Emergency Room and Acute Care of the Critically Ill Burned Patient

Burned Patient

E. Bittner, L. Grecu, and J.A.J. Martyn

Introduction

The natural history of serious burns is characterized by burn shock, which can be fatal within the first few hours to days, particularly in those with untreated large burns. Burn wound sepsis is the major cause of mortality among those who survive the burn shock. Survival and outcome after major burn injury have improved over the last 20 years due to improved understanding of the pathophysiologic nature of burn injury, better resuscitation, and advances in control of post-burn sepsis includ- ing early, aggressive surgical treatment [1].

Burn Injury Pathophysiology

Severe burn injury results in significant hypovolemic shock and tissue trauma. The volume loss is related to the release of local and systemic inflammatory mediators at local and distant sites. Increases in pulmonary and systemic vascular resistance in association with myocardial depression occur despite adequate fluid resuscitation [1]. Mediators implicated in the pathogenesis of burn injury include histamine, sero- tonin, kinins, oxygen free radicals, and products of the arachidonic acid cascade [2 – 4]. These mediators alter vascular permeability directly and/or indirectly by increasing microvascular hydrostatic pressure or surface area via arteriolar vasodila- tion. Because of the multiplicity of mediators, therapy to antagonize one single mediator (e.g., histamine) has not proved successful. Sympathetic stimulation and hypovolemia related to the injury result in release of catecholamines, vasopressin, angiotensin II, and neuropeptide Y leading to vasoconstriction and increased sys- temic vascular resistance (SVR) [3]. Increased SVR immediately after burn injury is also partly the result of increased blood viscosity secondary to hemoconcentration from fluid loss, which contrasts with other forms of trauma where red cells are also lost. Organs particularly susceptible to ischemia due to inadequate resuscitation and vasoconstriction are the kidneys and gastrointestinal (GI) tract. Myoglobinemia due to muscle damage can also contribute to the renal insult [5]. Sustained vasoconstric- tion of the GI tract can occur even with adequate resuscitation, leading to ischemia and bacterial translocation [6].

The fluid loss of burns occurs not only at the area of burn wound but also at dis-

tant non-burned tissues and can occur up to at least 24 – 48 hours after the injury

[7]. The generalized capillary leak leads to decreased plasma volume, cardiac output,

and urine output. Thus, the initial therapeutic goal is restoration of intravascular

volume in order to preserve tissue perfusion and minimize the ischemia/reperfusion

injury. Pulmonary edema is not uncommon, especially after the fluid resuscitation phase and restoration of capillary integrity (48 – 72 hours after burn injury), when the edema fluid is reabsorbed leading to hypervolemia. Initially, the pulmonary edema is the result mainly of increased capillary pressure secondary to increased pulmonary vascular resistance. It is likely that some left heart failure also contrib- utes to the pulmonary edema [8]. Developing hypoproteinemia may be an important contributing factor for post-burn pulmonary edema [9]. Pulmonary dysfunction associated with inhalation injury is discussed later.

The early phase of burn injury (first 1 – 2 days), characterized by decreased car- diac output, and metabolic rate, is followed by a phase of increased cardiac output and metabolic rate, which plateaus around post-burn day five. This hypermetabolic and hyperdynamic response is more severe and sustained than any other form of trauma [3, 10] and lasts even as long as 9 to 12 months post-injury in patients with major burns [11]. As a result, lean muscle mass continues to decrease with a nega- tive nitrogen balance despite aggressive nutritional support even with insulin. Loss of a quarter of total body nitrogen balance can be fatal and this limit can easily be reached within 3 – 4 weeks in burn patients not receiving maximal nutritional sup- port [12].

Initial Evaluation

Between 5 – 7 % of patients admitted to burn centers suffer from non-thermal trau- matic injuries. Therefore, all burn patients should be approached initially as multi- ple trauma patients [13]. Securing the airway is the first priority during the initial evaluation; safe airway management begins with its assessment. The presence of air- way injury, signs of airway obstruction, and presence of preexisting airway abnor- mality should be obtained as soon as the patient arrives at the hospital. Airway inju- ries may not be evident initially but, with massive fluid resuscitation, airway edema may result. As a general rule it is safer to intubate the patient early than risk a diffi- cult intubation later when airway swelling has occurred. With severe injuries of the face or neck, direct laryngoscopy may be difficult or impossible. When laryngoscopy and endotracheal intubation are anticipated to be difficult, options include a crico- thyroidotomy or tracheostomy.

