Welcome to the bed. We'll go ahead and give you
the story. This is all going to happen super
fast. Welcome to the emergency room. Welcome
back to the deep dive. Today, we are wrestling
a giant of critical care, thermal and cold injury
management, and we're going to forge an immediate.
High Yield Clinical Guide. Exactly. This isn't
just about reading the rule book. It's about
identifying those small, timely interventions.
that really make the difference between a successful
outcome and, well, a cascading failure in those
first few critical hours. Yeah, and today we're
really focusing on that Pareto principle, you
know, the 20 % of knowledge that's going to give
you 80 % of your success. It's tailor -made for
those of you in emergency medicine and nursing.
Right. Burn injury is, it's unique because it's
not just a wound. It's a systemic inflammatory
insult. A systemic insult. Our mission today
is to dissect that acute management minutiae.
We're really targeting three major areas of error,
failing to secure the airway early, mismanaging
the fluid resuscitation, and missing those secondary
complications. Things like compartment syndrome.
Compartment syndrome and the dreaded muscle breakdown,
which we call rhabdomyolysis. That distinction
you made, a systemic inflammatory insult versus
just a wound, that is absolutely the key to understanding
why burn care is so complex, isn't it? It is.
When we talk about rhabdomyolysis, for instance,
we're talking about damaged skeletal muscle breaking
down, releasing all these harmful proteins and
electrolytes into the bloodstream, which then,
of course, threatens the kidneys. It's a direct
threat. It just illustrates how one local injury
can become this massive multi -organ systemic
threat. Exactly. The injury sets off this catastrophic
but predictable domino effect. The extent and
the depth of the burn directly correlate to the
amount of inflammatory mediators that get released.
And this cascade causes a massive capillary leak,
which is why we see this profound generalized
edema. And here's where timing is everything.
This process might be, you know, explosive and
immediate in a high -intensity flame burn, or
it could be dangerously delayed and insidious
in a deep chemical injury. Okay, so let's unpack
this by starting at minute zero. The patient
arrives. We have to stop the burning process,
that energy transfer immediately. This is where
those basic steps can prevent progression from
say a second degree to a third degree injury.
The absolute first priority is prevention of
further injury. If the patient arrives still
smoldering or covered in hot material, you have
to completely remove all of the patient's clothing.
All of it. All of it. But a major caveat exists
here. You do not peel off adherent clothing.
Okay, so if the clothing is stuck, why? is trying
to remove it a mistake. What's the hidden injury
risk there? Well, if the fabric is adhered, and
this is usually synthetic material that's literally
melted onto the skin trying to peel it off, we'll
just rip off the underlying viable dermis. Oh,
I see. And you're basically converting a partial
thickness burn into a full thickness injury.
You're dramatically increasing pain, infection
risk, and scarring. You just cut around the adherent
parts and you leave them for specialized wound
care later. The non -adherent clothes, though,
they have to go immediately. And the rationale
for that immediate removal is really the type
of fabric we all wear today. It's a double -edged
sword, these synthetic fabrics. They ignite easily,
they burn hot, and crucially, they melt into
this persistent high -temperature residue that
continues to transfer heat to the tissue long
after the flame is out. So it's like a time release
injury. It is exactly a time release injury.
By removing them, you are effectively stopping
that process. OK, so once the insult is stopped,
We immediately have to pivot to temperature control,
which I know is a cornerstone of initial stabilization.
Why does the burn patient become hypothermic
so rapidly, and what are the essential nursing
interventions to combat that? The loss of skin
integrity? It instantly compromises the body's
ability to thermoregulate. Right. So you couple
that with the rapid exposure you need for a thorough
assessment and the constant use of room temperature
fluids, hypothermia is nearly guaranteed in major
brands. And this isn't just uncomfortable. Hypothermia
below 36 degrees Celsius worsens quailopathy.
It increases mortality and it impairs healing.
