Acute treatment of severely burned pediatric patients

Introduction

Over 440 000 children receive medical attention for burn injuries each year in the US [1]. Children younger than 14 years of age account for nearly half of all emergency department–treated thermal burns [2]. With approximately 1100 children dying of burn-re- lated injuries in the United States every year [2] severe burns represent the third most common cause of death in the pediatric patient population [3] and account for a significant number of hospital admissions in the United States [2, 4]. The devastating consequences of burns have been recognized by the medical community and significant amounts of resources and research have been dedicated, successfully improving these dismal statistics: Recent reports revealed a dramatic decline in burn-related deaths and hospital admissions in the USA over the last 20 years; mainly due to effective prevention strategies, decreasing the number and severity of burns [5–7]. Advances in therapy strategies, based on improved understanding of resuscitation, more appropriate infection control and improved treatment of inhalation injury, enhanced wound coverage and better support of hypermetabolic response to injury, have further improved the clinical outcome of this unique patient population over the past years. While other chapters within this book mostly summarize the general treatment of burn victims, this article is focusing on current and emerging thera-

Marc G. Jeschke et al. (eds.), Handbook of Burns

peutic strategies for the acute treatment of severely burned pediatric patients.

Initial management of the burned child

In general, initial management of the burned child should be the same as for any other burn or trauma patient, with special attention directed to the airway, breathing, circulation and cervical spine immobilization according to the guidelines of the American College of Surgeons Committee on Trauma and the Advanced Trauma Live Support Center [8]. The algorithms for trauma evaluation should be diligently applied to the burn patient and the primary survey begins with the ABCs (airway, breathing, circulation) and the establishment of an adequate airway as described elsewhere in this book [9]. Note worth to mention is to provide adequate pain control and relieve the patient from pain and stress. Pain medications should be carefully administered not to overdose and induce adverse side effects. In addition, the amount of pain medication should be reasonable and be based on the burn size and subjective pain of the patient [10]. Dosing of pain medication needs to be according to pediatric guidelines.

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Fluid resuscitation

Severe burn causes significant hemodynamic changes, which must be managed carefully to optimize intravascular volume, maintain end-organ tissue perfusion and maximize oxygen delivery to tissues [11]. Massive fluid shifts after severe burn injury result in the sequestration of fluid in both burned and non-burned tissue [12]. Release of pro-inflammatory mediators early post-burn, such as histamine, bradykinin and leukotriene leads to increased microvascular permeability, generalized edema and burn shock, a leading cause for mortality in severely burned patients [13–15]. Early and accurate fluid resuscitation of patients with major burns is thus critical for survival [16]. Calculations of fluid requirements are based on the amount of body surface involved in second or third degree burns (not first degree burns). The “Rule of Nines” (Fig. 1a) is commonly utilized to estimate the body surface area burned, but this does have limitations in the pediatric patient population where the head is proportionally larger than the body when compared to the adult. A more accurate assessment can be made of the burn injury, especially in children, by using the Lund and Browder chart, which takes into account changes brought about by growth (Fig. 1b). Many different fluid resuscitation formulas have been suggested, each of which can be used effectively to resuscitate a severe burn. The various formulas differ in the amount of crystalloid and colloid to be given, as well as in the tonicity of the fluid [11]. The American burn association has recently published practice guidelines on burn shock resuscitation in order to review the principles of resuscitation after burn injury, including type and rate of fluid administration, and the use of adjunct measures. It presents an excellent approach for the initial treatment of burn patients [17]. However, it is important to mention that there is no formula that will accurately predict the volume requirements of the individual patient: all resuscitation formulas are designed to serve as a guide only. The modified Brooke and Parkland (Baxter) formulas are the most commonly used early resuscitation formulas throughout the world [18]. They use 2–4 ml/kg/%BSA burn of Lactated Ringers solution respectively. The calculated needs are for the total fluids to be given over 24h [15]. In children, maintenance require-

