Burn Shock


Resuscitation of Burn Shock

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Burn Shock Resuscitation

Related Conditions

Major Burns


1. Description of the problem

Burn shock occurs in a major burn injury (covering >20% total body surface area [TBSA]) with disruption of normal organism homeostasis. This disruption is secondary to both local and systemic responses, including release of cytokines and other inflammatory mediators. Burn shock is similar to an ischemia-reperfusion injury that manifests at a cellular level and then systemically.

The thermal injury itself and the inflammatory mediators released are associated with increased capillary permeability and massive intravascular volume deficits, which peak within 24 hours following the burn. Burn shock is a unique combination of distributive and hypovolemic shock, recognized by intravascular volume depletion, low pulmonary artery occlusion pressure (PAOP), increased systemic vascular resistance and depressed cardiac output.

Decreased cardiac output is secondary to decreased preload, increased afterload and decreased contractility. The depressed contractility is caused by circulating mediators such as tumor necrosis factor-alpha (TNF-alpha), though the mechanism is not well defined. Impaired calcium exchange at the cellular level may also contribute to the myocardial dysfunction seen in burn shock. Early and adequate resuscitation of major burns has been the foundation to improving survival of burn patients with burn shock. The maintenance of ECF volume, until capillary integrity and cardiovascular function recover spontaneously 24-36 hours post-injury, is life-saving but has very little effect on the pathophysiologic course of burn shock.

When burn size exceeds 20% TBSA, heat injury releases cytokines, inflammatory mediators that increase capillary leak, and severe hypoproteinemia ensues. This causes intravascular volume shifts with resultant interstitial edema formation, vascular volume depletion and electrolyte imbalance. Isotope dilution studies have demonstrated up to 50% loss of ECF in unresuscitated burn shock. This intravascular depletion is associated with decreased cardiac output and increased pulmonary and systemic vascular resistance and results in shock.

Key management points

The first 48 hours following injury are focused on acute resuscitation with patient assessment, airway protection and fluid replacement. Optimal resuscitation aims to minimize rather than treat burn shock by maintenance of organ perfusion with the least amount of fluid necessary. Most patients with burn shock can be resuscitated successfully using various fluid regimens as demonstrated by multiple different resuscitation guidelines, mostly based on body weight and burn size. Radioisotope experiments by Baxter and Pruitt have shown that plasma expansion during early resuscitation was independent of the type of fluid given. The question of optimal fluid resuscitation (volume and type) remains open for debate. While under-resuscitation leads to decreased perfusion, acute kidney injury and ultimately death, over-resuscitation is also associated with complications, such as edema formation, abdominal compartment syndrome, acute respiratory distress syndrome, and multiple organ dysfunction.

2. Emergency Management

Fluid resuscitation is focused on supporting the patient through the first 24-48 hours of profound hypovolemia and cardiac dysfunction following the thermal injury. The National Institutes of Health consensus stated that the minimum fluid resuscitation required to maintain adequate organ perfusion should be provided. This volume infused should be titrated to avoid either over- or under-resuscitation.

The volume of isotonic crystalloid fluid necessary to maintain extracellular fluid (ECF) volume and cardiovascular function during burn shock is in the range of 2-4 mL/kg per percent TBSA of second- and third-degree burns in the first 24 hours post-injury for 80-95% of patients. Increased volume resuscitation requirements are associated with inhalational injury, electrical burn, full-thickness injury with extensive tissue trauma and a delay in resuscitation (considered to be >2 hours post-injury).

3. Diagnosis

The Lund-Browder Chart (Figure 1) is usually completed at the time of admission to calculate the TBSA of the burn. If TBSA burned is >20%, or associated with an inhalational injury, electrical injury, trauma or a full-thickness burn it will likely result in burn shock if the patient is not promptly and adequately resuscitated. Most clinicians overestimate the size and depth of a burn, which may have the unintended consequence of over-resuscitation with its known adverse outcomes of edema, ARDS, abdominal compartment syndrome and extension of burn injury.

Figure 1.

Lund-Browder Chart to evaluate the size of the burn.

