Chapter 61: Critical Care of Burn Patients

Caring for critically ill patients is even more challenging when the largest organ, the first barrier against any external insult, is damaged by a burn injury. Care of the severely burned patient requires prompt resuscitation and definitive surgical management to reduce morbidity and mortality. The approach is multidisciplinary and involves intensivists, surgeons, and skilled nursing teams among others. The need for psychologic and social support is considerable.

Mortality rates from severe burn injuries have steadily declined over the last 30 years attributed in part to a multidisciplinary approach and specialized care delivered in burn centers. Most burns are the result of fire or scalding and involve less than 10% of the total body surface area (TBSA) with a mortality of close to 0.5%. Patients with major burns (≥ 25% TBSA) require management in an intensive care unit.

Burn survival correlates with 3 major factors: patient age, burn size, and the presence of inhalational injury.

Burns are classified as thermal, electrical, chemical, friction, or radiation injuries that result in coagulative necrosis of tissues. The clinical severity is determined by the depth and extent of injury. Depending on the depth of injury, burns are further classified as superficial (first degree), partial thickness (second degree), and full thickness (third degree) when all skin layers are affected (Figure 61–1). A fourth degree burn signifies deeper tissue involvement down to bone or muscle.

Burns affecting the epidermis are usually red with mild pain and no blisters. Burns extending beyond the epidermis tend to be erythematous, painful and with blisters; a dry aspect is seen on deeper dermal burns due to the effect of coagulative necrosis sealing the tissues. Full thickness burns are always dry and in the vast majority insensible, as there is destruction of the entire dermis.

A thermal injury triggers responses in every mayor organ system. Immediately after a burn, intense inflammation and systemic manifestations are generated; inflammatory mediators cause loss of capillary integrity with edema formation mainly in the first hours extending up to 24 hours or more, postburn. The same cascade causes volume depletion, depressed cardiac contractility, and systemic hypoperfusion producing a shock state. Contributing to this process is leukocyte and endothelial activation with cytokine production, complement activation, histamine release, xanthine oxidase, and lysosomal enzyme activation that augment microvascular permeability and wound edema, similar to the cascade that causes acute respiratory distress syndrome (ARDS).

Cortisol, epinephrine, glucagon are also persistently secreted generating glucose intolerance and a hypermetabolic or catabolic state that extends beyond the initial recovery.

The initial management is triage and acute resuscitation in the first 24 to 48 hours. Prehospital care and stopping the burning process is the most important component for first responders. Clothes that are burning, smoldering, or soaked with chemicals should be removed. The patient should be removed away from an electrical source. In chemical injuries copious water lavage should be performed. A sequential assessment (primary survey) to avoid missing serious associated injuries as described by the American College of Surgeons in Advanced Trauma Life Support should be followed.

Estimating the total burned body surface area is a key component for resuscitation. Fluid resuscitation by formula is recommended if the TBSA is more than 15%. All current formulas and methods for resuscitation in burned patients are based on body weight and the percentage of TBSA burned. The initial history and physical exam should also include the body weight and an estimate of the second and third degree burn areas used to calculate resuscitation. The “rule of nines” allows a simple, rapid estimate of TBSA: (in an adult [units = % TBSA]): entire head & neck = 9; each arm = 9; upper 1/2 torso front = 9; lower 1/2 torso front = 9; upper 1/2 torso back = 9; lower 1/2 torso back = 9; each leg = 18—anterior leg = 9; and posterior leg = 9.

In burn patients a reevaluation of the airways and breathing should be done upon hospital arrival. Inhalational injury should be suspected in all patients exposed to smoke, flames, or steam, especially those trapped in a closed environment or rescued in an unconscious state. Early intubation should be performed in the presence of distinct features: deep facial burns, full thickness neck burns, oropharyngeal edema, hypoxemia, stridor, hypercapnia, or a Glasgow Coma Scale less than 8. In the early stages intubation is technically easier if there is minimal or no airway edema. If intubation is performed the internal diameter of the endotracheal tube should be at least 7.5 mm or greater (eg, 8.0-9.0 mm) if possible, in anticipation of the need for later bronchoscopy. Emergency tracheostomy or cricothyroidotomy is rarely needed if intubation is performed early; tissue edema in the head and neck can make these procedures complicated (Figure 61–2).