Inhalation Injury

Inhalation injury increases the resuscitation fluid requirements by up to 50 % and is

a major source of mortality in burn patients [14]. A history of exposure to fire in a

closed space, loss of consciousness, and presence of chemical irritants, in combina-

tion with the physical examination revealing carbonaceous sputum, singed nasal or

facial hair are all suggestive of inhalational injury. Chest X-rays are usually normal

until secondary complications, such as atelectasis or pneumonia develop. Fiberoptic

bronchoscopy may be used to support the diagnosis, which may reveal carbona-

ceous debris, erythema, or ulceration. The mechanism of inhalation injury consists

of a combination of: 1) direct thermal injury to the upper airway from inhalation of

hot gases; 2) damage to the cellular and oxygen transport processes by inhalation of

carbon monoxide and cyanide; and 3) chemical injury to the lower airways caused

by inhalation of the toxic products from the fire.

Direct heat injury to the upper airway can lead to marked swelling of the tongue, epiglottis, and glottic opening resulting in airway obstruction [15]. Airway swelling may not occur immediately but may develop over a period of hours (especially with concurrent fluid resuscitation). Therefore, a high index of suspicion and frequent re- evaluations are essential. Upper airway edema will have more immediate conse- quences in smaller children. Signs of impending upper airway obstruction include hoarseness, chest retraction, and stridor. If the history and physical examination are suggestive of inhalational injury one should have a low threshold for early intuba- tion, particularly in children. If intubation is delayed and significant swelling occurs, intubation can become difficult or impossible. Upper airway edema usually resolves in 7 – 14 days and is facilitated by elevation of the head of the bed and avoidance of excessive fluid administration.

Carbon Monoxide Poisoning

Because carbon monoxide binds to hemoglobin, 200 times more readily than oxy- gen, it can significantly reduce the oxygen carrying capacity of blood [16]. Binding of carbon monoxide to hemoglobin also shifts the oxyhemoglobin dissociation curve to the left. In addition, carbon monoxide interferes with peripheral oxygen utiliza- tion by binding to molecules such as myoglobin, NADPH reductase, and the cyto- chrome oxidase system resulting in impaired oxidative phosphorylation at the mito- chondria [16]. The mitochondrial dysfunction due to carbon monoxide has best been documented in the heart, where it produces myocardial stunning [17]. The decreased oxygen delivery to the tissues, impaired release of the available oxygen at the capillaries, and weakened ability to utilize the delivered oxygen results in tissue hypoxia and metabolic acidosis.

The clinical findings of carbon monoxide poisoning are variable and largely non- specific, and include headache, nausea, shortness of breath, tachypnea, angina, and changes in mental status [17]. The half-life of carboxyhemoglobin is 4 hours when breathing room air. This is reduced to 40 – 60 minutes when breathing 100 % oxygen.

Hyperbaric oxygen will further reduce the half-life of carboxyhemoglobin to 23 min- utes [17]. In those patients with more severe exposures (carboxyhemoglobin level greater than 30 % or neurologic changes), hyperbaric oxygen has been suggested to diminish the incidence of long term neurological sequelae [18]. The hyperbaric chamber is a difficult environment to monitor, administer fluid resuscitation, and provide acute burn care.

The absorbance spectrum of carboxyhemoglobin and oxyhemoglobin are similar.

Therefore, standard pulse oximeters cannot distinguish between the two forms of

hemoglobin. Oximeter readings will therefore be normal even when lethal amounts

of carboxyhemoglobin are present in the blood. The PaO

measured from arterial

blood gas sample reflects the amount of oxygen dissolved in blood and does not

indicate oxygen bound to hemoglobin (saturation). Thus, the PaO

can be normal

even with high levels of carboxyhemoglobin. The diagnosis of carbon monoxide poi-

soning is made by measuring the carboxyhemoglobin level in arterial blood,

expressed as a percent saturation of hemoglobin. Because of the inevitable time

delay between exposure and testing, prophylactic high concentrations of oxygen

therapy are indicated even before results of carbon monoxide levels. The levels of

carboxyhemoglobin measured may not reflect the true extent of poisoning especially

if the patient has been breathing a high concentration of oxygen.

Cyanide Poisoning

Hydrogen cyanide (HCN) is a toxic gas produced in fires by the burning of nitroge- nous materials, including natural fibers (wool and silk) and synthetic polymers (polyurethane, polyacrylonitrile and acrocyanate). HCN binds to mitochondrial cytochrome oxidase, which catalyzes the last step in the oxidative phosphorylation (ATP formation) pathway, preventing utilization of oxygen by mitochondria. HCN also arrests the tricarboxylic acid cycle. The pathophysiological sequel of cyanide poisoning is that cells can only generate ATP via anaerobic metabolism, which results in a metabolic acidosis from lactic acid production.