Investigations for major burns
  • General

    Full blood count – the hematocrit can increase to 55-60%, an indicator of profound intravascular depletion

    Urea and electrolyte concentration – electrolyte abnormalities (hyponatremia and hyperkalemia) are common and must be corrected

    Clotting screen – evaluation for the depletion of coagulation factors

  • Electrical Injuries

    12-lead electrocardiography to rule out arrhythmias

    Cardiac enzymes to evaluate for myocardial injury with high-voltage injuries

  • Inhalational Injuries

    Chest x-ray – evaluation of secondary injuries such as aspiration or trauma

    Arterial blood gas analysis – evaluation for carbon monoxide exposure, and base deficit and lactate may be predictive of the volume of resuscitation required.

Concomitaqnt injuries

The primary and secondary burn survey must evaluate the patient for concomitant injuries.

4. Specific Treatment

Effective fluid resuscitation is one of the cornerstones of modern burn care and strives to mitigate the effect of burn shock. Patients with burns >20% TBSA should undergo guided fluid resuscitation based on body size and surface area burned. Most burn centers follow a variant of the Parkland resuscitation formula, now also known as the Consensus formula. Most guided resuscitation formulas strive to maintain a minimum perfusion pressure (MAP > 65 mmHg) and a minimum urine output of 0.5-1 mL/kg/hr. The challenge in resuscitating burn shock is to provide enough fluid replacement to maintain organ perfusion without causing overload.

Consensus (Parkland) resuscitation formula

First 24 hours

  • Adults and children >20 kg

    Ringer’s Lactate: 2-4 mL/kg/% TBSA burnt/24 hours with half infused within the first 8 hours from time of injury

    Colloid: none

  • Children <20 kg

    Ringer’s Lactate: 2-4 mL/kg/% TBSA burnt/24 hours with half infused within the first 8 hours from time of injury

    Ringer’s Lactate with 5% dextrose: maintenance rate (approximately 4 mL/kg/hr for first 10 kg, 2 mL/kg/hr for next 10 kg, and 1 mL/kg for weight >20 kg)

    Colloid: none

Second 24 hours

  • All patients

    Crystalloid: to maintain urine output (0.5-1 mL/kg/hr); if silver nitrate is used, sodium leeching will mandate the continued isotonic fluid; if other topical is used, free water requirement is significant; serum sodium should be monitored closely; nutritional support should begin, ideally by the enteral route.

    Colloid (5% albumin in Ringer’s Lactate)

    0-30% burn: none

    30-50% burn: 0.3 mL/kg/%burn/24 hours

    50-70% burn: 0.4 mL/kg/%burn/24 hours

    70-100% burn: 0.5 mL/kg/%burn/24 hours

Inhalational injury, a delay in resuscitation (>2 hours from time of injury) and full-thickness burns require higher fluid requirements to maintain adequate perfusion pressure and urine output. If resuscitation requires >6 mL/kg/% TBSA burnt/24 hrs to maintain adequate urine output, more invasive monitoring should be obtained to measure intravascular volume status.

Patients who have adequate volume status but who are still in shock may require vasopressor or inotropic agents to improve cardiac dysfunction and maintain systemic perfusion pressures. Over-resuscitation of patients with burns has become a major source of morbidity and mortality for burn patients.

This “fluid creep” phenomenon noted by Pruitt has been around for as long as the Parkland formula, as Baxter acknowledged some patient groups routinely required more fluid. Recent publications have reported increased volume resuscitation requirements for the majority of routine patients with major burn injuries.

The myriad reasons for this phenomenon of fluid creep are beyond the scope of this chapter but include resuscitation of larger burns with patients surviving longer, increasing opioid doses for treatment of pain, goal-directed resuscitation with central monitoring and the unintended influence of crystalloid infusion on Starling forces, without the use of colloid to maintain oncotic pressure.

Morbidities associated with fluid overload include pulmonary edema with impaired gas exchange and prolonged intubation; abdominal compartment and intestinal ischemia syndrome; delayed wound healing; and an increased incidence of sepsis and multiorgan failure.