So the minute the clothes are off, what are we
doing? Immediately cover the patient with warm,
clean, dry linens. A thermal blanket if you have
one available. The environment itself, the room
must be warm, and all intravenous fluids you
use for resuscitation must be actively warm.
Actively warm, not just room temp. No, absolutely
not. We need to be judicious in exposing the
patient. So you only uncover the necessary area
for the immediate assessment and then you recover
it immediately. This active temperature management
starts in the ambulance or the emergency department
and it continues throughout the entire resuscitation.
Let's talk about chemical burns for a second
because they require a completely different triage
pathway. If it's a dry powdered chemical, what
is the sequence? The sequence is, uh, it's counterintuitive
for many. If a dry powder like certain industrial
lime products cause the burn, you must brush
the powder off first. Brush first. Brush first.
The mistake is immediately rushing to irrigation,
which can activate the chemical, turning a surface
exposure into this deep penetrating liquid that
just accelerates tissue destruction. And once
that dry powder is removed, or if it was a liquid
chemical to begin with, then the irrigation process
starts. What are the specifics for that decontamination?
Decontamination is an exhaustive effort We use
copious amounts of warm saline or a warm shower.
And the duration here is critical. At least 20
to 30 minutes of continuous rinsing. That's a
long time. It's a very long time. And if the
chemical is an alkali, the irrigation needs to
be sustained even longer. We're talking often
45 minutes to an hour because they penetrate
so deeply. You mentioned that acids and alkalis
injure tissue fundamentally differently. If I'm
a clinician stabilizing this patient, why does
understanding the difference between coagulation
and liquefaction necrosis influence my management?
Well, it dictates the urgency and the depth of
the injury you're facing. Acids cause something
called coagulation necrosis. Think of it like
frying an egg. The tissue protein coagulates,
creating a tough, often yellow -white, escher.
OK. This coagulated layer acts as a kind of temporary
barrier, which slows the acid's penetration into
deeper tissue. Right. So it kind of walls itself
off, in a way. In a way, yes. Alkalis, on the
other hand, cause liquefaction necrosis. They
dissolve proteins and fats through saponification,
essentially turning the tissue into this soapy
liquid mass. That sounds significantly worse.
It is because there is no self -limiting barrier.
The alkali just penetrates continuously and deeply,
inflicting damage over a wider area, often reaching
down to the bone or other vital structures. This
is why alkali burns are considered universally
more destructive and why they require such prolonged
irrigation to dilute and remove the agent completely.
Shifting back to the body's systemic response,
that inflammatory cascade. We highlighted that
massive edema is coming, and it's often delayed.
This isn't just about swelling, is it? It's about
preventing harm caused by the very equipment
we're putting on the patient. What are the specific
nursing alerts for preventing that iatrogenic
harm as the edema progresses? This is one of
the most critical high -yield nursing details,
I think. You know, you place the lines in tubes
when the patient was stable, but as that capillary
leak progresses, which can take hours, that same
equipment becomes a source of injury. It becomes
a tourniquet. It becomes a tourniquet. You must
vigilantly monitor all your intravenous lines,
endotracheal, and nasogastric tubes. The ties
securing these tubes, often just cotton tape
or some commercial restraint, they need to be
checked hourly to ensure they are not becoming
circumferential tourniquets, which can cause
pressure necrosis. What about simple things,
like an ID band? Absolutely crucial. An identification
band that you put on snugly in the first hour
can cause a severe skin and nerve compression
injury by hour six. They must be loose, ideally
taped to clothing, or affixed non -circumferentially,
maybe on a bed rail or a monitor cable, if the
swelling risk is really extreme. So this is a
continuous process. Edema takes time, typically
six to 12 hours, to fully manifest. If you wait
until the patient is visibly swollen, you've
already missed the window for prevention. That
transforms the action. of securing a two from
a one -time task to a continuous assessment priority.
It's checking the tie, not just the two position.
Exactly. Okay, let's move on. Airway management
is the pinnacle of immediate critical care and
burns. It is. Obstruction is a two -fold threat.
