- •Preface
- •List of contributers
- •History, epidemiology, prevention and education
- •A history of burn care
- •“Black sheep in surgical wards”
- •Toxaemia, plasmarrhea, or infection?
- •The Guinea Pig Club
- •Burns and sulfa drugs at Pearl Harbor
- •Burn center concept
- •Shock and resuscitation
- •Wound care and infection
- •Burn surgery
- •Inhalation injury and pulmonary care
- •Nutrition and the “Universal Trauma Model”
- •Rehabilitation
- •Conclusions
- •References
- •Epidemiology and prevention of burns throughout the world
- •Introduction
- •Epidemiology
- •The inequitable distribution of burns
- •Cost by age
- •Cost by mechanism
- •Limitations of data
- •Risk factors
- •Socioeconomic factors
- •Race and ethnicity
- •Age-related factors: children
- •Age-related factors: the elderly
- •Regional factors
- •Gender-related factors
- •Intent
- •Comorbidity
- •Agents
- •Non-electric domestic appliances
- •War, mass casualties, and terrorism
- •Interventions
- •Smoke detectors
- •Residential sprinklers
- •Hot water temperature regulation
- •Lamps and stoves
- •Fireworks legislation
- •Fire-safe cigarettes
- •Children’s sleepwear
- •Acid assaults
- •Burn care systems
- •Role of the World Health Organization
- •Conclusions and recommendations
- •Surveillance
- •Smoke alarms
- •Gender inequality
- •Community surveys
- •Acknowledgements
- •References
- •Prevention of burn injuries
- •Introduction
- •Burns prevalence and relevance
- •Burn injury risk factors
- •WHERE?
- •Burn prevention types
- •Burn prevention: The basics to design a plan
- •Flame burns
- •Prevention of scald burns
- •Conclusions
- •References
- •Burns associated with wars and disasters
- •Introduction
- •Wartime burns
- •Epidemiology of burns sustained during combat operations
- •Fluid resuscitation and initial burn care in theater
- •Evacuation of thermally-injured combat casualties
- •Care of host-nation burn patients
- •Disaster-related burns
- •Epidemiology
- •Treatment of disaster-related burns
- •The American Burn Association (ABA) disaster management plan
- •Summary
- •References
- •Education in burns
- •Introduction
- •Surgical education
- •Background
- •Simulation
- •Education in the internet era
- •Rotations as courses
- •Mentorship
- •Peer mentorship
- •Hierarchical mentorship
- •What is a mentor
- •Implementation
- •Interprofessional education
- •What is interprofessional education
- •Approaches to interprofessional education
- •References
- •European practice guidelines for burn care: Minimum level of burn care provision in Europe
- •Foreword
- •Background
- •Introduction
- •Burn injury and burn care in general
- •Conclusion
- •References
- •Pre-hospital and initial management of burns
- •Introduction
- •Modern care
- •Early management
- •At the accident
- •At a local hospital – stabilization prior to transport to the Burn Center
- •Transportation
- •References
- •Medical documentation of burn injuries
- •Introduction
- •Medical documentation of burn injuries
- •Contents of an up-to-date burns registry
- •Shortcomings in existing documentation systems designs
- •Burn depth
- •Burn depth as a dynamic process
- •Non-clinical methods to classify burn depth
- •Burn extent
- •Basic principles of determining the burn extent
- •Methods to determine burn extent
- •Computer aided three-dimensional documentation systems
- •Methods used by BurnCase 3D
- •Creating a comparable international database
- •Results
- •Conclusion
- •Financing and accomplishment
- •References
- •Pathophysiology of burn injury
- •Introduction
- •Local changes
- •Burn depth
- •Burn size
- •Systemic changes
- •Hypovolemia and rapid edema formation
- •Altered cellular membranes and cellular edema
- •Mediators of burn injury
- •Hemodynamic consequences of acute burns
- •Hypermetabolic response to burn injury
- •Glucose metabolism
- •Myocardial dysfunction
- •Effects on the renal system
- •Effects on the gastrointestinal system
- •Effects on the immune system
- •Summary and conclusion
- •References
