Introduction:

 Pediatric burn injuries are a significant problem worldwide, particularly

affecting children between the ages of 5 and 9 (Jordan et al., 2022). These
injuries can be caused by various sources including heat, electricity, friction,
chemicals, and radiation. The majority of childhood burn injuries are scald
burns resulting from exposure to hot liquids (Jordan et al., 2022).
 The severity of a burn depends on factors such as the temperature of the heat
source, duration of contact, and the thickness of the skin. Electrical
discharge can cause damage to cell membranes, and the extent of the injury
depends on the pathway, resistance, and strength of the current. Friction can
cause tissue injury through mechanical disruption and the generation of heat.
Exposure to caustic chemicals can lead to various reactions, and the severity
of the injury depends on the duration of exposure and the nature of the
chemical. Radiation from the sun and medical procedures can damage the
skin and tissues, with the severity depending on factors such as dose, time of
exposure, and type of radiation particle (Jordan et al., 2022).
 According to the World Health Organization Global Burn Registry, pediatric
patients account for 42% of burn injuries worldwide, with young children
(ages 1-5 years) comprising the largest group at 20% (Jordan et al., 2022).
Scald burns are the most common type of burn injury in children aged 1-5
years, followed by flame burns. More than half of pediatric patients were
from centers in middle-income countries, and more boys were reported than
girls (Jordan et al., 2022).
 Accurately estimating the extent of burn injuries is crucial for proper
management, particularly in pediatric patients. Two widely used methods for
estimating burn surface area are the Lund-Browder method and the rule of
nines (Murari & Singh, 2019). The Lund-Browder Chart, developed by Dr.
Charles Lund and Dr. Newton Browder, offers a more precise estimation of
the percentage of total body surface area burned in children, as it considers
age-related changes in body proportions (Murari & Singh, 2019). This chart
takes into account that the proportions of body parts differ between children
and adults, such as the larger head size in pediatric patients. By assigning
different percentages of body surface area to specific body sections, varying
with the age of the child, the Lund-Browder Chart provides a more accurate
estimate (Murari & Singh, 2019). In contrast, the rule of nines gives a rough
estimate of burn surface area without considering age-related changes
 (Murari & Singh, 2019). Overall, the use of the Lund-Browder Chart is
recommended for precise estimation of burn surface area in pediatric
patients, as it accounts for age-related changes in body proportions, aiding in
effective management (Murari & Singh, 2019).