You've got the direct injury from smoke or heat
inhalation, and then you've got massive edema
compressing the airway from the outside. The
crucial point for listeners is that signs of
impending obstruction are subtle at first, and
waiting for that overt crisis, like a complete
inability to ventilate, means you've waited far
too long. Based on specific risk factors, what
are the absolute high -risk clinical factors
that should trigger an immediate call to intubation
readiness? We're looking for a constellation
of factors. A burn size or depth exceeding 40
% to 50 % total body surface area, or TBSA massive
burns produce massive edema. Makes sense. Any
burn to the head, the face, or inside the mouth
suggests high heat exposure to the upper airway.
Also, always consider associated trauma and,
of course, a confirmed inhalation injury. pediatric
patient is fundamentally at higher risk, right?
Regardless of the burn size. Precisely. Because
of their smaller diameter airways and the high
compliance of their tracheal rings, children
can progress from just mild upper airway swelling
to complete obstruction much, much faster than
adults. A child with a moderate facial burn needs
vigilance that, frankly, borders on paranoia.
So if those risk factors are present, we consult
the Advanced Burn Life Support, the ABLS indications
for early intubation. This list essentially forces
clinicians to intervene based on anticipation,
not just the current clinical status. Let's break
down those key indicators that just scream, secure
the airway now. These are non -negotiable guidelines.
First, any sign of obstruction, hoarseness, accessory
muscle use, or difficulty breathing. But let's
clarify the late sign. OK. Stridor. Stridor,
that high -pitched, harsh sound on inspiration,
means the airway is already critically narrowed
and it demands immediate intubation. Waiting
another 15 minutes is risking a completely impossible
airway. What about physical findings on the head
and neck? Extensive and deep facial or mouth
burns are a clear indication. as is significant
edema or just the visible risk for edema progression.
If the patient has difficulty swallowing their
own secretions, swelling is already impeding
their laryngeal function. Right. We also must
secure the airway if there are circumferential
full thickness neck burns. Why? Because as that
massive edema develops, that leathery inelastic
burn tissue on the neck acts like a vice. It
just strangles the airway from the outside. And
what about level of consciousness or just the
logistical problem of transferring a patient?
Well, if the patient has a decreased level of
consciousness or impaired airway protective reflexes,
maybe due to associated trauma or CO poisoning,
they need immediate intubation just to prevent
aspiration. And logistically, if you have a large
burn patient who needs transport and you don't
have personnel qualified to intubate en route,
you must secure the airway before they leave
your facility. That makes a lot of sense. And
finally, a carboxyhemoglobin, or HBCO, level
greater than 10 % following a fire, especially
in an enclosed space, strongly indicates the
need for airway protection due to deep inhalation
damage. So that emphasizes that if transport
time is prolonged, or if you anticipate significant
fluid requirements, you intubate. Once they're
intubated, What's the mechanical challenge that
swelling presents to the tube itself? Swelling
makes endotracheal tube or ETT management very
difficult. When you place it, you must use an
adequately sized ETT, preferably an 8mm internal
diameter or at least a 7 .5mm ID in adults. And
why is that so important? It's twofold. Swelling
may compress the soft tissues around the tube,
making a small tube even smaller. And second,
smaller tubes make subsequent necessary procedures
like bronchoscopy to clear out necrotic material,
extremely difficult, or even impossible. Let's
talk about the invisible killer, carbon monoxide
poisoning, which has to be assumed in any enclosed
space burn. The underlying biochemistry here
is terrifying. It is. The primary danger comes
from CO having an affinity for hemoglobin that
is a staggering 240 times greater than oxygen's.
Wow. So CO just displaces oxygen, effectively
suffocating the blood. But it gets worse. The
remaining oxygen that does bind to hemoglobin
is then held too tightly. CO shifts the oxyhemoglobin
dissociation curve to the left, which prevents
the release of oxygen to the tissues. The patient
is suffering from profound cellular hypoxia.