Fluid creep prevention strategies

Strategies to prevent fluid creep in the resuscitation of burn shock should be pursued and should include:

  • Use of resuscitation protocols

  • Accurate assessment of size and depth of burn with concomitant assessment for inhalational burn, electrical burn or associated trauma injury

  • Prompt institution of resuscitation, but restriction in the early resuscitation period to meet patient requirements, while avoiding overzealous administration of fluids

  • Rescue colloid infusions after 24 hours after burn or after 12 hours following injury if resuscitation requirements exceed 120% normal

  • The use of colloid, hypertonic saline, antioxidant therapy and plasma exchange may be considered as adjuncts to decrease required volume resuscitation in patients refractory to crystalloid administration.

  • Monitor resuscitation and its complications:

    Routine bladder pressure monitoring

    Early decompressive laparotomy for abdominal compartment syndrome

    Escharotomy for limb edema

Colloid resuscitation

The addition of colloids to the resuscitation can decrease total volume requirements, but this strategy remains controversial, with a wide variation in clinical practice. Plasma proteins maintain intravascular oncotic pressure to balance the outward hydrostatic pressure. Large-volume crystalloid resuscitation in burn shock exacerbates the low oncotic pressure by decreasing the plasma protein concentration further, thus promoting local and systemic edema formation. Colloid resuscitation may replenish the intravascular oncotic pressure and limit the ensuing tissue edema. Capillary integrity, which is restored at 24 hours, may allow for the manipulation of intravascular oncotic pressure by administration of colloid. Studies have shown little clinical benefit of colloid resuscitation in first 12 hours post-injury with an increase in lung water in the post-resuscitation phase. Most U.S. burn centers will add albumin to the resuscitation 17-24 hours following the injury with a TBSA burn >40%.

Hypertonic saline resuscitation

Extracellular sodium deficit is noted in acute burn shock, which makes hypertonic saline an attractive resuscitation solution. Intravascular hyperosmolarity as a result of hypertonic saline resuscitation expands the plasma volume at the expense of intracellular water depletion; whether or not this is deleterious to cellular function has not been established. Monafo and others have demonstrated smaller volumes of fluid to maintain adequate urine output when hypertonic saline is used for resuscitation of burn shock, with the expected benefit of less edema formation and improved respiratory function in the post-resuscitation phase. Severe hypernatremia, acute renal failure and cerebral edema induced by rapid correction of hyponatremia are known complications of this management strategy. Huang et al. compared outcomes of patients resuscitated with hypertonic saline vs. the Parkland formula and found increased renal failure and mortality in the hypertonic saline resuscitation group. Hypertonic saline resuscitation should be done with close monitoring of sodium and serum osmolarity by experienced burn physicians.

Antioxidant therapy

Systemic burn-mediated changes in the liver increase peroxidation and decrease antioxidant capacity. Pharmaceutical agents with antioxidant properties, high-dose ascorbic acid (optimal dose of ascorbic acid is unknown), may reduce the severity of burn shock by preventing the membrane lipid peroxidation and by scavenging the oxygen-derived free radicals, which are major components of burn shock pathophysiology. Matsuda et al. demonstrated decreased volume requirements in animals and humans following a major burn using high-dose ascorbic acid, with no deleterious effects noted.

Plasma exchange

This strategy may limit the humorally mediated systemic inflammatory response and restore leukocyte chemotaxis. Plasmapharesis may remove the circulating mediators of burn shock, and the plasma removed is replaced with fresh frozen plasma (FFP). FFP has been shown to reverse specific leukocyte abnormalities and is an excellent source of proteins, coagulation factors and other components depleted by the burn injury. Plasma exchange may return the altered milieu to normal by removing circulating toxins or replenishing deficiencies, or a combination of the two.

Transfusion of FFP has many risks and cannot be recommended secondary to expense and disease transmission unless to correct a coagulopathy. Plasma exchange studies have failed to show decrease in fluid requirements, though it is sometimes used as a salvage maneuver to avoid end-organ damage when conventional therapy fails.

5. Disease monitoring, follow-up and disposition

Effective resuscitation of burn shock will not achieve complete normalization of physiologic variables, as the burn injury leads to ongoing cellular and hormonal responses. Consequences of excessive resuscitation – pulmonary edema, myocardial edema, conversion of superficial to deep burns, need for fasciotomies in unburned limbs and abdominal compartment syndrome – are detrimental to the injured patient.