 Pediatric burn patients require special attention in their management, as they

exhibit unique characteristics. One important concept to consider is fluid
creep, which refers to the gradual accumulation of excess fluid in burn
patients due to ongoing resuscitation efforts (Saffle, 2016). This
phenomenon is reported in 30% to 90% of patients with major burns, and its
incidence increases with burn size (Saffle, 2016).
 The excessive fluid given in the initial hours after injury can lead to fluid
overload, resulting in complications such as pulmonary edema, abdominal
compartment syndrome, and increased mortality (Atiyeh et al., 2012). In
fact, reports have shown that modern burn patients often receive far more
resuscitation fluid than predicted by the standard Parkland formula, which is
used to calculate the amount of fluid needed for burn resuscitation (Saffle,
2007).
 To reduce fluid creep, strategies include avoiding early over-resuscitation,
incorporating colloid as a routine component of resuscitation or for "rescue,"
and adhering to protocols for fluid resuscitation (Saffle, 2007). Additionally,
 a study found that early albumin treatment in burn children resulted in better
outcomes in terms of fluid creep, surgery procedures, and length of hospital
stay (Dittrich et al., 2020).
 In summary, fluid creep is a significant issue in the management of pediatric
burn patients, and excessive fluid resuscitation can lead to complications and
increased mortality. Strategies such as avoiding over-resuscitation, using
colloids, and following fluid resuscitation protocols can help mitigate fluid
creep. (Jeschke et al., 2020).
 It is crucial to monitor fluid balance carefully to avoid overhydration.
Pediatric patients exhibit distinct changes in response to burn injuries
compared to adults. These changes include an exaggerated immune and
inflammatory response, metabolic alterations such as increased metabolic
rate and hyperglycemia, and a higher susceptibility to distributive shock
(Burgess et al., 2022). This immune and inflammatory response can
contribute to the severity of the burn injury and impact the healing process
(Burgess et al., 2022). Effective management of metabolic alterations is
essential in pediatric burn patients. This includes addressing increased
metabolic rate and managing hyperglycemia to support the healing process
(Snell et al., 2013). Pediatric burn patients are more susceptible to
distributive shock, which is characterized by peripheral vasodilation,
increased capillary permeability, and fluid shift into the interstitial space
(Jeschke et al., 2020). Prompt recognition and management of distributive
shock are crucial. Although rare, pediatric burn patients can develop
abdominal compartment syndrome (ACS), a potentially life-threatening
complication. Early recognition and management of ACS are essential for
optimal patient outcomes (Snell et al., 2013).
Understanding the pathophysiology of burn injuries and advancements in
their treatment is crucial for improving outcomes in pediatric burn patients.
Definition and Classification of Burns: A burn is defined as a traumatic injury to
the skin or other organic tissue primarily caused by heat or exposure to electrical
discharge, friction, chemicals, and radiation. Several classification systems are
used to describe burn injuries, with the most commonly employed being depth,
extent, and severity classifications.
Depth classification: Burn depth classification is important for understanding the
severity and potential complications of a burn injury.
Superficial (First-degree) Burns: These burns only affect the epidermis. They are
characterized by redness, pain, and mild swelling. Sunburn is a typical example of
a first-degree burn.
Partial-Thickness (Second-degree) Burns: These burns involve both the epidermis
and the underlying dermis layer of the skin. They can be further divided into two
subcategories: Superficial Partial-Thickness (Superficial Second-degree) Burns:
These burns affect the epidermis and the superficial dermis. They present with
blistering, severe pain, redness, and swelling. Deep Partial-Thickness (Deep
Second-degree) Burns: These burns extend into the deeper dermis layer. They may
appear white, waxy, mottled, or pale. They typically have a reduced sensation to
touch and are less painful than superficial partial-thickness burns.
Full Thickness (Third-degree) Burns: These burns destroy the entire epidermis and
dermis layers, reaching the subcutaneous tissue below. They result in a hard,
leathery, dry, and charred appearance. Third-degree burns are often painless due to
damage to nerve endings.
Devastating Full Thickness (Fourth-degree) Burns: Some classifications include a
fourth-degree burn category, which describes burns that extend beyond the
subcutaneous tissue, affecting deeper structures such as muscles, tendons, or
bones. These burns are usually charred or blackened and require immediate
medical attention.
Extent classification: When assessing burn severity, determining the total body
surface area (TBSA) affected by the burn is crucial. Various methods exist to
estimate the TBSA affected, each with its advantages, limitations, and variations.
One commonly used method is the rule of nines. This method involves dividing the
body into regions, with each accounting for 9% (or multiples of 9%) of the total
body surface area. These regions consist of the head, each upper extremity, the
anterior trunk, the posterior trunk, each lower extremity, and the perineum. The
rule of nines is quick and easy to use, making it particularly useful for initial triage.
However, it lacks accuracy, especially when dealing with patients who have
irregular body proportions. Another method is the Lund-Browder Chart, which
divides the body into smaller, more specific regions and assigns a percentage of