And what are the clinical correlations? What
are we looking for in the field? We often classify
symptoms by the level of HBCO saturation. So
below 20%, often asymptomatic, maybe a mild headache.
20 % to 30%, you're looking at a clear headache,
nausea, mild confusion. OK. 30 % to 40%, significant
confusion, maybe dizziness. 40 % to 60 %? Coma
is likely, and above 60 % is typically rapidly
fatal. And that classic cherry red skin. It's
a myth for clinical practice. It only occurs
in moribund patients because high concentrations
of deoxyhemoglobin are absent. It is a completely
unreliable and rare sign. Don't look for it.
So if the history suggests exposure, what is
the fastest, most effective management strategy?
The management is 100 % oxygen delivered via
a non -rebreathing mask. This treatment leverages
the principle of mass action. Breathing room
air, which is 21 % oxygen, gives carbon monoxide
a half -life of about four hours. If you increase
the environmental oxygen concentration to 100%,
you rapidly displace the CO, reducing that half
-life dramatically to about 40 minutes. That's
a huge difference. It's a massive difference.
Empiric treatment with high -flow oxygen for
Four to six hours is a reasonable and essential
intervention if a closed space fire occurred,
even if you're still waiting on blood gas results.
And here is the pitfall that can kill a patient
being monitored by even the most vigilant nurse
or clinician, the pulse oximeter reading. This
is a mistake we see far too often. Standard pulse
oximetry, it operates by measuring light absorption
at two wavelengths, and it distinguishes between
oxygenated and deoxygenated hemoglobin. The problem
is it cannot reliably distinguish between oxyhemoglobin
and carboxyhemoglobin. So it looks the same to
the machine. It looks the same. A patient could
have 40 % of their hemoglobin saturated with
CO, be severely hypoxic, and the pulse oximeter
will still happily read 98 to 100 % saturation.
So if the pulse oximeter is basically useless
here, how do we confirm CO poisoning? You must
measure baseline HBCO using a co -oxymetry device,
which analyzes multiple wavelengths, or you can
do it via an arterial blood gas machine that's
capable of measuring specific CO levels. Clinically,
a strong warning sign is often a discrepancy
between the partial pressure of oxygen in arterial
blood, the PaO2, which might be normal, and that
high pulse oximeter reading. That's the tip -off.
While we're covering toxic inhalation, let's
briefly touch on cyanide toxicity. less common,
but equally devastating. We put structure fires.
Cyanide is produced when materials like plastics
and wool burn in confined spaces. The clinical
clue is often subtle. It's a persistent, profound,
unexplained metabolic acidosis. If your patient
is getting adequate resuscitation and ventilation,
but their pH and their bicarbonate levels remain
alarmingly low without an obvious cause, you
have to suspect cyanide and consult poison control
immediately for the specific antidotes. and finally
the mechanical damage caused by the smoke inhalation
injury itself. What does all that particle and
fume damage actually do to the lower airways?
It's a dual mechanism of injury. First, the heat
and the toxic fumes damage the mucosal cells
below the vocal cords, which triggers an explosive
local inflammatory response. Right. This not
only increases the patient's overall systemic
inflammation, meaning they're going to require
significantly more fluid for resuscitation, but
it also causes the damaged necrotic cells to
slap off. And those slew cells, they cause obstruction.
Exactly. They accumulate, they form casts and
plugs that physically obstruct the bronchioles,
impairing the patient's ability to clear secretions,
and significantly increasing the risk of subsequent
pneumonia and acute respiratory distress syndrome,
or ARDS. And that's a huge driver of mortality.
This injury is so severe that it is known to
double the patient's overall mortality compared
to a burn injury of the same size without inhalation.