Pulmonary insufficiency and failure in severely burned patients is multifactorial, due to direct pulmonary and upper airways injury, indirect or secondary injury due to systemic inflammatory response, and delayed injury due to sepsis and pneumonia. Ventilation can also be impaired due to edema within the torso and abdomen; torso escharotomy can avoid laparotomy and improve ventilation.

Severe inflammation and endothelial activation can lead to significant pulmonary capillary leak and ARDS which is common in burn patients with an incidence as high as 30%.¹ It can be exacerbated by sepsis and over resuscitation.

Reduced lung compliance and chest wall rigidity can lead to higher airway pressures. Lung injury may not be a result of higher airway pressures because there is also less stretch on the alveoli as is also seen in other situations where compliance is reduced such as abdominal hypertension. Ventilator strategies may include low tidal volume ventilation with permissive hypercapnia with conventional ventilator modes, airway pressure-release ventilation or high-frequency oscillation in selected patients with inhalational or chest wall injuries. Inhaled nitric oxide may be used for the treatment of hypoxic vasoconstriction improving ventilation/perfusion mismatching and tissue oxygenation. Extracorporeal membrane oxygenation, used more often in pediatrics, may be helpful in selected adults with severe refractory ARDS.²

The indications and timing of tracheostomy (either open or percutaneous) after burns are similar to critically ill patients in general, however, caution is needed in the selection of patients with severe facial and neck burns or upper airway edema for tracheostomy because of the increased potential for loss of the airway and local skin complications. Tracheostomy in a burned neck tends to be a difficult procedure due to anatomy disruption, with increased complications such as bleeding, infection, and poor wound site healing.

As in other critical illnesses such as septic shock, prompt and adequate resuscitation is of great importance. However due to external burn injuries, the degree of systemic inflammation and tissue edema, fluid losses are much more prominent. The main focus on resuscitation strategies is to minimize resuscitation complications of under or over resuscitation. Protocols unique to the burned patient take into account fluid losses via the skin.

Two large-bore peripheral intravenous catheters should be inserted through unburned skin if possible and baseline laboratories sent. Frequently unusual peripheral venous sites or central venous access is required. The groins are often spared; so femoral venous cannulation is usually possible. Burns are usually the immediate cause of hypovolemia, however, bleeding from other injuries should also be ruled out.

Fluid resuscitation should be individualized based on age, comorbidities, organ function, burn area and hemodynamics. Fluid resuscitation guidelines are often based on the Parkland burn formula. Typically a lactated Ringer’s solution is infused at an initial volume of 4 mL/kg body weight × % burn area in 24 hours with 50% given in the first 8 hours and the remainder over the next 16 hours. However, balanced isotonic crystalloids such as plasmalyte containing acetate, a bicarbonate precursor, may also be used; either Ringer’s lactate or plasmalyte will result in less hyperchloremic metabolic acidosis than normal saline. Continuing fluid administration may be based on the formula 0.3 to 0.5 mL/kg × % burn area over 24 hours, but fluid resuscitation must be modified depending on organ function and hemodynamics. In adults, a urine output of at least 30 to 50 mL/h is commonly targeted. Under resuscitation results in reduced cardiac output (CO), inadequate tissue/organ perfusion, oliguria and increasing lactate trends; over resuscitation can result in a constellation of complications including worsening of upper airway edema, pulmonary edema, prolongation of mechanical ventilation, cerebral edema and compartment syndromes (CS) (abdomen, extremities, ocular).³ Elevated lactate appears to be a biomarker for increased mortality in burn patients but a normal lactate alone does not mean that fluid resuscitation is adequate.

Fluid resuscitation with hypertonic saline (eg, 7.5% NaCl) or colloids (eg, albumin) has not been demonstrated to improve outcomes, although as expected the total resuscitation volume is usually less with colloid administration.

