the initial 24 to 48 hours postburn, which results in hypovolemia from third spacing and fluid shifts. This led Baxter and Shires to develop and implement the Parkland formula, which estimates the amount of replacement fluids in the first 24 hours in a burn patient. Total replacements needs are calculated by the formula: total fluids = 4 mL × weight (kilograms) × % total body surface area (TBSA) of second and third-degree burns. The first half is given within 8 hours from the injury, and the second half is given over the remaining 16 hours. The body surface area is estimated using the Wallace rule of nines (Fig. 8‑2). 37 , 38 , 39 , 40 , 41

Fig. 8.2 Wallace Rule of Nines (a) Adult and (b) Child.

The patient’s response to resuscitation is dependent upon age, depth of burn, pre-existing comorbidities, associated injuries, and concomitant inhalation injury. 38 Smoke inhalation injuries require up to one third more fluid during acute resuscitation compared to burn patients without inhalational injury. 41 The current first-line crystalloid solution is lactated ringers. 37 , 38 During the inflammatory state, 25% of the infused volume remains intravascular; therefore, larger amounts of crystalloid are needed, contributing to the edema seen in burn patients. 38 , 40 The Parkland formula grossly underestimates requirements with inhalational injury, alcohol intoxication, electrical injury, and postescharotomy. Hypertonic saline has been used in early resuscitation with benefits seen in decreased tissue edema and abdominal compartment pressures, but is currently not routinely used. 37 , 38 , 40

Colloid fluid administration (albumin and fresh frozen plasma) can be given 12 to 72 hours postinjury after the capillary leak phase has ceased in patients with low urine output and hypotension, despite crystalloid administration. The standard belief that colloid use increases mortality in burn injury patients and may be due to the notion that colloids leak into lung parenchyma. Blood transfusions increase mortality in burn patients and a restrictive strategy with hemoglobin goals of 7 to 9 g/dL is recommended. 37

Intravenous fluid administration is critical to reverse the pathophysiology of burn shock by restoring plasma fluid loss, increasing body fluid reservoir, and restoring preload. 38 , 40 Care should be taken not to over-resuscitate the patient, which can lead to abdominal compartment syndrome, renal failure, pulmonary edema, extremity compartment syndrome, and orbital compartment syndrome. 38 , 40 The adequacy of resuscitation is monitored constantly and urine output of 0.5 to 1.0 mL/kg/h is an adequate indicator of vital organ perfusion. 41 Some studies suggest that the use of IV ascorbic acid decreases edema, intravascular fluid requirement, and respiratory dysfunction severity. 37 , 41

Upon initial evaluation, the clinician should be aware of both the admission and transfer criteria for burn-injured patients. Current recommendations for admission and transfer are listed in Box 8.1. 42

Box 8.1 Admission/Transfer criteria after burn injury (American Burn Association Guidelines)

  • Second-/third-degree burns: >10% TBSA (<10 years old/>50 years old).

  • Second-degree burns: >20% TBSA.

  • Hands/Face/Feet/Genitalia/Perineum burns.

  • Third-degree burns: >5%.

  • Electrical/Chemical burns.

  • Inhalational burn.

  • Polytrauma.

  • Significant comorbidities.

  • Child abuse/neglect.

  • Social/Emotional/Long-term rehabilitation.

8.4.2 Topical Antimicrobial Therapy

Topical agents are used on burn wound to hinder bacterial proliferation and fungal colonization. The three most commonly used topical antimicrobials are silver sulfadiazine (Silvadene), mafenide acetate (Sulfamylon), and silver nitrate, all of which have varying coverage of bacterial pathogens. Silver sulfadiazine is mainly used for prevention of burn wound bacterial infection, rather than treatment, because of poor eschar penetration. Also, it should not be used on the face. Mafenide acetate is used for both treatment and prevention of bacterial infection of burn wounds because of excellent eschar penetration. However, mafenide’s disadvantages include painful application in partial thickness burns and inhibition of carbonic anhydrase, leading to metabolic acidosis. Silver nitrate is another topical agent with broad-spectrum antibacterial activity; however, it has poor eschar penetration and is associated with electrolyte abnormalities. Mupirocin and bacitracin are commonly used for superficial facial burns and care should be taken to only apply to small areas given their nephrotoxic quality (Table 8‑6). 41

Table 8.6 Topical antimicrobial agents

Drug

Mechanism of action

Side effects

Silver sulfadiazine (Silvadene)