So we need definitive criteria for diagnosis,
which often involves a scope, right? Diagnosis
is established by requiring both an exposure
to a combustible agent and visual signs of exposure
soot, inflammation, necrotic tissue in the lower
airway, as seen on bronchoscopy. Management is
largely supportive, but if a high probability
of inhalation injury exists and the burn is significant,
we use the cutoffs of greater than 20 % TBSA
in an adult or greater than 10 % in a child or
elderly. Patient early intubation and aggressive
pulmonary hygiene are mandatory. Okay. Airways
secured, toxic gases are managed. Now we address
circulation, or more accurately, the management
of burn shock. We aren't replacing blood. We
are replacing these massive fluid losses from
capillary leak. This is where the math and the
timing of that math is paramount. The goal is
very specific. We have to maintain end organ
perfusion by counteracting the massive ongoing
volume losses from that inflammatory capillary
leak. We treat this profound hypovolemia with
volume replacement for deep partial and full
thickness burns that are greater than 20 % TBSA.
But before we even get to the math, we need the
access. Right. What are the immediate rules for
IV access? Two large caliber peripheral IVs,
at least an eight engaged catheter, must be established
immediately. The preferred site is the upper
extremities. Why the upper extremities specifically?
Well, if we place IVs in the lower extremities,
specifically using the saphenous veins, there
is a significantly increased risk of developing
phlebitis and septic phlebitis, especially as
the patient's condition evolves over the next
few days. What if the extent of the burn? makes
placing an IV through unburned skin impossible.
Do we spend precious time looking for a central
line? No. Time is perfusion. If placing the IV
through unburned skin is genuinely impossible
due to the extent of the injury, you must place
the peripheral IV directly through the burn skin
into an accessible vein. The risk of infection
from a properly secured and maintained peripheral
IV through the burn is lower than the risk of
delayed resuscitation. And let's revisit that
high -yield nursing detail regarding the swelling
and the catheters. Yeah, this is important. Given
the guarantee of massive edema, standard short
IV catheters are highly susceptible to dislodgement
or kinking as the soft tissue just swells up
around them. So we advocate for the use of longer
IV catheters in patients with larger burns. To
give you more of a margin for error. It gives
you a much greater margin of safety, ensuring
the catheter remains securely seated in the vessel
despite that aggressive tissue swelling. OK,
so The fluid choice is warm disatonic crystalloid,
usually lactated ringers. But how do we monitor
efficacy when traditional vital signs like blood
pressure are notoriously unreliable in these
patients? You're right to question the traditional
monitoring. Blood pressure can be inaccurate,
it's difficult to obtain in severely burned extremities,
and it's often falsely elevated early on due
to high catecholamine levels from pain and stress.
So what do we use instead? The primary monitoring
tool that reflects true end organ perfusion is
the indwelling urinary catheter and the hourly
urine output, or UOP, target. This is the gold
standard for guiding resuscitation. Now, for
the crucial math, the consensus fluid formulas,
this is what every clinician has to calculate
immediately upon presentation. And we have to
use the current guidelines, which aim to prevent
the over -resuscitation we saw with older, higher
-volume formulas. For adults, defined as 14 years
and older, the baseline calculation is 2 mL times
kilograms times percent TBSA. Just for partial
and full thickness burns, right? Correct, only
for partial and full thickness. The target UOP
for adults is pretty narrow, 0 .5 mL per kilo
per hour, which translates roughly to 30 to 50
mL per hour. And the requirements escalate dramatically
for children. why the higher volume for the pediatric
patient. Children have a much greater body surface
area relative to their weight compared to adults.
That means they lose heat and volume proportionally
faster. So for children under 14 years, the starting
calculation is 3 mL times kilogram times percent
TBSA. Their target UOP is higher at 1 mL per
kilo per hour. And for the youngest patients?
For infants and young children, so those less
than or equal to 30 kilograms, they also start
at 3 mL times kilogram times TBSA, plus they
require maintenance fluids, specifically D5LR.
And why the D5, the dextrose in that younger
group? They have much smaller glycogen stores
and a higher metabolic rate. That places them
at significant risk for hypoglycemia during the
shock phase. The dextrose in the maintenance
fluids prevents this while ensuring they receive
the necessary volume. Their UOP target remains
1 ml per kilo per hour. Okay, let's nail down
the critical timing and the administration schedule.