- •Anesthesia for patients with acute burn injuries
- •Introduction
- •Preoperative evaluation
- •Monitors
- •Pharmacology
- •Postoperative care
- •References
- •Diagnosis and management of inhalation injury
- •Introduction
- •Effects of inhaled gases
- •Carbon monoxide
- •Cyanide toxicity
- •Upper airway injury
- •Lower airway injury
- •Diagnosis
- •Resuscitation after inhalation injury
- •Other treatment issues
- •Prognosis
- •Conclusions
- •References
- •Respiratory management
- •Airway management
- •(a) Endotracheal intubation
- •(b) Elective tracheostomy
- •Chest escharotomy
- •Conventional mechanical ventilation
- •Introduction
- •Pathophysiological principles
- •Low tidal volume and limited plateau pressure approaches
- •Permissive hypercapnia
- •The open-lung approach
- •PEEP
- •Lung recruitment maneuvers
- •Unconventional mechanical ventilation strategies
- •High-frequency percussive ventilation (HFPV)
- •High-frequency oscillatory ventilation
- •Airway pressure release ventilation (APRV)
- •Ventilator associated pneumonia (VAP)
- •(a) Prevention
- •(b) Treatment
- •References
- •Organ responses and organ support
- •Introduction
- •Burn shock and resuscitation
- •Post-burn hypermetabolism
- •Individual organ systems
- •Central nervous system
- •Peripheral nervous system
- •Pulmonary
- •Cardiovascular
- •Renal
- •Gastrointestinal tract
- •Conclusion
- •References
- •Critical care of thermally injured patient
- •Introduction
- •Oxidative stress control strategies
- •Fluid and cardiovascular management beyond 24 hours
- •Other organ function/dysfunction and support
- •The nervous system
- •Respiratory system and inhalation injury
- •Renal failure and renal replacement therapy
- •Gastro-intestinal system
- •Glucose control
- •Endocrine changes
- •Stress response (Fig. 2)
- •Low T3 syndrome
- •Gonadal depression
- •Thermal regulation
- •Metabolic modulation
- •Propranolol
- •Oxandrolone
- •Recombinant human growth hormone
- •Insulin
- •Electrolyte disorders
- •Sodium
- •Chloride
- •Calcium, phosphate and magnesium
- •Calcium
- •Bone demineralization and osteoporosis
- •Micronutrients and antioxidants
- •Thrombosis prophylaxis
- •Conclusion
- •References
- •Treatment of infection in burns
- •Introduction
- •Clinical management strategies
- •Pathophysiology of the burn wound
- •Burn wound infection
- •Cellulitis
- •Impetigo
- •Catheter related infections
- •Urinary tract infection
- •Tracheobronchitis
- •Pneumonia
- •Sepsis in the burn patient
- •The microbiology of burn wound infection
- •Sources of organisms
- •Gram-positive organisms
- •Gram-negative organisms
- •Infection control
- •Pharmacological considerations in the treatment of burn infections
- •Topical antimicrobial treatment
- •Systemic antimicrobial treatment (Table 3)
- •Gram-positive bacterial infections
- •Enterococcal bacterial infections
- •Gram-negative bacterial infections
- •Treatment of yeast and fungal infections
- •The Polyenes (Amphotericin B)
- •Azole antifungals
- •Echinocandin antifungals
- •Nucleoside analog antifungal (Flucytosine)
- •Conclusion
- •References
- •Acute treatment of severely burned pediatric patients
- •Introduction
- •Initial management of the burned child
- •Fluid resuscitation
- •Sepsis
- •Inhalation injury
- •Burn wound excision
- •Burn wound coverage
- •Metabolic response and nutritional support
- •Modulation of the hormonal and endocrine response
- •Recombinant human growth hormone
- •Insulin-like growth factor
- •Oxandrolone
- •Propranolol
- •Glucose control
- •Insulin
- •Metformin
- •Novel therapeutic options
- •Long-term responses
- •Conclusion
- •References
- •Adult burn management
- •Introduction
- •Epidemiology and aetiology
- •Pathophysiology
- •Assessment of the burn wound
- •Depth of burn
- •Size of the burn
- •Initial management of the burn wound
- •First aid
- •Burn blisters
- •Escharotomy
- •General care of the adult burn patient
- •Biological/Semi biological dressings
- •Topical antimicrobials
- •Biological dressings
- •Other dressings
- •Exposure
- •Deep partial thickness wound