As with carbon monoxide poisoning, HCN toxicity can be difficult to diagnose, but should be suspected in any patient with a history of inhalation injury. Concentrations greater than 20 parts per million (ppm) are considered dangerous. Early symptoms include headache, dizziness, tachypnea, and tachycardia. HCN toxicity may manifest as S-T segment elevation on the electrocardiogram (EKG), mimicking acute myocar- dial infarction. Cyanide increases minute ventilation through carotid body and peripheral chemoreceptor stimulation. Concentrations of 100 ppm can lead to sei- zures, coma, respiratory failure, and death. Laboratory findings include an anion gap metabolic acidosis that does not respond to oxygen administration. The mixed venous oxygen saturation (SvO

) in cyanide poisoning is often elevated suggesting an inability to utilize oxygen [19]. Direct detection of cyanide poisoning in the blood is difficult.

Cyanide has a short half-life in blood and measurement is not universally available.

The deleterious effects of HCN are normally neutralized by the conversion of cya- nide to thiocyante, which is excreted in the urine. This can be enhanced by the administration of exogenous thiosulfate [20]. Cyanide can also combine with hydroxycobalamin (vitamin B12), which forms cyanocobalamin. Nitrate administra- tion results in the oxidation of hemoglobin to methemoglobin, which can combine with cyanide to form cyano-methemoglobin. Methemoglobin, however, does not transport oxygen and may thus be harmful in a patient whose oxygen carrying capacity is already compromised because of carboxyhemoglobin.

Chemical Injury to the Lower Airways

The burning of many materials in a house fire can release combustion products that are toxic and damaging to the lower airways, including respiratory epithelium and capillary endothelium of the airway and alveoli. The damage to epithelium results in destruction of mucociliary transport, which impairs clearance of bacteria. Alveolar collapse and atelectasis can occur because of loss of surfactant production or from plugging due to mucus debris [21]. Chemical damage to alveoli and its capillaries will lead to extravasation of plasma proteins. Activation of injury-induced alveolar macrophages will lead to further inflammatory response and damage. Bronchial swelling and bronchospasm can lead to obstruction of both large and small airways.

The end result is respiratory failure from increased V/Q mismatch, decreased lung compliance, and increased dead-space ventilation generally occurring 12 – 48 hours after the inhalation event [15]. The respiratory failure may further worsen several days later from continued airway mucosal sloughing, barotrauma, bacterial invasion, and pneumonia [22].

Injury to the lung can occur in patients with severe cutaneous burns in the

absence of inhalational injury [23]. Mechanisms include inflammatory mediators

from the burn-injured area, effects of fluid resuscitation, and infection. Pulmonary

edema often occurs after a large burn injury because of decreased oncotic pressure, and pulmonary artery hypertension. After restoration of the capillary integrity, the edema fluid from throughout the body is resorbed and can lead to hypervolemic pulmonary edema.

Fluid Resuscitation

Multiple fluid resuscitation formulae exist for estimating fluid needs. As a general rule, burns of ‹ 15 % total body surface area (TBSA) are not associated with exten- sive capillary leak and can be managed with fluid of 1.5 times maintenance rate and careful attention to the hydration status. The commonly used resuscitation formulae differ somewhat in their recommendations of the amount of crystalloid and colloid (Table 1). Most formulae recommend isotonic crystalloid initially and later use of colloids [24]. The time at which colloid administration is initiated varies from insti- tution to institution, and depending on the size of the burn, patient age and other cardiorespiratory parameters. Lactated Ringer’s solution, or similar composition- solutions, is often the crystalloid chosen as it contains physiologic concentrations of major electrolytes and lactate replaces some of the chloride in the solution resulting in less hyperchloremic metabolic acidosis compared to normal saline. In younger children and patients where hypoglycemia is a potential concern, 5 % dextrose can be added to the lactated Ringer’s solution.

Once capillary integrity returns, generally by 24 – 48 hours, most resuscitation formulae recommend administration of colloid. Most authorities advocate 5 % albu- min in isotonic crystalloid, which is ideally administered by continuous infusion at a dose adjusted by burn size. Side effects of large volume crystalloid resuscitation include pleural and pericardial effusions, and intestinal ileus with abdominal com- partment syndrome. Thus, more burn units are advocating early use of colloids.