This is where pre -hospital delays become a huge
factor. The clock for fluid administration starts
at the exact moment of injury, not when the patient
arrives at the hospital. This piece of information
is absolutely essential. And how is the total
volume administered? It's staggered. You give
half of that total calculated volume in the first
eight hours from the time of injury. Then you
give the remaining half over the subsequent 16
hours. Let's run a quick example to illustrate
the pressure. Say a 70 kilo adult has a 40 percent
TPS A burn and arrives six hours post injury.
Total fluid. 2 ml times 70 kilos times 40 percent.
That's 5 ,600 ml. Right. So half of that is 2
,800 ml. Since six of the first eight hours are
already gone, the team has to infuse 2 ,800 ml
in only two hours. That's a staggering rate of
1 ,400 ml per hour just to catch up. That is
the reality. And it highlights why obtaining
the precise time of injury is absolutely non
-negotiable. But here is the most crucial management
point for the nursing staff. Okay. The formulas
are a starting point, not a rigid prescription.
Titration is the key. If the UOP drops below
target, the best intervention is to increase
the fluid rate by 20 to 30 percent, not to administer
large sudden boluses unless the patient is profoundly
hypotensive. And the trap at the eight -hour
mark, what happens then? Do not under any circumstances
precipitously drop the infusion rate by half
at the eight -hour mark simply because the time
guideline changed. You must maintain whatever
rate is required to hit your UOP goal. If the
UOP is excellent, say 50 ml per hour in our 70
kilo patient, you may continue decreasing the
rate gradually, but the primary driver of fluid
adjustment must always be the urine output. What
are the consequences of missing this narrow window?
the pitfalls of under and over resuscitation.
Under resuscitation is obvious. You get hypoperfusion
and organ ischemia, acute kidney injury. The
less obvious and often more dangerous threat
in modern burn care is over resuscitation. Excess
fluid leads to even greater edema, which can
actually drive burn depth progression. A superficial
partial thickness burn can be converted to a
deep partial or even a full thickness injury
simply by excessive swelling cutting off the
local blood supply. And this edema contributes
directly to our secondary complication risk like
compartment syndrome. Absolutely. The excess
fluid is the fuel for abdominal and extremity
compartment syndromes. It's a very delicate balance
to achieve hemodynamic stability without drowning
the tissues in unnecessary fluid. Finally, what
about monitoring other vital signs? Why is tachycardia,
which is a classic sign of hypovolemia, such
a poor marker here? Burned patients are in severe
pain and stress, and they often have a baseline
hypermetabolic state. Therefore, tachycardia
is common and it's persistent, regardless of
their hydration status. Relying on it as a primary
measure of resuscitation is really misleading.
So what should we focus on instead? You should
focus instead on UOP mental status and their
acid -based balance. Persistence in acidemia,
for instance, might signal inadequate volume
replacement leading to anaerobic metabolism,
or conversely, it could indicate a massive infusion
of normal saline, which is acidotic. ECG monitoring
is vital, as dysrhythmias may be the first sign
of hypoxia or electrolyte imbalance. Okay, so
with immediate life threats managed and resuscitation
underway, we move to the secondary survey. Gathering
the history using the Amy Kille framework is
essential here, specifically to determine associated
injuries and the precise time of the burn. History
is often neglected in the chaos, but it informs
every aspect of care. We need to know the exact
time of injury for our fluid calculation. We
need to know the mechanism. Was the patient escaping
a fire, suggesting fractures or head injury?
Was there an explosion, suggesting potential
internal injuries like blast lung or blunt trauma?