TBSA to each region. This method takes into account varying proportions in
different age groups, making it more accurate, especially for pediatric patients
whose body proportions change with age. However, it requires more time and
effort to use compared to the rule of nines.
The Lund-Browder method is recommended for estimating burn size in pediatric
patients due to its consideration of changes in body proportions with growth. By
adjusting the percentages of TBSA burned based on the age of the child, the Lund-
Browder chart provides a more precise estimation of the TBSA affected in
children. On the other hand, the rule of nines provides a quick estimation but does
not consider changes in body proportions. It assumes that the body surface area is
evenly distributed and is commonly used for adults and older children but may not
be as accurate for pediatric patients.
In conclusion, the Lund-Browder method is preferred for estimating burn size in
pediatric patients due to its ability to account for changing body proportions with
growth. However, healthcare professionals may choose the most appropriate
method based on the specific circumstances of the patient. Both methods have their
uses and can be valuable tools in assessing burn severity.
The location of the burn: The location of the burn can help determine the severity
of the injury. Different areas of the body have different levels of sensitivity and
vulnerability to burns. For example, burns to the face, hands, feet, or genitals are
generally considered sever.
Burn injuries to the respiratory tract, whether from direct thermal injury or
exposure to smoke or chemicals, can have life-threatening consequences. Damage
to the airway can lead to airway obstruction, respiratory distress, and the risk of
respiratory failure. Immediate medical intervention and close monitoring are vital
in such cases to ensure adequate oxygenation and prevent further complications
such as pneumonia or respiratory distress syndrome.
severity classification: A severe (major) burn injury refers to any burn that is
complicated by major trauma or inhalation injury, chemical burns, high-voltage
electrical burns, or burns that cover more than 20 percent of the total body surface
area (TBSA) in adults, excluding superficial burns like sunburn. In older adults and
young children, a burn covering less than 20 percent of the TBSA may still be
considered severe. Individuals at the highest risk for death from severe burns are
those at the extremes of age and those with serious underlying medical conditions.
Initial care for severe burns typically requires treatment in a specialized intensive
care unit of a burn center.
3. Phases of burn injury: The three main phases of burn injury are:
 1. Inflammatory Phase: This initial phase begins immediately after the burn
injury and lasts for approximately 48-72 hours. During this phase, there is an
immediate and intense inflammatory response triggered by tissue damage.
Blood vessels in the affected area dilate, leading to increased permeability and
leakage of fluid and proteins into the surrounding tissues. The release of pro-
inflammatory mediators, such as cytokines and chemokines, attracts immune
cells to the site of injury. Neutrophils migrate to the burn site and release
reactive oxygen species, causing further tissue damage. Symptoms during this
phase may include erythema (redness), edema (swelling), pain, warmth, and
impaired function.
2. Catabolic Phase: The catabolic phase follows the inflammatory phase and can
last for several days to weeks, depending on the severity of the burn injury.
During this phase, the body experiences an increased metabolic demand and
breakdown of muscle protein. This phase is characterized by a hypermetabolic
state, with elevated resting energy expenditure and increased oxygen
consumption. Hormonal and cytokine imbalances occur, including increased
levels of cortisol, catecholamines, glucagon, and pro-inflammatory cytokines.
The breakdown of muscle protein leads to muscle wasting, negative nitrogen
balance, and diminished immune function. Patients may experience significant
weight loss, weakness, malaise, and increased susceptibility to infections.
3. Resolution Phase: The resolution phase begins once the acute physiological
response to the burn injury subsides, usually after several weeks to months. In
this phase, the body shifts from a catabolic state to an anabolic state, focused
on tissue repair and regeneration. Wound healing and re-epithelialization
occur, with the formation of granulation tissue. Collagen synthesis and
remodeling take place, contributing to scar formation and wound strength.
Metabolism begins to normalize, with a decrease in resting energy expenditure
and the resolution of the hypermetabolic state. Patients may experience
improved appetite, decreased weight loss, and decreased susceptibility to
infections.
4. Local and Systemic Responses to Burn Injury:
Local response at the burn wound site: The local injury in burns, is often described
in terms of three zones of damage that occur in the skin. These zones were first
described by Jackson in 1947 and include the zone of coagulation, the zone of
stasis, and the zone of hyperemia.
The zone of coagulation is located in the central part of the burn and is
characterized by complete coagulative necrosis. This means that the tissue in this
area has undergone irreversible damage and tissue loss. It is unlikely for any
recovery or regeneration to occur in this zone.
The zone of stasis surrounds the zone of coagulation and is characterized by
sluggish tissue perfusion. In this area, the blood vessels may constrict
(vasoconstriction) or even become completely blocked (ischemia), resulting in
decreased blood flow and oxygen supply to the tissues. However, with early and
adequate resuscitation, along with proper wound care, the effects in this zone have