Bactericidal (cell membrane/wall)

Broad spectrum anti-microbial coverage

Exact MOA unknown

No eschar penetration

Use: superficial and intermediate thickness burns

  • Sulfa allergy

  • Neutropenia

  • Thrombocytopenia

  • Not for facial burns or ear burns

  • Contraindicated on areas of new skin grafting (destructive to grafts)

Mafenide Acetate (Sulfamylon)

Bacteriostatic

Inhibits folic acid synthesis

Pseudomonal coverage

Good eschar penetration

Good for cartilage (ears)

Prevention and Treatment

Use: Intermediate thickness and deep burns (full thickness)

  • Painful

  • Metabolic Acidosis (difficult ventilator management)

  • Sulfa allergy

  • Skin hypersensitivity reactions

Silver Nitrate

Antiseptic

Denatures proteins (cell wall/membrane)

No eschar penetration

Advantage: doesn’t need to be removed

  • Hyponatremia

  • Hypochloremia

  • Hypocalcemia

  • Hypokalemia

  • Methemoglobinemia

  • Black tissue staining

Neomycin

Use: superficial partial thickness burns on face

  • Nephrotoxic

Polymyxin B

Use: superficial facial burns

  • Nephrotoxic

Bacitracin

Use: superficial burns, raw wounds

Helps keep wounds moist

  • Anaphylaxis

Mupirocin

Use: superficial MRSA infection

  • Nephrotoxic

8.4.3 Nutrition and Local Injury

Severely burned patients (>40% TBSA) have a metabolic rate that approaches 200% of the basal rate, resulting in greater energy and protein requirements. 41 Providing nutrition is crucial for wound healing, cellular function, and resistance to infection. 41 Early enteral feeding, within the first 24 hours, in burn patients decreases the catabolic response, improves nitrogen balance, maintains gut mucosal integrity, and decreases length of hospital stay. The recommended formula consists of 20% of calories from protein, 30% as fat, and 50% as carbohydrates. The general formula is 25 kcal/kg + 40 kcal/5% burn. 41 High-carbohydrate diet improves the net balance of skeletal muscle protein, but aggressive monitoring and treatment of hyperglycemia is recommended. Uncontrolled glucose levels are associated with increased bacteremia, reduced skin graft take, and increased mortality. 37 The protein requirement in severely burned patients is 1.5 to 2.0 g/kg per day, which attenuates the increased oxidation rate of amino acids. 37

8.4.4 Anesthesia

Pain management after burn injury is difficult and requires a methodical, rational approach. 40 Burn injury is one of the most painful types of trauma due to injury of both sensory organelle receptors in the dermis and afferent nerve fibers leading to the skin. 42 Debridement, daily wound care, excision and grafting, and physical therapy, all further affect sensory feedback loops. The guidelines for providing adequate pain relief for burn patients begin with differentiating background pain from procedural and breakthrough pain, while treating from anxiety, depression, and possible substance abuse. The goal is for the patient to be comfortably awake and alert. 43

Classic recommendations of avoiding succinylcholine after 72 hours are still valid. 40 Some studies suggest the use of intravenous opioids from the time resuscitation begins and addressing breakthrough pain with short-acting opioids and nonsteroidal anti-inflammatory medications. During procedures or dressing changes, ketamine, inhaled nitrous oxide, and benzodiazepines have been used with success. Propofol or Precedex has been used for sedation while the patient is mechanically ventilated; however, it is important to note that these infusions do not provide analgesia. Opioids are the mainstay of treatment; however, anxiolytics, anticonvulsants, and nonsteroidal anti-inflammatory drugs (NSAIDs) can be used as adjuncts to control the patient’s relentless pain. 43 The prevention of chronic neuropathic pain is critical and therefore other adjuncts are utilized, such as laser therapy, acupuncture, fat grafting, and nerve decompression.