Almost immediately after a major thermal injury, CO tends to decrease within an hour. This is, in part, due to myocardial depression from tumor necrosis factor (TNF)-alpha and endotoxin. After adequate resuscitation, the CO tends to normalize and is often followed by a hyperdynamic circulation with vasodilation. Evaluation of hemodynamic parameters typically involves invasive or noninvasive blood pressure measurement and some form of cardiac monitoring. Pulmonary artery catheters are less commonly used, being supplanted by transpulmonary thermodilution devices and noninvasive techniques such as ultrasound of the heart, inferior vena cava (IVC), and lung that can provide accurate information in monitoring resuscitation of the acute burn patient.

Restrictive strategies of red blood cell transfusion (hemoglobin 7.0-9.0 g/dL) may be superior or at least equivalent to the liberal strategy (hemoglobin 10.0-12.0 g/dL) in critically ill patients. This appears to also be applicable in burn patients as increased mortality is associated with blood transfusion. The use of erythropoietin is not helpful to prevent or improve anemia in burn patients due blunting of erythropoietic response.

Acute renal failure may result from severe hemodynamic instability, delayed or inadequate resuscitation during the initial burn treatment or later as a result of sepsis or rhabdomyolysis. Patients who have sustained high-voltage electrical injuries are at increased risk of acute tubular necrosis, as the large myoglobin molecules released after such an injury can damage the renal tubules. Patients with evidence of myonecrosis or rhabdomyolysis have a reported mortality of more than 70% in severe burns.⁴ Intravenous fluid rates should be increased for a target urine output of 1 mL/kg/h, commonly between 75 and 100 mL/h. In difficult cases, diuresis with mannitol or furosemide may be instituted but may result in hypovolemia and invalidates urine output as a reliable measure of resuscitation. Although nothing has been proved to be superior to saline administration, alkalization of the urine with sodium bicarbonate is advocated to prevent precipitation of myoglobin in the renal tubules.

Acute burn patients are at risk for electrolyte derangements, especially hyperkalemia, due to renal failure and rhabdomyolysis. Serum electrolytes—sodium, potassium, calcium, and phosphorus—and creatinine kinase (CK) must be monitored frequently with initial treatment aiming for intravenous (IV) fluid administration and electrolyte management until CK is less than 5000 U/L. In cases that do not respond and develop oliguric or anuric renal failure, fluid resuscitation will no longer be beneficial and if continued will exacerbate volume overload. In this setting with volume overload and/or persistent hyperkalemic acidosis, renal replacement therapy should be initiated.

Edema is almost always present in the burn patient, even in the absence of excessive fluid administration. Edema is seen in tissues affected by the thermal injury and also in unburned areas related to systemic inflammation and resuscitation. Complications due to the edema can be cumbersome; facial and neck swelling create more difficult airway management, requiring prophylactic intubation in some instances.

Compartment syndrome (CS) in the extremities, torso, or abdomen have been linked to the presence of deep, full-thickness circumferential burns and the volume resuscitation.

Limb CS: Clinical suspicion is increased in the presence of delayed capillary refill, cyanosis, paresthesias, and diminished pulses. Compartment pressures can be measured by placement of an 18 grams needle connected to an arterial pressure transducer under the eschar into the subfascial tissue. Pressures above 25 to 30 mm Hg in any compartment are considered diagnostic of CS, but the clinical exam is important in diagnosis regardless of pressure measurements that can be inaccurate or misleading. The diagnosis of CS mandates decompression via escharotomy and/or fasciotomy. Escharotomy includes incision along the full length of eschar with extension into viable unburned tissue, typically using electrocautery. Fasciotomies involve the surgical opening of the full length of fascial compartments. In both cases, a tissue bulge is often noted indicating adequate release of compartment pressure. Escharotomies are commonly performed at the bedside using mild sedation; fasciotomies may need to be performed in an operating room under general anesthesia. Failure to diagnose and promptly treat CS can lead to ischemia, myonecrosis, and limb loss.