the potential to be reversed. If not properly treated, though, the zone of stasis can
quickly progress into necrosis due to further decreased perfusion, edema (fluid
accumulation), and infection.
The zone of hyperemia is located at the outer edge of the zone of stasis. In this
area, viable cells are still present, and the blood vessels dilate (vasodilation) due to
local inflammatory mediators. The tissues in this zone have the ability to recover
fully, unless they are complicated by infection or severe hypo-perfusion (a
decrease in blood flow).
Systemic response following burn injury:
• Burn injuries involving more than 15% of the total body surface area (TBSA)
have the potential to cause severe shock and organ dysfunction.
• Burn shock is caused by three main factors: hypovolemia due to fluid leaking into
the interstitial space, causing burn edema; cardiac depression caused by humoral
factors and loss of preload; and increased systemic vascular resistance. Later in the
resuscitation process, vasoplegia, or low systemic vascular resistance, can replace
the initial increase in resistance. Burn shock is a complex process involving
circulatory and microcirculatory dysfunction that is not easily fixed by fluid
resuscitation alone. Severe burns result in distributive shock and tissue trauma,
leading to the production and release of various inflammatory mediators. These
mediators affect both the microcirculation and the function of the heart and lungs.
Despite correcting hypovolemia, burn shock can still persist, with increases in
pulmonary and systemic vascular resistance and myocardial depression, even with
adequate preload and volume support. These cardiovascular dysfunctions can
worsen the overall inflammatory response, leading to organ dysfunction.
• Burn injury leads to hypovolemia and rapid edema formation due to extravasation
of plasma into the burn wound. This causes hemodynamic changes, including
decreased plasma volume, cardiac output, and urine output, as well as increased
systemic vascular resistance (SVR) resulting in reduced peripheral blood flow. The
primary goal of treatment for hypovolemic shock caused by burn injury is to
promptly restore intravascular volume, preserve tissue perfusion, and minimize
tissue ischemia. However, burn resuscitation is complicated by severe burn wound
edema, as well as extravasated and sequestered fluid and protein in unburned soft
tissue. Large volumes of resuscitation solutions are needed to maintain
intravascular volume in the first few hours after an extensive burn.
• Edema formation occurs when fluid filtration out of capillaries exceeds the flow
in lymph vessels. It often follows a biphasic pattern, with an immediate and rapid
increase in water content of burned tissue within the first hour after injury,
followed by a more gradual increase in fluid flux in both burned and unburned
tissue over the next 12-24 hours. The amount of edema formation depends on the
type and extent of injury, fluid resuscitation provided, and the type and volume of
fluid administered. Fluid resuscitation increases blood flow and capillary pressure,
contributing to further fluid extravasation. Without sustained intravenous
replacement of fluid losses, edema formation is somewhat self-limited as tissue
blood flow and capillary pressure decrease..
• Burn injury can also lead to myocardial dysfunction, which further complicates
the management of burn shock. The release of inflammatory mediators and cellular
damage resulting from the burn injury can impair the function of the heart. This
myocardial dysfunction can manifest as reduced contractility, impaired relaxation,
and abnormalities in the electrical conduction of the heart. These cardiac
abnormalities can contribute to a further decrease in cardiac output and tissue
perfusion, exacerbating the overall shock state. Therefore, in addition to addressing
hypovolemia and edema formation, it is crucial to monitor and manage myocardial
dysfunction in patients with severe burns.
In summary, burn injury leads to hypovolemia and rapid edema formation due to
the leakage of plasma into the burn wound. Prompt restoration of intravascular
volume is crucial to maintain tissue perfusion and minimize tissue ischemia.
Edema formation occurs in two phases, with an initial rapid increase in water
content followed by a slower increase over the next 12-24 hours. Adequate fluid
resuscitation is necessary to maintain intravascular volume, but excessive fluid
administration can exacerbate fluid extravasation. The management of burn shock
also requires attention to myocardial dysfunction, as the release of inflammatory
mediators and cellular damage from burn injury can impair cardiac function.
Therefore, monitoring and addressing myocardial dysfunction is an important
aspect of burn resuscitation.
 Hypermetabolic Response to Burn Injury:
The hypermetabolic response to burn injury is a complex physiological reaction
characterized by various changes in the body. These changes include increased
blood pressure and heart rate, peripheral insulin resistance, increased breakdown of
proteins and lipids, elevated resting energy expenditure, higher body temperature,
loss of total body protein, muscle wasting, and increased production of acute-phase
proteins.
The exact cause of this response is not fully understood but is believed to be
initiated by a significant and sustained increase in the secretion of hormones and
neurotransmitters such as catecholamines, glucocorticoids, glucagon, and
dopamine. Cytokines such as Interleukins 1 and 6, platelet-activating factor, tumor
necrosis factor (TNF), endotoxin, neutrophil-adherence complexes, reactive
oxygen species, nitric oxide, and coagulation and complement cascades have also
been implicated in regulating this hypermetabolic response.