- •Total wound excision
- •Serial wound excision and conservative management
- •Full thickness burns
- •Excision and autografting
- •Topical antimicrobials
- •Large full thickness burns
- •Serial excision
- •Mixed depth burn
- •Donor sites
- •Techniques of wound excision
- •Blood loss
- •Antibiotics
- •Anatomical considerations
- •Skin replacement
- •Autograft
- •Allograft
- •Other skin replacements
- •Cultured skin substitutes
- •Skin graft take
- •Rehabilitation and outcome
- •Future care
- •References
- •Burns in older adults
- •Introduction
- •Burn injury epidemiology
- •Pathophysiologic changes and implications for burn therapy
- •Aging
- •Comorbidities
- •Acute management challenges
- •Fluid resuscitation
- •Burn excision
- •Pain and sedation
- •End of life decisions
- •Summary of key points and recommendations
- •References
- •Acute management of facial burns
- •Introduction
- •Anatomy and pathophysiology
- •Management
- •General approach
- •Airway management
- •Facial burn wound management
- •Initial wound care
- •Topical agents
- •Biological dressings
- •Surgical burn wound excision of the face
- •Wound closure
- •Special areas and adjacent of the face
- •Eyelids
- •Nose and ears
- •Lips
- •Scalp
- •The neck
- •Catastrophic injury
- •Post healing rehabilitation and scar management
- •Outcome and reconstruction
- •Summary
- •References
- •Hand burns
- •Introduction
- •Initial evaluation and history
- •Initial wound management
- •Escharotomy and fasciotomy
- •Surgical management: Early excision and grafting
- •Skin substitutes
- •Amputation
- •Hand therapy
- •Secondary reconstruction
- •References
- •Treatment of burns – established and novel technology
- •Introduction
- •Partial thickness burns
- •Biological membranes – amnion and others
- •Xenograft
- •Full thickness burns
- •Dermal analogs
- •Keratinocyte coverage
- •Facial transplantation
- •Tissue engineering and stem cells
- •Gene therapy and growth factors
- •Conclusion
- •References
- •Wound healing
- •History of wound care
- •Types of wounds
- •Mechanisms of wound healing
- •Hemostasis
- •Proliferation
- •Epithelialization
- •Remodeling
- •Fetal wound healing
- •Stem cells
- •Abnormal wound healing
- •Impaired wound healing
- •Hypertrophic scars and keloids
- •Chronic non-healing wounds
- •Conclusions
- •References
- •Pain management after burn trauma
- •Introduction
- •Pathophysiology of pain after burn injuries
- •Nociceptive pain
- •Neuropathic pain
- •Sympathetically Maintained Pain (SMP)
- •Pain rating and documentation
- •Pain management and analgesics
- •Pharmacokinetics in severe burns
- •Form of administration [21]
- •Non-opioids (Table 1)
- •Paracetamol
- •Metamizole
- •Non-steroidal antirheumatics (NSAID)
- •Selective cyclooxygenasis-2-inhibitors
- •Opioids (Table 2)
- •Weak opioids
- •Strong opioids
- •Other analgesics
- •Ketamine (see also intensive care unit and analgosedation)
- •Anticonvulsants (Gabapentin and Pregabalin)
- •Antidepressants with analgesic effects
- •Regional anesthesia
- •Pain management without analgesics
- •Adequate communication
- •Psychological techniques [65]
- •Transcutaneous electrical nerve stimulation (TENS)
- •Particularities of burn pain
- •Wound pain
- •Breakthrough pain
- •Intervention-induced pain
- •Necrosectomy and skin grafting
- •Dressing change of large burn wounds and removal of clamps in skin grafts
- •Dressing change in smaller burn wounds, baths and physical therapy
- •Postoperative pain
- •Mental aspects
- •Intensive care unit
- •Opioid-induced hyperalgesia and opioid tolerance
- •Hypermetabolism
- •Psychic stress factors
- •Risk of infection
- •Monitoring [92]
- •Sedation monitoring
- •Analgesia monitoring (see Fig. 2)
- •Analgosedation (Table 3)
- •Sedation
- •Analgesia
- •References
- •Nutrition support for the burn patient
- •Background
- •Case presentation
- •Patient selection: Timing and route of nutritional support
- •Determining nutritional demands
- •What is an appropriate initial nutrition plan for this patient?