Abdominal CS: Abdominal distention, oliguria, and high airway pressures on mechanical ventilation may signal the development of an abdominal compartment syndrome (ACS). ACS significantly decreases perfusion to vital organs including the small and large bowel, liver, and kidneys, contributing to the development of multisystem organ failure. Early recognition of abdominal hypertension through serial bladder pressure measurement can allow for timely decompressive laparotomy and avoidance of the sequelae caused by prolonged tissue ischemia. In many centers, caring for burned patients there are institutionalized protocols to monitor for abdominal hypertension, especially in patients with greater TBSA percentages, large torso burns, and those who require large volume resuscitation (> 500 mL/h).

Another complication of postburn edema is elevated ocular pressure. Measuring intraocular pressure (IOP) is required in some patients with large facial burns and eyelid edema; when the IOP is persistently high, decompression is indicated to avoid optic nerve damage and visual loss.

Sepsis is an independent risk factor for mortality following thermal injury, especially when multiorgan system failure is present. Open wounds, injured lungs, central venous catheters and urinary catheters place the burn patient at increased risk of infection and sepsis, in that order. Signs of systemic inflammatory syndrome (SIRS) are all normal findings induced by burn injury, leading to diagnostic uncertainty. Laboratory markers including peripheral white blood cell (WBC) levels, procalcitonin, C-reactive protein, human leukocyte antigen D-related (DR) expression and others have been proposed as early indicators of sepsis in the burn patient, all with mixed results. Absolute values and trends in WBC, neutrophil percentage and body temperature are unable to predict bloodstream infection in the burn patient. The promise of early markers is to provide earlier diagnosis and treatment of infection. Although controversial, the use of procalcitonin levels has been advocated due to its sensitivity, specificity and mortality correlation in patients with burns having sepsis. However there is insufficient evidence to support the use of procalcitonin as a single diagnostic marker for sepsis in patients with burn injury.

The largest entrance of infection in burns is the breakdown of the skin barrier. The monitoring of wounds and the use of topical and surgical therapies is the first line for prevention of burn wound infection.

Ventilator associated pneumonia (VAP) in severe burn patients is associated with increased mortality but the diagnosis of VAP is nebulous. Due to severe underlying inflammatory pulmonary pathology, accurate clinical diagnosis of VAP can be very difficult in burn patients and infiltrates may be due to noncardiogenic pulmonary edema (ie, ARDS) from SIRS. The emergence of multidrug resistant bacteria is a major problem as is the use of prolonged antibiotherapy.

Bloodstream and urinary tract infections are also of concern. Timing of central access exchange in the patient with burns is determined by the risk of colonization, need for placement through burned versus unburned tissue, and physician preference. The use of peripherally inserted central catheters lines may not decrease the risk of central-line-related bloodstream infections.³ Prompt removal of all indwelling catheters when no longer warranted provides the best balance between benefit and risk in the patient with burns. Blood and urinary tract infections are treated with removal of the catheter whenever possible and appropriately tailored antibiotic therapy. The use of systemic antibiotic prophylaxis has not been shown to decrease wound infection or any others in the burned patient and may promote infection with multidrug resistant organisms and fungal infections. Protocols vary in when surveillance cultures of burn wounds are performed. Burn wounds often become colonized but may or may not be causing sepsis. Systemic antibiotics are added to standard local wound care if infection is suspected (see Sec. “Wound Care”).

Less Common Infections

Acute infective endocarditis has a low prevalence in burn patients, but adds considerable morbidity and mortality. A common pathogen is Staphylococcus aureus and persistent bacteremia should prompt investigation for endocarditis. Other less frequent infections in burn patients include parotitis, sinusitis, chondritis of the ear and ocular infections.