The release of damage-associated molecular patterns (DAMPs) during burns can

disrupt the innate immune response, leading to an immunosuppressive state. This
increases the risk of systemic inflammatory response syndrome, acute respiratory
distress syndrome, and multiorgan dysfunction.

The hypermetabolic response in burn patients occurs in two distinct phases: the
ebb phase and the flow phase. The ebb phase occurs within the first 48 hours after
the burn injury and is characterized by a decrease in cardiac output, oxygen
consumption, and metabolic rate. Glucose tolerance is impaired, leading to
hyperglycemia.

The flow phase is a gradual increase in metabolism that reaches a plateau within
the first five days after the injury. This phase is characterized by a hyperdynamic
circulation and the development of insulin resistance. Insulin release in response to
glucose load is twice that of controls, leading to markedly elevated plasma glucose
levels.

The hypermetabolic response can persist for more than 12 months after the initial
injury, even after wound closure. Sustained elevations in stress mediators, such as
cortisol and cytokines, continue to contribute to the increased metabolic rate.
Impaired glucose metabolism and insulin sensitivity can persist for up to three
years after severe burn injury. The magnitude of the hypermetabolic response is
proportional to the size of the burn, with larger burns resulting in a more
significant response.
Altered hemodynamics during the hypermetabolic response include a low cardiac
index and extreme vasodilation initially, followed by a hyperdynamic state with
tachycardia and increased cardiac output. Children may experience heart rates and
cardiac outputs that exceed predicted values for their age, which can remain
elevated for up to two years after the injury.

Altered glucose metabolism is a prominent feature of the hypermetabolic response.

Hyperglycemia persists due to the failure to suppress hepatic glucose release and
the attenuated suppressive effect of insulin on hepatic glucose release.
Catecholamines also contribute to hyperglycemia by enhancing glycogenolysis and
impairing glucose disposal in muscle and adipose tissue, resulting in peripheral
insulin resistance.

Protein and lipid metabolism are also affected during the hypermetabolic response.
Proinflammatory cytokines contribute to lean muscle breakdown, leading to
wasting of lean body mass. Lipid utilization as an energy source is reduced, and
skeletal muscle becomes the primary substrate for glucose production. This further
contributes to insulin resistance and muscle wasting.

It is important to note that immobility during this response can exacerbate the
wasting of lean body mass and lead to various complications. Early mobility
protocols have been shown to be safe and effective in mitigating these
complications and promoting recovery.
4. Burn wound healing: Burn wound healing refers to the process through which
the body repairs and regenerates skin tissue after a burn injury. This healing
process involves several stages, including inflammation, cell proliferation, and
tissue remodeling.
Inflammation: Immediately after a burn injury, the body responds with
inflammation. This immune response helps to clean the wound, remove dead
tissue, and prevent infection. Blood vessels in the area expand, allowing increased
blood flow to the wound, and white blood cells are sent to the site to fight off
bacteria.
Cell proliferation: After the initial inflammatory response, the body starts the
process of cell proliferation. Skin cells around the burn site begin to multiply and
move across the wound, forming a new layer of tissue called granulation tissue.
This tissue contains new blood vessels, collagen, and other proteins necessary for
wound healing.
Tissue remodeling: Over time, the granulation tissue transforms into mature skin
tissue through tissue remodeling. Collagen fibers, which provide strength and
structure to the wound, are rearranged and realigned to create a stronger scar tissue.
This process can take several months to complete.
5. complications of severe burn injury
1)Coagulation Changes and Hematological Considerations: The thermal injury
disrupts the normal clotting cascade and can lead to a state of coagulopathy. These
changes are important considerations in the management of pediatric burn patients.
Burn-induced coagulopathy is characterized by a combination of both procoagulant
and anticoagulant effects. The release of pro-inflammatory cytokines and other
mediators of the systemic inflammatory response contribute to an activation of the
coagulation system. This can result in increased levels of procoagulant factors,
such as fibrinogen and factor VIII, and an increased risk of clot formation. At the
same time, the burn injury also triggers an anticoagulant response, with decreased
levels of antithrombin III and protein C, which inhibit clot formation.

The combination of procoagulant and anticoagulant effects in burn-induced

coagulopathy can lead to a state of hypercoagulability and an increased risk of
thrombosis. This is particularly relevant in pediatric burn patients who often have
extensive burns and may require prolonged periods of immobilization, further
increasing the risk of thromboembolic complications.