- •Formulations for nutritional support
- •Monitoring nutrition support
- •Optimal monitoring of nutritional status
- •Problems and complications of nutritional support
- •Conclusion
- •References
- •HBO and burns
- •Historical development
- •Contraindications for the use of HBO
- •Conclusion
- •References
- •Nursing management of the burn-injured person
- •Introduction
- •Incidence
- •Prevention
- •Pathophysiology
- •Severity factors
- •Local damage
- •Fluid and electrolyte shifts
- •Cardiovascular, gastrointestinal and renal system manifestations
- •Types of burn injuries
- •Thermal
- •Chemical
- •Electrical
- •Smoke and inhalation injury
- •Clinical manifestations
- •Subjective symptoms
- •Possible complications
- •Clinical management
- •Non-surgical care
- •Surgical care
- •Coordination of care: Burn nursing’s unique role
- •Nursing interventions: Emergent phase
- •Nursing interventions: Acute phase
- •Nursing interventions: Rehabilitative phase
- •Ongoing care
- •Infection prevention and control
- •Rehabilitation medicine
- •Nutrition
- •Pharmacology
- •Conclusion
- •References
- •Outpatient burn care
- •Introduction
- •Epidemiology
- •Accident causes
- •Care structures
- •Indications for inpatient treatment
- •Patient age
- •Total burned body surface area (TBSA)
- •Depth of the burn
- •Pre-existing conditions
- •Accompanying injuries
- •Special injuries
- •Treatment
- •Initial treatment
- •Pain therapy
- •Local treatment
- •Course of treatment
- •Complications
- •Infections
- •Follow-up care
- •References
- •Non-thermal burns
- •Electrical injury
- •Introduction
- •Pathophysiology
- •Initial assessment and acute care
- •Wound care
- •Diagnosis
- •Low voltage injuries
- •Lightning injuries
- •Complications
- •References
- •Symptoms, diagnosis and treatment of chemical burns
- •Chemical burns
- •Decontamination
- •Affection of different organ systems
- •Respiratory tract
- •Gastrointestinal tract
- •Hematological signs
- •Nephrologic symptoms
- •Skin
- •Nitric acid
- •Sulfuric acid
- •Caustic soda
- •Phenol
- •Summary
- •References
- •Necrotizing and exfoliative diseases of the skin
- •Introduction
- •Necrotizing diseases of the skin
- •Cellulitis
- •Staphylococcal scalded skin syndrome
- •Autoimmune blistering diseases
- •Epidermolysis bullosa acquisita
- •Necrotizing fasciitis
- •Purpura fulminans
- •Exfoliative diseases of the skin
- •Stevens-Johnson syndrome
- •Toxic epidermal necrolysis
- •Conclusion
- •References
- •Frostbite
- •Mechanism
- •Risk factors
- •Causes
- •Diagnosis
- •Treatment
- •Rewarming
- •Surgery
- •Sympathectomy
- •Vasodilators
- •Escharotomy and fasciotomy
- •Prognosis
- •Research
- •References
- •Subject index
J. Knighton, M. Jako
Possible complications
Complications can arise throughout all phases of burn care, although the potential for development is greater in the acute stage of recovery. Prompt identification and management are essential in order to effect the best possible patient outcome. The systems most commonly affected are cardiovascular, respiratory, gastrointestinal and renal.