Abdominal compartment syndrome in severe burns has significant detrimental effects on multiple organ systems and is associated with a 70-100% mortality rate. Consequences of under-resuscitation include worsening shock and death.

First-line monitoring

The American Burn Association Practice Guidelines for Burn Shock Resuscitation recommend 0.5 mL/kg/hr urine output in adults and 0.5-1 mL/kg/hr in children weighing <30 kg. Urine output less than this on an hourly basis is indicative of inadequate resuscitation. Hemodynamic monitoring with a pulse rate <110 bpm indicates adequate volume, and rates >120 bpm are usually indicative of hypovolemia. This can be complicated by pain, medication effects and other individual characteristics. Narrowed pulse pressure is a more sensitive indicator of shock than systolic blood pressure alone.

Arterial line vs. blood pressure cuff

Non-invasive cuff measurements can be inaccurate secondary to tissue edema and will typically read lower than actual blood pressure. They may also be difficult to place on burned tissue. Arterial catheterization of the radial artery is ideal, with the femoral artery as a second choice. Placement of the invasive arterial line may be dictated by the area of the burn, as it is preferred that invasive lines be placed through normal tissue.

Central venous catheterization and pulmonary artery catheters (PAC)

Central venous access may be required for fluid administration, but no benefit has been found with goal-directed therapy or demonstrating adequate oxygen delivery in burn shock resuscitation. This has limited the use of PACs in burn shock management. PAOP and central venous pressure are not good indicators of preload in burn patients, and thus if adequate tissue perfusion is noted, filling pressures should not be normalized at the risk of causing volume overload.


A high initial lactate level is a strong predictor of mortality, but lactate clearance itself may not be a sensitive marker for the adequacy of resuscitation. There is minimal correlation between urinary output, mean arterial pressure, serum lactate and base deficit. At present there are insufficient data to recommend the use of base deficit or lactate clearance as endpoints of resuscitation or as independent predictors of outcome in burn shock.

Resuscitation end points

Urine output, heart rate and mean arterial pressure are still considered the gold standard, but they may be too insensitive to ensure adequate fluid replacement in burn injuries. Urine output does not mirror renal blood flow but remains the most accessible and easily monitored index of resuscitation. Goal-directed therapy for the resuscitation of burn shock has not been shown to have improved outcomes in prospective studies. Using central venous catheters and PACs, many investigators have aggressively attempted to restore preload and cardiac output in the first 24 hours and were able to show restoration of preload, but prospective randomized trials failed to show any outcome benefit while noting a 68% increase in fluid administration with this preload-driven strategy.

Burn care transfer criteria

Burn care requires expertise, personnel and equipment that are expensive to train and maintain. Patients with major burns requiring burn shock resuscitation should be transferred to verified burn centers for guided resuscitation and management.

American Burn Association burn center transfer criteria

  • Second- and third-degree burns on >10% TBSA in patients <10 or >50 years of age

  • Second- and third-degree burns on >20% of TBSA in other age groups

  • Second- and third-degree burns that involve the face, hands, feet, genitalia, perineum, and major joints

  • Third-degree burns on >5% of TBSA in any age group

  • Electrical burns including lightning injury

  • Chemical burns

  • Inhalational injury

  • Burn injury in patients with pre-existing medical disorders that could complicate management, prolong recovery or affect mortality

  • Any patient with burns and concomitant trauma (such as fracture) in which the burn injury poses the greatest risk of morbidity or mortality.

  • Hospitals without qualified personnel or equipment for the care of children should transfer children to a burn center with these capabilities.

  • Burn injury in patients who will require special social/emotional and/or long-term rehabilitative support, including cases involving suspected child abuse and substance abuse.


Burn shock at the cellular level occurs immediately following the thermal or chemical injury and is manifest by a decreased cellular membrane ATP-ase activity and reduced transmembrane potential. This results in increased intracellular sodium and extracellular potassium concentrations, leading to cellular swelling and acidosis in both injured and non-injured tissue. Local release of inflammatory cytokines produces tissue and systemic effects.