Management of coagulopathy in pediatric burn patients involves a multimodal

approach. Early recognition and aggressive correction of coagulation abnormalities
are essential. Serial monitoring of laboratory parameters such as prothrombin time
(PT), activated partial thromboplastin time (aPTT), fibrinogen levels, platelet
count, and D-dimer can help guide therapy. Transfusion of blood products may be
necessary to correct coagulation abnormalities. Fresh frozen plasma (FFP) is often
given to replenish clotting factors, while platelet transfusions are used to restore
platelet counts when necessary. Cryoprecipitate, which contains high levels of
fibrinogen and factor VIII, may also be administered in cases of severe
coagulopathy.

In addition to coagulopathy, pediatric burn patients may also experience

hematological changes, including anemia. The burn injury itself can lead to
hemolysis and increased red blood cell destruction. Furthermore, the inflammatory
response can suppress erythropoiesis, resulting in decreased production of new red
blood cells. Anemia in burn patients can have significant consequences, including
impaired oxygen delivery, delayed wound healing, and increased susceptibility to
infections. Close monitoring of hemoglobin levels and prompt treatment of anemia
with transfusion of packed red blood cells may be necessary to optimize
oxygenation and promote healing.
2)Respiratory Complications in Pediatric Burn Patients: Inhalation injury is a
critical aspect of burn injuries, particularly in pediatric patients. It refers to the
damage caused to the respiratory system due to the inhalation of heat, smoke, or
toxic gases during a burn incident. Inhalation injury can lead to significant
morbidity and mortality in burn patients, as it can result in airway obstruction,
respiratory failure, pneumonia, and other complications. In pediatric burn patients,
inhalation injury is of particular concern due to their smaller airway diameter and
potential for airway obstruction. It is estimated that up to 40% of pediatric burn
patients may develop inhalation injury, with higher rates observed in those who
experience burns in enclosed spaces or have injuries to the face or neck. The
assessment of inhalation injury in pediatric burn patients includes a thorough
history of the burn incident, including the presence of a closed space fire or
exposure to smoke. Physical examination findings such as hoarseness, stridor,
singed facial hair, or carbonaceous sputum may raise suspicion of inhalation
injury. However, these findings are not specific, and additional diagnostic
modalities may be necessary to confirm the diagnosis. Imaging studies, such as
chest X-rays or computed tomography (CT), can help identify signs of inhalation
injury, including airway edema, bronchial wall thickening, or an infiltrate
suggestive of pneumonia. Fiberoptic bronchoscopy is considered the gold standard
for diagnosing inhalation injury, as it can directly visualize the airway and assess
the extent of injury. Inhalation injury significantly impacts the resuscitation and
management of pediatric burn patients. It requires early and aggressive airway
management, which may include intubation and mechanical ventilation. Fluid
resuscitation should be tailored to the individual patient's needs, taking into
account the extent of burn, associated injuries, and the presence of inhalation
injury.
3)Acute Renal Failure in Association with Thermal Injury: The mechanisms
underlying the development of AKI in burn patients are multifactorial and involve
both systemic and local factors.

1. Decreased renal blood flow: Burn injuries can lead to a decrease in renal blood
flow due to hypovolemia resulting from fluid loss through the burned skin.
This reduced blood flow can impair kidney function and contribute to the
development of AKI.
2. Ischemic injury: Severe burns can cause ischemic injury to the kidneys due to
decreased blood supply. The release of vasoactive substances and a decrease in
 oxygen delivery to the renal tissues can lead to tubular damage and renal
dysfunction.
3. Myoglobin-induced renal injury: In extensive burns or deep muscle
involvement, myoglobin, a protein from damaged muscle tissue, can be
released into the bloodstream. High levels of myoglobin can cause renal
tubular injury by obstructing the tubules, leading to myoglobin-induced renal
failure.
4. Systemic inflammation: Burn injuries trigger a systemic inflammatory
response characterized by the release of pro-inflammatory cytokines and
activation of the immune system. This inflammatory response can contribute
to renal injury by causing endothelial dysfunction, tubular damage, and
inflammation in the kidneys.
5. Complications of resuscitation: Fluid resuscitation is a crucial aspect of burn
management, but it can also be associated with the development of AKI.
Overaggressive fluid resuscitation or the use of inappropriate fluid formulas
can lead to fluid overload, which in turn can contribute to renal dysfunction.
Management and prevention strategies for acute renal failure in burn patients
include:

 Monitoring and maintaining adequate fluid balance during the resuscitation

phase, ensuring appropriate fluid rates and composition.
 Early detection and intervention of AKI by closely monitoring renal function,
urine output, and electrolyte levels.
 Using techniques such as renal replacement therapy (dialysis) when necessary
to support renal function.
 Implementing measures to reduce systemic inflammation, such as early wound
excision and debridement to remove necrotic tissue and control the source of
inflammatory mediators.
 Preventing and treating complications that can contribute to renal injury, such
as infection, hypovolemia, and compartment syndrome.
Further research and advancements in burn management aim to improve outcomes
and reduce the incidence and severity of acute renal failure in burn patients. This
includes optimizing fluid resuscitation strategies, developing novel therapies to
mitigate the inflammatory response, and early identification and management of
renal complications in this specific population.
4) Electrolyte disturbances in association with thermal injuries: Severe burns, can
cause significant electrolyte disturbances. These imbalances can arise due to
multiple factors, including fluid loss, tissue damage, and systemic inflammatory
response. Common electrolyte disturbances seen in association with thermal
injuries include:
1. Hyponatremia: Burn patients may develop hyponatremia, which refers to
low serum sodium levels. This can result from fluid resuscitation with
hypotonic solutions, excessive water intake, or inappropriate secretion of
antidiuretic hormone (SIADH) due to the stress response and release of
inflammatory mediators.

2. Hyperkalemia: Hyperkalemia, or high serum potassium levels, can occur in

burn patients. Burn injuries cause cellular damage, particularly in muscle
tissues, which releases intracellular potassium into the bloodstream.
Additionally, reduced renal function in the context of renal injury or acute
kidney injury can impair potassium excretion, leading to hyperkalemia.

3. Hypokalemia: While hyperkalemia is a common electrolyte disturbance,

burn patients may also develop hypokalemia, which is characterized by low
serum potassium levels. The loss of potassium can occur through increased
renal excretion, gastrointestinal losses (e.g., vomiting or diarrhea), or shifts
of potassium into cells due to the stress response.

4. Hypocalcemia: Thermal injuries can cause hypocalcemia, which refers to

low serum calcium levels. Calcium binds to damaged tissues and can be lost
through the burn wound, leading to decreased circulating levels.
Additionally, the inflammatory response triggered by burns can affect the
regulation of calcium metabolism.

5. Hypomagnesemia: Burns can result in hypomagnesemia, defined as low

serum magnesium levels. Similar to calcium, magnesium can bind to tissue
debris and be lost through the burn wound. Additionally, stress responses
and inflammation can impair magnesium homeostasis.

6. Hyperphosphatemia: In severe burns, hyperphosphatemia, or high serum

phosphate levels, may develop. The release of intracellular phosphorus from
damaged tissues, coupled with decreased renal clearance, contributes to this
electrolyte disturbance.

Managing electrolyte disturbances in burn patients includes ongoing monitoring

and correction of imbalances. Treatment strategies may involve providing fluids
with electrolyte compositions that address specific imbalances, administering
intravenous electrolyte supplements, or using renal replacement therapy in cases of
severe renal dysfunction. Regular monitoring of electrolyte levels and adjusting
treatment accordingly is essential to prevent further complications and optimize
patient outcomes.

5)Burn wound infection and sepsis: Burn wound infection and sepsis are
significant complications in burn patients and can lead to morbidity and mortality.
Risk factors include the severity and size of the burn, delays in wound excision,
extremes in age, impaired immunity, and certain organisms. The most common
organisms associated with these infections are Staphylococcus and Pseudomonas,
but the epidemiology can vary. Burn injuries create an environment conducive to
microbial colonization and proliferation due to the disruption of the skin's natural
barrier and the avascular necrotic tissue (eschar) that forms. Gram-positive bacteria
initially populate the wound, but gram-negative bacteria dominate after the fifth
day. Fungi and multiresistant organisms can also cause infections, especially after
antibiotic use and prolonged hospital stays. Clinical features may include fever,
signs of sepsis, changes in wound appearance, increased pain, and signs of
intolerance to enteral feedings. Diagnosis relies on clinical features, cultures, and
histopathology from burn wound biopsy. Treatment involves wound cleansing,
debridement, antimicrobial therapy, and burn wound excision or grafting.
Monitoring and controlling systemic signs of sepsis are also important.

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