Cardiovascular system – Cardiovascular system complications include hypovolemic shock and arrhythmias. When the intravascular volume is reduced immediately post-burn, the cardiac output decreases dramatically and blood flow through the tissues and coronary artery is reduced. Prompt and adequate fluid resuscitation can effectively address the decrease in circulating volumes. Circulation to the extremities can also be impaired by the decreased volumes, the presence of circumferential burns and the formation of edema. Incisions through the leathery, devitalized burned tissue may be necessary in order to restore circulation to these limbs. That procedure is called an escharotomy (Fig. 11). Deeper burns (severe electrical or prolonged flame exposure) may require a fasciotomy. Patients with preexisting cardiac disease may be more prone to the development of arrhythmias, brought on by the stress of a major burn injury. Direct cardiac damage may have also occurred from the passage of electrical current through the heart. All moderate to major burns should be monitored, using an external cardiac monitor, and invasive lines transduced. Hemodynamic parameters, such as heart rate, central ven-
Fig. 11. Chest escharotomy
ous pressure and blood pressure/mean arterial pressure, are set within targeted ranges [3]. Attention should also be paid to electrolyte levels, especially sodium and potassium. Early post-burn, sodium shifts into the interstitial spaces, only to return at the end of the hypovolemic shock phase. Potassium is initially released into the extracellular spaces by hemolyzed red blood cells and those cells injured by the burn. As fluids are mobilized, potassium levels increase in the vascular spaces. As plasma leaks into the interstitial space, there is a temporary increase in blood viscosity. Appropriate fluid resuscitation can correct that situation satisfactorily. Arrhythmia management may require a collaborative consultation with Cardiology and medication on either a shortterm or long-term basis. Evidence-based, venous thromboembolism prophylaxis should also be instituted and medications, such as enoxaparin, commenced as the incidence of DVT’s in burns is estimated to be between 1 to 23% [4].
Respiratory system – There are, generally, two ways in which the respiratory system can be affected by a burn injury. One involves mechanical, upper airway obstruction due to heat injury and edema formation and/or constricting circumferential burns to the neck and chest. The other involves inhalation of noxious products of combustion, which produces a chemical irritation reaction to the middle and lower airways. Early in the emergent phase of care, the upper airway can close off very quickly, because of massive facial and neck edema. Upon initial assessment, if there is any indication that the patient has a pharyngeal burn, is hoarse or has stridor, the patient should be nasally or, preferably, orally intubated with an uncut endotracheal tube. This action serves to splint the airway open and maintain patency. Arterial blood gases (ABG’s) should then be drawn and oxygen saturation levels monitored. If necessary, the patient may need to be mechanically ventilated in order to maintain sufficient levels of oxygenation.
Mechanical ventilation protocols should be instituted and ventilator settings titrated to maintain desired PaCO2, PaO2 and SaO2 readings.