a

b

Fig. 1. a Estimation of burn size utilizing the rule-of-nines. b Estimation of burn size utilizing the Lund and Browder method

ments must be added to the resuscitation formula. For this reason, we recommend the Shriners Burns Hospital SBH-Galveston Formula, which calls for initial resuscitation with 5 000 ml/m2 BSA burn/d + 2 000 ml/m2 BSA/d of Lactated Ringers solution [19]. For both formulas, the first half is administered within the first 8 hours after the burn, and one-quarter in each of the next 16 hours. Intra-vascular volume status must be still reevaluated on a frequent basis during the acute phase. Fluid balance during burn shock resuscitation is typically measured by hourly urine output via an indwelling urethral catheter. It has been recommended to maintain urine output of approximately 0.5 cc/kg/h in adults [20] and between 0.5 and 1.0 ml/kg/h in patients weighing less than 30 kg [21], however, there have been no clinical studies identifying the optimal hourly urine output to maintain vital organ perfusion during burn shock resuscitation. Diuretics are generally not indicated during the acute resuscitation period. It is imperative to avoid over-aggressive resuscitation, particularly in small children under 4 years of age, which may potentially lead to increased extravascular hydrostatic pressure and pulmonary edema [22]. This is especially important in patients who have a concomitant inhalation injury, because they will also have increased pulmonary vascular permeability. Patients with high voltage electrical burns and crash injuries with myoglobin and/or hemoglobin in the urine have an increased risk of renal tubular obstruction. Therefore in these patients sodium bicarbonate should be added to IV fluids to alkalinize the urine, and urine output should be maintained at 1 and 2 cc/kg/h as long as these pigments are in the urine [23]. The addition of an osmotic diuretic such as mannitol may be needed to assist in clearing the urine of these pigments. Because large volumes of fluid and electrolytes are administered both initially and throughout the course of resuscitation, it is important to obtain baseline laboratory measurements of complete blood count, electrolytes, glucose, albumin, and acid-base balance [24]. Crystalloid, in particular lactated Ringer’s solution, is the most popular resuscitation fluid currently utilized [19]. Proponents of the use of crystalloid solutions alone for resuscitation report that other solutions, specifically colloids, are not better and are certainly more expensive than crystalloids for maintaining intravascular vol-

ume following burn trauma [25]. Perel and Roberts identified 63 trials comparing colloid and crystalloid fluid resuscitation across a wide variety of clinical conditions and found no improvement in survival when resuscitated with colloids [26]. The use of albumin in burns and critically ill patients has recently been challenged by the Cochrane Central Register of Controlled Trials, which demonstrated no evidence that albumin reduces mortality in this particular patient population when compared with cheaper alternatives such as saline [27]. Vincent et al. showed in a cohort, multicenter, observational study that albumin administration was associated with decreased survival in a population of acutely ill patients when compared to those who did not receive any albumin at any time throughout their ICU stay. It is noteworthy that in this study albumin receiving patients were more severely ill than patients who did not receive any albumin [28]. Even though, most burn surgeons agree that burn patients with very low serum albumin during burn shock may benefit from albumin supplementation to maintain oncotic pressure [29].

Sepsis

Sepsis is one of the leading causes of morbidity and mortality in critically ill patients [30]. Severely burned patients are markedly susceptible to a variety of infectious complications [31]. There are excellent criteria (fever, tachycardia, tachypnea, leukocytosis) for the diagnosis of infection and sepsis in most patients, however, the standard diagnoses for infection and sepsis do not really apply to burn patients, since these patients, according to the definitions of the ABA Consensus Conference to Define Sepsis and Infection in Burns, already suffer from a systemic inflammatory response syndrome (SIRS) due to their extensive burn wounds [32]. Consequently, experts in the field of burn care and/or research establish definitions and guidelines for the diagnosis and treatments of wound infection and sepsis in burns [Greenhalgh, 2007 #88]. However, it is important to realize that these definitions are sensitive but not specific screening tools to be used primarily for research purposes, and any direct application to the clinical setting must take into account the dynamic

and continuous nature of the sepsis disease process and the static and categorical nature of the definitions. In addition, clinical parameters used to define SIRS and organ dysfunction are greatly affected by the normal physiologic changes that occur as children develop [33]. A description of pediatric-specific definitions for SIRS, sepsis, severe sepsis, and septic shock based on age-specific risks for invasive infections, age-specific antibiotic treatment recommendations, and developmental cardiorespiratory physiologic changes has been recently published by Goldstein et al. [34] and are summarized in Tables 1 and 2.