Wound Care

Although wound sepsis in burns has steadily decreased, it remains a factor that adds morbidity and mortality. Cleansing and debridement of the wound is accomplished with mild soap and water or with chlorhexadine/normal saline washes. Most burn experts recommend debridement of all blisters larger than 0.5 cm to reduce the risk of bacterial colonization or infection. Burn wounds become colonized in the first few hours with gram-positive bacteria including S aureus and epidermidis, and by 5 days are predominantly colonized with gut flora such as Pseudomonas aeruginosa, Enterobacter cloacae, and Escherichia coli.

Health care workers must be vigilant in hand washing and maintenance of a clean environment around the wounds for prevention of cross-contamination in these immunocompromised patients. Culture swabs of all wound beds should be obtained upon admission and repeated serially to monitor for changes in colonization or if there is a clinical suspicion of wound sepsis. Quantitative cultures of the burn to diagnose wound invasion are best obtained by tissue biopsy, either in the operating room or at bedside. Bacterial colonization of burn wounds does not require systemic antibiotics but should be managed with early debridement and/or excision, together with appropriate topical and/or biologic dressings.

Cleansing and debridement is followed by application of a topical antimicrobial agent intended to control colonization, not sterilize the burn wound. Several layers of absorptive gauze and Kerlix cover the wound to decrease evaporative water losses. Minor burns can be managed with biologic dressings, silver-coated dressings, or tribiotic ointment covered with nonadherent gauze. Commonly utilized topical agents include silver sulfadiazine (silvadene), mafenide acetate (sulfamylon), and silver nitrate. Silvadene continues to demonstrate effective control of burn wound colonization, while remaining inexpensive and easy to apply. However, eschar penetration is minimal and complications related to leukopenia and hemolysis have been reported. Mafenide acetate cream (sulfamylon) is painful when applied to superficial partial thickness burns. Eschar penetration is greatest with sulfamylon, making it the topical agent of choice in burns where the eschar will not be excised immediately or when control of P aeruginosa is required. Metabolic acidosis may occur, as sulfamylon is a carbonic anhydrase inhibitor. Silver nitrate 0.5% solution has fallen out of favor due to electrolyte abnormalities and poor tissue penetration but may be used as a reasonably effective agent for treatment of gram-negative or fungal colonization. Other alternatives for topical treatment are available especially when patients are allergic to sulfas, such as bacitracin, neosporin, mupirocin (mainly gram-positive coverage), and polymyxin B.

Complications directly related to topical agents, frequent dressing changes often result in traumatized epithelialization and delayed wound healing. Silvadene has been shown to delay wound healing due to a direct toxic effect on keratinocytes. To avoid this silver impregnated dressings have been developed to provide antimicrobial coverage, adequate humidity, and decreased trauma, all with less frequent dressing changes. Biosynthetic products designed as epidermal substitutes are also used, allowing for faster reepithelialization, although their use is limited due to increased infection.

In addition to topical wound care, a great deal of wound care relies on the surgical management. Deep burns are managed with surgical excision and placement of xenograft, allograft, autograft, or cultured skin substitutes.

Most experienced burn centers advocate for an early wound excision within the first 1 to 7 days following thermal injury to attenuate the systemic inflammatory effects of burns and reduce the risk of sepsis. No significant difference in infection or mortality rates was found when burn excision was performed at any point between 2 and 7 days of management. The appropriate timing for burn wound excision and grafting involves a number of important factors including the age of the patient, extent and depth of burn, comorbidities, hospital resources, and physician preference. Mortality and length of stay is decreased in young populations of burn patients (< 30 years and children) with a TBSA more than 30% when early excision is performed.

After the wound is excised, bleeding is controlled and grafting occurs as per institution protocol, after the procedure a proper wound dressing, topical antibiotics are a must to avoid graft failure and infections. Skin substitutes and replacements require adequate wound bed preparation to ensure minimal graft loss.

Burns are associated with a hypermetabolic state. The increase in metabolic rate is proportional to the extent of the burn and the coexistence of infection; the metabolic rate peaks at 7 to 10 days and can persist for many months postinjury. Overfeeding excess carbohydrate or lipid calories can result in metabolic complications such as hyperglycemia and fatty liver.