When the edema subsides and/or ventilation parameters improve, the patient can be appropriately assessed and extubated safely. In most clinical settings, tracheostomies are performed if the patient is intubated for longer than 3 weeks. Patients, who
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do not have inhalation injury, may benefit from a face mask or nasal cannula to maintain oxygen saturations > 92%. If there are circumferential flame burns to the chest and back, escharotomies of the chest and/or abdomen may need to be performed in order to release the constricting eschar, decrease respiratory distress and improve chest expansion and ventilation. With an inhalation injury, it is not as obvious that there is damage to the middle or lower airways. At times, patients may present with bronchial and bronchiolar injury, such as bronchorrhea and/or expiratory wheezing. Examination of the lower respiratory tract, using fiberoptic bronchoscopy, should be performed. However, some may have an invisible injury at the level of respiratory gas exchange. This condition is often delayed and diagnosed by arterial blood gas analysis, rather than a chest x-ray. Impaired gas exchange may be related to carbon monoxide poisoning. Carboxyhemoglobin levels should be drawn on admission (Table 5). Treatment of inhalation injury includes aggressive chest physiotherapy, tracheobronchial suctioning, administration of nebulized heparin and acetylcysteine [5], use of bronchodilators (ipratropium) to treat severe bronchospasm and mechanical ventilation with positive end expiratory pressure (PEEP). PEEP prevents collapse of the alveoli and the development of progressive respiratory failure. If the patient’s condition deteriorates and conventional ventilation strategies prove to be inadequate, newer forms of ventilation have been utilized in recent years and include strategies such as high frequency oscillation and implementation of prone positioning techniques. Patients, who have pre-existing respiratory problems, such as a history of frequent pneumonia or chronic obstructive pulmonary disease, are more likely to succumb to respiratory infection. Pneumonia is commonly seen in these patients since they are relatively immobile, may be debilitated and have an abundance of microbial organisms that can settle in the lungs and require aggressive therapy to eradicate. Older, more debilitated patients are also more prone to the development of pulmonary edema as a consequence of the fluid resuscitation required by inhalation-injured patients.
Maintaining the airway is crucial in these patients and frequent assessments of tube placement and stability are an essential part of care. Before pa-
tients are extubated, there is a weaning process which involves adjusting ventilator settings, so the machine is doing less of the work associated with breathing and patients are essentially breathing on their own. If they meet certain criteria, patients are extubated, placed in high Fowler’s position and given 100% oxygen. In addition, they require chest physiotherapy, suctioning, frequent repositioning and deep breathing and coughing exercises. Mobilization at the bedside and in the hallways is also helpful in moving secretions from the upper and lower airways. Sometimes, patients tire too easily post-extubation and need to be reintubated. In situations where a patient cannot be weaned in the near distant future, a decision is made to perform a tracheostomy until such time as he/she can breathe unaided.
Gastrointestinal system – The gastrointestinal system is initially affected in the emergent phase by a lack of circulation to the splanchnic area. This hypoperfusion, secondary to hypovolemic shock, causes paralytic ileus and an absence of bowel sounds. The stress response post-burn causes a decrease in mucous production and an increase in gastric acid secretion, resulting in stress (Curling’s) ulcers. Prompt and effective fluid resuscitation and a restoration of circulation to the gastrointestinal region result in a return of bowel sounds and indicate a functional gut. Bladder pressures should be measured q4h for 72 hours in body surface area burns > 30% and pressures > 20 mm Hg reported. Abdominal compartment syndrome is a life-threatening complication of high-volume fluid resuscitation [6,7]. Management includes keeping the patient NPO for a few hours post-admission until things stabilize and then, beginning early enteral feeds to address the profound hypermetabolic effects of a burn injury. Anti-catabolic, anabolic agents, such as oxandralone and propanolol, may also prove to be valuable adjuncts to therapy. Enteral feeding also maintains the integrity of the gut and avoids bacterial translocation. The hourly rate of feeds is advanced, in a timely manner, to the desired goal rate, usually arrived at in consultation with the burn centre dietitian. A nasogastric (NG) tube, connected to either straight drainage or wall suction, can be inserted for the purposes of gastric decompression and medication administration. Water flushes preand post-medication help ensure the tubes remain patent. Medications include
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J. Knighton, M. Jako
prophylactic use of intravenous H2 antagonists (Ranitidine) to decrease hydrochloride secretion. During the acute phase of care, patients frequently become constipated as a result of codeine-contain- ing pain medication received during their hospitalization and immobility. Prompt institution of a bowel regimen, upon admission, and attention to diet and/ or choice of tube feedings can prevent or rectify the situation before it causes the patient unnecessary discomfort. Patients may also develop diarrhea, caused by certain tube feedings or antibiotics. Excessive diarrhea may warrant clostridium difficile testing. Recommendations from the dietitian or pharmacist should be sought to correct the problem. A bowel management system may need to be inserted if loose stools interfere with optimal wound care. Sepsis is the most common cause of gastric ileus occurring in the acute phase of care and should be monitored closely. Some burn centres are administering an anti-oxidant protocol, which includes selenium, acetylcysteine, ascorbic acid, vitamin E, zinc and a multivitamin. It is also important to monitor and, if necessary, institute potassium, calcium, magnesium and phosphate replacements, and administer thiamine and folic acid, particularly if the patient has a history of alcohol abuse. Blood glucose point- of-care testing should be performed and an insulin nomogram commenced, as per ICU protocol, in order to maintain strict glucose control of 80–110 mg/ dL.