Disrupted capillary integrity follows the instantaneous release of histamine from injured tissue. This leads to tissue edema formation, locally and systemically, which exacerbates intravascular volume depletion. Capillary leak allows for the rapid equilibration of water, inorganic solutes and plasma proteins (not cellular elements) between the intravascular and interstitial spaces. Intravascular hypovolemia and hemoconcentration rapidly ensue and are maximal 12 hours post-burn. Edema formation is also exacerbated by alterations in local blood flow, with increased arteriolar tone and pressure and post-capillary dilation of the venules.

Circulating cytokines, decreased plasma volume, increased afterload and impaired contractility all contribute to the reduced cardiac output noted immediately post-injury. This reduced cardiac output does not respond to maximizing preload but rather resolves spontaneously at 24 hours post-injury, an observation made by Baxter and Shires and repeated by Holm et al. in 2004. TNF- alpha causes myocardial depression with reduced cardiac output and activates other mediators and local vasodilators. Prostoglandins, leukotrienes, oxygen radicals, and a cascade of other cytokines contribute to the systemic response to burn.

Heat injury activates a systemic inflammatory response with release of inflammatory and vasoactive mediators, which cause local vasoconstriction, systemic vasodilation and capillary leak.

Presumed circulating mediators of burn shock include:

  • Vasoactive amines – Histamine, serotonin

  • Products of platelet activation – Thromboxanes

  • Products of complement activation – C3a, C5a (anaphylatoxins)

  • Products of arachidonic acid metabolism – Prostaglandins, leukotrienes

  • Kinin polypeptides, coagulation/fibrinolytic proteins

  • Exogenous substances – Endotoxin

  • Metabolic hormones – Catecholamines, cortisol

  • Other – Neutrophil products, denatured proteins, fibronectin


Burns are a major problem in the developed and developing world. They are common, devastating both physically and psychologically, and span the entire age spectrum. A 10-year review from the National Burn Repository published in 2006 showed 125,000 acute burn admissions to U.S. burn centers per annum. Of these admissions, 70% were male, with a mean age of 33 years; 10% were infants; and 8.5% were >70 years of age. Only 10% of patients had a burn size >30% TBSA, and inhalational injury was reported in 6.5% of patients. Flame and scald burns account for 78% of total cases, with 43% of these injuries occurring in the home and only 17% being work-related.


Survival has remained at 95%, with deaths from burn injury increased at the extremes of age, increasing burn size, and the presence of inhalational injury. The leading cause of death was multiple organ failure complicated by pneumonia, wound infection and cellulitis. Risk factors for mortality include age >60 years, TBSA burn >40%, and inhalational injury, with a predicted mortality of 0.3%, 3%, 33%, or 90% depending on whether 0, 1, 2, or 3 risk factors were present respectively. Inhalational injury has a disproportionate effect on mortality following burns, with an increase in mortality to 30% as opposed to 5% for the group as a whole.

Early and adequate treatment of burn shock is critical to the survival of the victim of a major burn. In the 1940s hypovolemic shock and acute renal failure were the leading causes of death after burn injury. Now mortality related to burn-induced volume loss has decreased considerably, with fewer deaths occurring in the first 48 hours post-burn.

Burn shock is rarely refractory to fluid resuscitation, with Baxter noting that 95% of children and 80-90% of adults will be adequately resuscitated using the Parkland formula. Certain high-risk patient groups, the extremes of age, patients with massive tissue trauma, electrical burns, inhalational injury, delayed resuscitation (>2 hours post injury) or pre-existing illness with limits on their cardiovascular or pulmonary reserve may require more resuscitation or may not tolerate adequate fluid resuscitation.

If the physiologic reserve and compensatory mechanisms of the burned patient are inadequate to respond despite the volume resuscitation, he or she will progress on to death. Adequate resuscitation may also lead to morbidity with edema formation and its associated complications.

The strongest predictor of discharge disposition and functional independence is TBSA of the burn. Only 27.6% of patients were discharged directly home if they had a burn injury with a TBSA >30.75%.

Special considerations for nursing and allied health professionals.


What's the evidence?

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