Inhalation injury

Even though mortality from major burns has significantly decreased during the past 20 years, inhalation injury still constitutes one of the most critical concomitant injuries following thermal insult. Approximately 80% of fire-related deaths result not from burns but from inhalation of the toxic products of combustion and inhalation injury has remained associated with an overall mortality rate of 25% to 50% when patients require ventilator support for more than one week following injury [35, 36]. Early diagnosis of bronchopulmonary injury is thus critical fior survival and is conducted primarily clinically, based on a history of closed-space exposure, facial burns and carbonaceous debris in mouth, pharynx or sputum [37]. Evidenced based experience on diagnosis of inhalation injury, however, is rare. Chest X-rays are routinely normal until complications, such as infections have developed. The standard diagnostic method should be therefore bronchoscopy of the upper airway of every burn patient. Gamelli et al. established a grading system of inhalation injury (0, 1, 2, 3, and 4) derived from findings at initial bronchoscopy and based on Abbreviated Injury Score (AIS) criteria [38]. Bronchoscopic criteria that are consistent with inhalation injury included airway edema, inflammation, mucosal necrosis, presence of soot and charring in the airway, tissue sloughing or carbonaceous material in the airway. The treatment of inhalation injury should start immediately with the administration of 100% oxygen via face mask or nasal cannula. Maintenance of the airway is critical. As

Table 1. Definitions of systemic inflammatory response syndrome (SIRS), infection, sepsis, severe sepsis, and septic shock [32, 34]

SIRS1

The presence of at least two of the following four criteria, one of which must be abnormal temperature or leukocyte count:

Core2 temperature of > 38.5 °C or > 36 °C.

Tachycardia, defined as a mean heart rate > 2 SD above normal for age in the absence of external stimulus, chronic drugs, or painful stimuli; or

otherwise unexplained persistent elevation over a 0.5- to 4-hr time period OR for children > 1 yr old: bradycardia,

defined as a mean heart rate > 10th percentile for age in the absence of external vagal stimulus, -blocker drugs, or congenital heart disease; or otherwise unexplained persistent depression over a 0.5-hr time period.

Mean respiratory rate > 2 SD above normal for age or mechanical ventilation for an acute process not related to underlying neuromuscular disease or the receipt of general anesthesia.

Leukocyte count elevated or depressed for age (not secondary to chemotherapy-induced leukopenia) or > 10% immature neutrophils.

Infection

A suspected or proven (by positive culture, tissue stain, or polymerase chain reaction test) infection caused by any pathogen OR a clinical syndrome associated with a high probability of infection. Evidence of infection includes positive findings on clinical exam, imaging, or laboratory tests (e. g. white blood cells in a normally sterile body fluid, perforated viscus, chest radiograph consistent with pneumonia, petechial or purpuric rash, or purpura fulminans)

Sepsis

SIRS in the presence of or as a result of suspected or proven infection.

Severe sepsis

Sepsis plus one of the following: cardiovascular organ dysfunction OR acute respiratory distress syndrome OR two or more other organ dysfunctions. Organ dysfunctions are defined in Table 4.

Septic shock

Sepsis and cardiovascular organ dysfunction as defined in

Table 4.

Modifications from the adult definitions are highlighted in boldface.

1 See Table 2 for age-specific ranges for physiologic and laboratory variables

2 Core temperature must be measured by rectal, bladder, oral, or central catheter probe