Renal system – With the renal system post-burn, an early warning sign of complications is an increase in the specific gravity, which usually occurs before the urinary output falls. Acute tubular necrosis is the most frequent emergent phase complication and is due to hypovolemic shock. Fluid resuscitation is usually sufficient to correct such problems. Careful attention to trends in urinary output and specific gravity is a more helpful strategy than haphazardly increasing or decreasing the intravenous fluids. Insertion of a urinary catheter should occur, upon admission, to allow for accurate intake/output. If the injury is deep to the tissue and/or muscle, there is the additional complication of high circulating levels of hemoglobin (red blood cell breakdown) or myoglobin (muscle cell breakdown) pigments blocking the renal tubules. This situation is so common in electrical burns that the fluid resuscitation formula
requires very aggressive resuscitation and the infusion of an osmotic diuretic (Mannitol). In the acute phase of care, a decrease in urinary output or the development of high output renal failure, with rising levels of BUN and creatinine, may be indicative of a septic episode. Consultation with the renal service is essential if the patient doesn’t respond to fluid challenges or diuretics. In the most serious of situations, the patient may require dialysis as a life-saving measure. Rising glucose levels indicate stress response, due to catecholamine release, and sepsis. High levels lead to compensatory osmotic diuresis, which means the burn patient needs more fluid.
Infection – Burn patients are at risk for the development of infection due to both the high bacterial loads on their devitalized, burn eschar and the loss of their primary barrier against infection – the skin. Infection is the leading cause of morbidity and mortality in burn patients. The degree of risk is increased due to the presence of devitalized burn eschar, which serves as an excellent breeding ground for organisms, invasive catheters and tubes, and a state of immunosuppression that continues long after the wounds have healed. The larger the burn wound, the greater the risk of infection. However, the advent of early burn excision and prompt wound closure has decreased the overall incidence of burn wound infection and, consequently, the incidence of sepsis and death. Evi- dence-based procedures for the insertion of central lines have resulted in impressive reductions in central line blood stream infection rates. Ventilator-acquired pneumonia (VAP) rates have also declined since the advent of evidence-based practice bundles, such as chlorhexidine mouth rinse, head-of-bed elevation to 300, gastrointestinal prophylaxis and turning patients, from side to side, q2h [8].
The primary sites for organisms are the burn wound, oral and pulmonary secretions, perineal and anal regions. Gram negative organisms, such as e. coli, klebsiella, pseudomonas and serratia, are largely responsible for more than 50% of all septic episodes. They release endotoxins, which serve as key triggers for the sepsis cascade. All burn wounds are colonized with bacteria, which can be identified through qualitative wound swabs. More specific determinations can be made using quantitative, burn wound biopsies. If the bacterial count on a wound rises above 1 × 105/gram of tissue, the wound is said
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