Resuscitation with hypertonic saline is not part of practice in most burn units since there was a significant increase in renal failure and deaths in patients treated with hypertonic saline compared to lactated Ringer’s solution [25].

The Parkland formula remains the most widely used resuscitation formula for burn injury in the United States. The Parkland formula, 4 ml per %TBSA burn per kg body weight, is administered over the first 24 hours with one half of the calcu- lated volume administered during the first eight post-injury hours [26]. The remain-

Table 1. Formulae for estimating burn resuscitation fluid needs Crystalloid formulae

Parkland Lactated Ringer’s 4 ml/kg/% TBSA burn

Modified Brooke Lactated Ringer’s 2 ml/kg/% TBSA burn

Colloid formulas

Evans Normal saline 4 ml/kg/% TBSA burn

Colloid 1 ml/kg/% TBSA burn

5 % dextrose 2000 ml/24 hours

Brooke Lactated Ringer’s 1.5 ml/kg/% TBSA burn

Colloid 0.5 ml/kg/% TBSA burn

5 % Dextrose 2000 ml/24 hours

TBSA: total body surface area

Table 2. Burn resuscitation end-points Arousable and comfortable

Warm extremities

Systolic blood pressure: For infants, 60 mmHg; for older children, 70 – 90 mmHg + 2 x age (in years);

for adults, mean arterial pressure 8 65 mmHg or within 20 % of baseline Heart rate: 80 – 150 bpm (age dependent)

Urine output 0.5 – 1 ml/kg/hr (glucose negative) Base deficit ‹ 2 mEq/l

ing half is administered over the next 16 hours. If resuscitation is delayed, this vol- ume is administered so that infusion is completed by the 8

post-injury hour. No matter which formula is used, it should serve only as a guideline and fluid resuscita- tion be titrated to physiologic endpoints (Table 2). Actual fluid requirements can vary depending on size of the burn, patient’s weight, interval from injury to start of resuscitation, presence of associated injuries and presence of inhalational injury.

Base deficit is another indicator of global tissue perfusion and is calculated from an arterial blood gas using normograms. In a retrospective study in burn patients, Kaups et al. showed the base-deficit was predictive of fluid requirements and sur- vival [27]. In burn injury, when tissue perfusion is not uniform throughout the body, an indirect measure of less well-perfused tissues may prove useful. One such measure that has been described is the intramucosal gastric pH (pHi), as measured by gastric tonometry. After burn injury, blood flow to the heart, brain, and kidneys is maintained at the expense of splanchnic blood flow. Several studies have shown that a lower pHi is predictive of organ failure and increased mortality and have sug- gested the use of pHi as a guide to resuscitation [28, 29]. This technique, however, has not become routine in clinical practice.

A small percentage of patients fail to respond to conventional fluid resuscitation.

These patients frequently have large, deep burns, are at extremes of age, or have inhalational injury or coexisting medical conditions [30]. If the total fluid require- ment exceeds 6 ml/kg/%TBSA/24 hours, it is advisable to obtain more information regarding intravascular volume. This information can be obtained by physical exam or by measurement of central venous pressure (CVP) and/or pulmonary artery pres- sure. Based on the information, inotropic support may be required. Echocardio- graphic evaluation of ventricular volume and function has been used in burns [31].

After 24 – 48 hours, capillary integrity returns to normal in non-burned areas espe- cially with repletion of circulating volume. At this stage, fluid requirements dramati- cally decrease; it is important to decrease fluid administration promptly as overzeal- ous administration of fluid can be associated with substantial morbidity.

Estimation of Size/Depth of burn

The magnitude of burns is classified according to the TBSA involved, depth of the

burn, and the presence or absence of inhalational injury. The burned TBSA can be

estimated in adults using the ‘Rule of Nines’. Each of the upper arms and head in the

adult contribute to 9 % of TBSA, while the front and back of the trunk, and each of

the lower limbs contribute to 18 % TBSA. Alternatively, estimation by palmar surface

of the hand (without the fingers, 0.5 % TBSA) is age invariant and can also provide

a quick estimate [32]. The depth of skin destruction is characterized as first-, sec-

ond- or third-degree, based on whether there is superficial, partial, or full thickness destruction of the skin. Fourth degree is used to describe burns that have injured deeper structures such as muscle, fascia and bone. Deep second and third degree burns require surgical debridement and grafting, whereas more superficial burns do not. Revisions of burn-depth estimations are often necessary in the first 24 to 72 hours. This is especially true in patients with thin skin, who often sustain deeper burn injuries than evident on initial examination. Skin can be presumed to be thin in young children and the elderly. Mortality from burn injury is related to the TBSA of deep second or third degree burns. A large analysis revealed three risk factors as predictive for death after burns: Age more than 60 years, burn size more than 40 % TBSA, and inhalation injury. Mortality rates were 0.3, 3, 33, or 90 % depending on whether 0, 1, 2, or 3 risk factors, respectively, were present [33].