Caloric requirements may be estimated using 120% to 150% of the Harris–Benedict formula calculation or 20 to 30 kcal/kg body weight/day, trending toward the higher 30 kcal/kg due to the increased metabolic rate. Supplying 1.5 to 2.0 gram of protein/kg body weight will help in maintaining the nitrogen balance due to excess protein losses via the burn wounds. Enteral nutrition is preferred and early enteral nutrition is beneficial. In patients with gastrointestinal complications (see the following section), unable to tolerate enteral feeding, TPN may be initiated.

Hyperactive metabolic response in the thermal injury is due to the increased levels of catecholamines and catabolic hormones. The use of beta-blockers is very common in burn units to attenuate the catabolic state reducing oxygen demand, resting energy expenditure and heart rate. Randomized prospective trials will be needed to assess the impact of beta-blockade after burn injuries.

Multiple complications affecting the gastrointestinal tract arise after the occurrence of severe burns, usually in patients with a Total Body Surface Burn (TBSB) more than 25%. Dysmotility problems vary from diarrhea (very common), mainly while using enteral feeds, high osmotic loads, overfeeding, and infection (Clostridium difficile, Cytomegalovirus). Ileus may develop due to hypovolemia, use of narcotics, infection, prompting nasogastric decompression and bowel rest.

Within hours of a severe burn injury, the stomach and the duodenal mucosa can develop focal injuries, progressing to larger and multiples lesions and even gastrointestinal bleeding (Curling’s ulcers). Rapid resuscitation, the use of proton-pump inhibitors or H-2 blockers and early enteral feeding has decreased this complication to less than 2% in the critically ill population.

The liver seems to be affected immediately following severe burn injury most likely related to severe systemic inflammation, shock, and hemolysis. There is a mild to moderate increase of aminotransferases that should resolve within a few days, the presence of early jaundice is associated with a poor prognosis.

The proposed etiology of hemolysis is the induction of morphologic changes in red cells. Schistocytes and spherocytes are identified due to direct effect of heat on the cells, hemolysis generally takes place during the first 24 to 48 hours and it correlates with the TBSA.

The incidence of pancreatitis has increased in patients with severe burns as more patients survive. Standard diagnostic and therapeutic modalities are used when clinically indicated (amylase, lipase levels) with temporary bowel rest. Acute cholecystitis (mostly acalculous, intestinal necrosis) can occur in any critically ill patient and is increased in patients receiving TPN. Acute cholecystitis is less commonly seen, possibly due to more effective resuscitation and enteral nutrition.

Pain as the result of an acute burn is usually a mixed picture (procedural pain and pain directly caused by the injury), multiple procedures from wound dressings changes, debridement, grafting, and physiotherapy will add severe pain to the patient, poor pain management will impede proper patient cooperation and ultimately good rehabilitation. In intubated patients the usual approach is continuous sedation and opiate infusion, in awake patients needing multiple procedures conscious sedation is ideal. Long-acting opiates and patient control analgesia are useful. Evaluation and follow up by an acute pain team can be beneficial by recommending other therapies, anxiolytics, nonopiate medications, and nonpharmaceutical strategies.

The incidence of deep vein thrombosis and pulmonary embolism in the burn patient is increased; unless contraindicated all critically ill burn patients should receive both mechanical (intermittent compression devices) and pharmacologic prophylaxis (fractionated or unfractionated heparin) until mobile.

Psychologic and psychiatric support is often not needed in the acute ICU setting; however, an assessment and treatment should be addressed as soon as needed, taking into account that most of every severe burned patient will live with not only physical sequels from their misfortune but also with a pronounced posttraumatic stress disorder. Caregivers should start a clear and honest conversation with the patient and family when feasible, for a better understanding of the implications of the injuries sustained.

A multidisciplinary approach including nurses, physiotherapists, counselors, occupational therapists, and social workers is fundamental to aid rehabilitation and reduce long-term disability. It should start at the time of injury and during the acute care and continue postdischarge. Physical therapy can decrease muscle mass loss and bone mineralization, and improve mobility and function in the burned patient.