8.4.5 Infection/SIRS/MSOF

Burn wound infections are common after burn injury and the practitioner must be vigilant during clinical assessment (Table 8‑7). The larger the size of the burn injury, the greater the risk of infection, which is due to decreased cell mediated immunity, as thermal injury results in less phagocytic activity and lymphokine production by macrophages. 44 Specifically, the large surface burns have a systemic immunomodulatory effect by skewing the system toward an interleukin-mediated response. 45 Multiple studies have looked at the role of prophylactic antibiotics and current recommendations do not support their use. 46

Table 8.7 Burn wound infections

Signs

Common bacteria

Other infectious agents

Diagnosis

Rapid eschar separation

Edema

Partial-thickness conversion to full thickness

Hemorrhage within the wound

Green fat discoloration

Necrotic skin around wound bed

Erythema Gangrenosum

Malodor from wound bed

P. aeruginosa (most common)

S. aureus (2nd most common)

E. coli

Acinetobacter

Enterobacter

Enterococcus

C. difficile

Stenotrophomonas

Herpes simplex Virus (most common virus)

C. Albicans (most common fungus)

Mucormycosis

Aspergillus

Biopsy (gold standard): > 105 organisms

Hospital-associated infections (HAIs) in severely burned patients remain a major cause of morbidity and mortality. Weber et al used HAI surveillance data at a single institution over 5 years and found the most common sites to be the respiratory tract (ventilator-associated pneumonia [VAP] and tracheobronchitis), the urinary tract, burn surgical site infection, burn wound cellulitis, superficial thrombophlebitis, peritonitis, Clostridium difficile colitis, and device-related bacteremias (central-line associated bloodstream infections). 44

Pneumonia, specifically VAP, is one of the most common infections and most common cause of death in severely burned patients (greater than 30% TBSA). Burn patients become susceptible secondary to immunosuppression, impaired secretory clearance of pulmonary secretions, inflammatory cascade activation, and leakage of plasma into the lung parenchyma. Diagnosis remains difficult in the burned patient, but the cornerstone of accurate diagnosis involves the use of bronchoalveolar lavage with quantitative cultures. 37

Central line-associated blood stream infections (CLABSIs) are common among patients with burn injuries due to the immunosuppressed state and potential burn wound bacterial colonization. Van Duin et al implemented interventions to decrease CLABSIs in a burn intensive care unit. These interventions included enhanced education of medical staff, mandatory nursing training on IV line care and maintenance, central line changes over a guide-wire every three days with the use of a new site every six days, introduction of antibiotic-impregnated central venous catheters, universal glove and gown use, and use of chlorhexidine patch at insertion site. The interventions decreased the incidence of CLABSIs and the number of CLABSIs caused by Staphylococcus aureus. 45

The most common pathogens among burn intensive care units vary among institutions. Throughout the literature, Pseudomonas aeurginosa is recognized as the most common pathogen isolated, followed by Staphylococcus aureus. At UNC, the most common pathogens isolated among the burn ICU patients are Pseudomonas and Acinetobacter spp (Table 8‑7). 44

8.5 Treatment

8.5.1 Airway

Treating the burn patient is complex and requires a multidisciplinary approach in order to limit morbidity and mortality. Initial management should start with airway, breathing, and circulation under Advanced Trauma Life Support guidelines. In the severely burned patient, early intubation and ventilator support is appropriate for airway management. The burned patient has reduced pulmonary compliance and increased chest wall rigidity, leading to high airway pressures and exacerbation of the lung injury. Therefore, using of low tidal volumes with permissive hypercapnia is recommended. Another ventilator strategy is using high-frequency oscillator or percussive ventilation. 37 As a last resort, extracorporeal membrane oxygenation can be considered. The benefits have been studied in the pediatric population and adult patients with inhalation injury. Supplemental therapies with inhaled nitric oxide, aerosolized heparin, and N-acetylcysteine have some benefit in selected patients. Early tracheostomy provides shorter time to extubation and increases patient comfort, but offers no advantage in ventilatory support, length of stay, or survival. 37 Burn-induced hypermetabolism is an important sequela that leads to complications and death; therefore, the management recommendations are outlined in Table 8‑8. 37 , 47 , 48

Table 8.8 Burn induced hyper-metabolism management

Recommendation

Effect

Early excision of full-thickness burns

Halts inflammatory mediators

Strict glucose control: Insulin

Target: 80–110 mg/dL

Decreases infectious complications and mortality rates

Non-selective beta-blocker: propranolol

Blunt cardiac response

Reverses muscle protein catabolism

Decreases wound infection rates

Decreases wound healing time

Decreases mortality

Testosterone analog: Oxandrolone

May improve catabolic response, skeletal muscle growth, wound healing

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Feb 21, 2021 | Posted by in General Surgery | Comments Off on 8 Burn and Thermal Injury

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