Burn Center Referral and Organ Specific Care

Data exist linking improved outcomes from major burns with early referral to a burn center [34]. It is recognized that burn care requires specialized expertise, per- sonnel, and equipment which are not cost-effectively maintained in low volume cen- ters. Following establishment of the airway and correction of immediate life-threat- ening problems, the next section focuses on aspects of the neurologic, otolaryngolo- gic, ophthalmic, chest, cardiac, abdomen, genitourinary, and extremity issues that are related to acute burn injury.

Neurologic

Central nervous system (CNS) function can be altered by inhalation of neurotoxic chemicals, effects of hypoxia and hypotension, and from the effects of anxiety and pain or their treatment. It is essential to rule out coexisting intracranial and cervical spine injury by history, clinical examination and radiologic imaging. Patients with serious injuries commonly become obtunded because of hemodynamic instability as well as from the administration of drugs for sedation and analgesia. Therefore, it is important to know that this change does not represent a missed intracrainal injury.

In rare instances, patients with deep neck burns may need escharotomies at that site to facilitate venous drainage.

Otolaryngologic and Ophthalmic

The primary otolaryngologic and ophthalmic evaluation includes assessment and initial treatment of burns to the airway, corneal epithelium, and the external ear.

Signs of airway involvement include perioral and oropharyngeal burns, presence of carbonaceous sputum, and signs of hoarseness. Hot liquid can be aspirated in con- junction with a scald injury to the face and can result in rapid airway compromise.

One should have a low threshold for intubation when potential airway involvement

exists. The globes of the eye should be examined early since adnexal swelling can

make the examination difficult. Severe corneal burns are usually obvious by the

cloudy appearance they impart, but damage is more often subtle requiring florescein

staining. Topical antibiotics are the initial treatment if an injury is present. Burns to

the external ear can be complicated by suppurative chondritis. Treatment with topi-

cal mafenide acetate cream may decrease its development.

Chest

The focus of the initial evaluation of the chest is to ensure chest wall compliance of both hemithoraces. Impaired chest wall compliance can result from deep circumfer- ential eschar impairing chest wall excursion and/or bronchospasm resulting from inhalation of airway irritants. The inhalation of toxic fumes may precipitate bron- chospasm in a patient with a previous history of asthma. A patient with decreased compliance because of a circumferential eschar will exhibit rapid shallow respira- tions. A patient on a ventilator will show an increase in peak airway pressures.

Escharotomy is the treatment of the latter condition while bronchodilators, pulmo- nary toilet, and ventilation strategies to minimize breath stacking are used to treat bronchospasm. Severe inhalational injury may result in thick secretions and the slo- ughing of airway mucosa, which can occlude the endotracheal tube or distant bron- chi resulting in atelectasis and collapse. In these instances, suctioning and bronchos- copy may be required.

Abdomen

Primary objectives in the evaluation of the abdomen are to exclude associated inju- ries, ensure that eschar does not impair adequate abdominal wall compliance to per- mit ventilation, decrease the risk of gastric dilation, and prevent gastrointestinal ulceration. Coincident abdominal trauma should be evaluated with imaging studies or diagnostic peritoneal lavage if indicated. Occult abdominal trauma can explain excessive fluid resuscitation requirements or a paradoxical fall in hematocrit in the early phase of burn injury. In some cases, torso escharotomies may be necessary to facilitate spontaneous respiration or mechanical ventilation in patients with deep circumferential eschars. Circumferential abdominal eschar, accumulation of intra- peritoneal fluid, or bowel edema can lead to abdominal compartment syndrome, leading to diminished urine output, decreased pulmonary compliance, and hemody- namic instability [35]. Obtaining bladder pressure measurements can be useful in the diagnosis. In some cases abdominal decompression may be necessary. Patients with severe burns often develop a paralytic ileus and require nasogastric decom- pression for varying lengths of time. Gastroduodenal ulceration is a risk in severe burn injury and ulcer prophylaxis with H

receptor antagonists or proton pump inhibitors should be initiated as early as possible.

Genitourinary

Catheterization of the bladder is important in patients with moderate to severe

burns, who, therefore, require intravenous fluid resuscitation, since it facilitates the

use of urine volume and quality as an indicator of adequacy of resuscitation. Soft

tissue swelling in the genital area can be significant with severe burn injury whether

or not the burn involves the genital region. This can make urinary catheterization

more difficult as time passes in the acute resuscitation phase. For this reason an

appropriate size Foley catheter should be inserted as early as possible. In males it is

important to ensure that the foreskin is reduced over the urinary catheter after its

insertion to prevent the development of paraphimosis as soft tissue edema develops.

Extremities

Exclusion of associated (non-burn) injuries and monitoring of peripheral perfusion are the initial priorities in evaluation of the extremities. Extremity perfusion can be compromised by soft tissue swelling in the noncompliant fascial compartments or by circumferential eschar. Extremities that are at risk for ischemia, especially in those with circumferential burns or with electrical injury, should be monitored closely for tense fascial compartments and signs of impaired perfusion. Frequent checks of pulses, capillary filling, venous congestion, and Doppler blood flow are important. Dressings should be loosely applied to facilitate frequent examination.

Tense extremities should be decompressed by escharotomy and/or fasciotomy when clinical examination reveals signs of impaired perfusion. Escharotomies can be per- formed at the bedside with use of electrocautery to minimize blood loss. The need for escharotomy usually becomes apparent in the early hours of acute resuscitation.

Fasciotomies are generally performed in the operating room to minimize damage to the underlying structures that can be obscured by the tissue edema.

Antibiotics

Prophylactic antibiotics have no proven role in burn care and are not routinely given [36]. All burn injuries are potentially contaminated soft tissue wounds, and, there- fore, tetanus toxoid should be given to all burned patients [37]. If the patient has not been previously immunized, tetanus immunoglobulin as well as tetanus toxoid should be administered.

Electrical Injuries

Electrical burns can have acute and chronic effects not seen with other types of burn injury, and with morbidity much higher than expected based on burn size alone [38]. Approximately 15 % of patients sustaining electrical injury suffer other trau- matic injury in addition to their burn. These injuries often involve falls, being thrown against an object, or result from tetanic muscle contractions.

Both arrhythmias and direct myocardial injury can result from electrical injury.

Creatine kinase and MB-creatine kinase enzymes are poor indicators of myocardial injury in the absence of EKG findings, particularly if muscle injury is present [39].

The diagnostic value of cardiac troponin levels has not been evaluated in this set- ting. The myocardial injury behaves more like a cardiac contusion than a myocardial infarction, with minimal hemodynamic consequences. This may be related to the fact that the heart, unlike the skeletal muscle cannot sustain tetanic contractions.

Virtually any cardiac arrhythmia can result from electrical injury. Ventricular fibril- lation is the most common cause of death at the scene of the injury. Arrhythmias from electrical injury are managed using the same medical therapies as those result- ing from any other cause. Patients with electrical injury should have EKG monitor- ing during transport to the hospital, in the emergency room, and afterwards. Indica- tions for more prolonged cardiac monitoring include: 1) documented cardiac arrest;

2) cardiac arrhythmia on transport or in the emergency room; and 3) abnormal EKG [40].

The hidden (deeper) injury associated with electrical burn makes the standard

fluid resuscitation formula inaccurate. Adequate fluid resuscitation is obtained by

achieving the standard resuscitation endpoints described previously. Myoglobinuria due to muscle damage will manifest as pigmented urine and usually indicates more severe muscular damage. Myoglobin and hemoglobin pigments pose risk for acute renal failure and require prompt treatment with crystalloid loading to a target urine output of 2 ml/kg/hr. Addition of sodium bicarbonate to intravenous fluid may facil- itate pigment clearance and minimize renal injury. Mannitol and furosemide are also effective in promoting a prompt diuresis, but compromise the value of urine output as an indicator of adequacy of resuscitation.

Conclusion

Care of the severely burned patient requires the team effort of emergency room phy- sicians, anesthesiologists/intensivists, psychiatrists, surgeons, nursing staff, and the paramedical personnel. Intensive care management of the patient necessitates an understanding of the early and late pathophysiology of the injury and careful atten- tion to detail. An organized team approach will lead to safe management and avoid- ance of complications, and thus decrease morbidity and mortality.

Acknowledgement: This work was supported in part by grants from Shriners Hospi- tal Research Philanthropy and NIH GM31569, GM21500 Project IV, and GM55082 to Jeevendra Martyn.

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