And tetanus status. And we also need to immediately
establish and manage tetanus status as all deep
burns are considered contaminated wounds. Let's
talk about the assessment tools, particularly
the estimation of burn size, which directly influences
resuscitation. What is the fundamental rule when
applying the rule of nines? The fundamental rule
is to avoid overestimation. So do not include
superficial burns or first degree burns in your
TBSA calculation. First degree burns, like a
standard sunburn, are characterized by erythema
and pain, but they lack blistering. This means
the dermal layer is intact and there's no significant
capillary leak or fluid shift that requires resuscitation
calculation. We only include partial and full
thickness burns in the formula. And what's the
critical difference between using the rule of
nines for an adult versus a child? The standard
rule of nines, 9 % for the head, nine for each
arm, 18 for the trunk, front and back, 18 for
each leg, that's all based on adult body proportions.
Children have a proportionately much larger head
and smaller, lower extremities. For example,
an infant's head might be 18 to 20 % of the TBSA,
while each leg is only 13 to 14%. So clinicians
must use adjusted pediatric burn diagrams, like
one broader charts, or if they're unavailable,
rely on the quick, practical method for irregular
burns. Which is using the patient's palm. Yes,
the patient's palm, including their fingers,
is used to represent approximately 1 % TBSA.
This is a reliable way to estimate small, irregular,
or scattered burns. And never, ever forget to
log roll the patient to assess the back. Burns
are notoriously often hidden posteriorly. Let's
quickly review the clinical distinction of burn
depth, as this also affects prognosis and management.
We use tactile and visual clues. Superficial
partial thickness, or second degree, this is
the Hallmark blister, the wound is moist, usually
pink or red, very painfully hypersensitive even
to air movement, and most importantly, it blanches
briskly to touch, which indicates intact capillary
perfusion. Okay, and deeper. A deep partial thickness
burn has a drier appearance. It's modeled red
or white. The key clinical distinction is that
it's less painful, sensitive primarily to deep
pressure, and critically, it does not blanch
to pressure or it blanches very slowly. That
indicates microvascular damage. And finally,
full thickness. Full thickness, or third degree,
is leathery, dry, and classically waxy white,
opaque, or translucent. It is painless to light
touch or pinprick because the nerve endings are
destroyed. This tissue is non -pliable and it
will require excision and grafting. That lack
of pliability and full thickness burns, especially
when they're circumferential, is the direct mechanism
behind our most feared local complication. Compartment
syndrome is a circulatory emergency. It results
from two simultaneous factors, the inelastic
nature of the burn escher, that leathery dead
skin, and the mass of edema accumulating beneath
it. driven by our resuscitation fluids. So the
pressure just builds and builds. It rapidly compresses
the muscles and nerves within the closed fascial
compartments. If that pressure exceeds 30 millimeters
of mercury, muscle necrosis, and permanent nerve
damage begin. What are the high alert need to
know warning signs that should trigger immediate
concern, especially since the patient may be
unconscious or sedated? Well, we teach the classic
four P's, pain, pallor, or paresthesias, pulselessness,
but we need the burn specific nuances. One, pain
out of proportion to the injury or pain that
persists despite adequate IV narcotics. Two,
pain on passive stretch of the muscle group.
For example, passively flexing the wrist for
a forearm burn. How about it? tense swelling
of the affected compartment. It will feel rock
hard. And four, parasieges or altered sensation
distal to the compartment. We have to have a
high index of suspicion because pulselessness
is often a late sign signifying that ischemia
is already established. So what are the immediate
proactive nursing actions before surgical intervention
is needed? Early action is key. Remove all jewelry
and any constricting items, watches, rings, ties,
anything before significant swelling occurs.
These items have to be cut off if removal is
otherwise difficult. And we must repeatedly assess
distal circulation, check and capillary refill,
color, temperature, and progressive neurologic
signs. And when assessing pulses through burned
tissue, the Doppler is the definitive tool. Absolutely.
The Doppler ultrasonic flow meter provides the
most objective and reliable assessment of peripheral
pulses beneath the escher. If pulses are diminished
or absent, especially in a circumferential burn,
surgical intervention is required. And that intervention
is an escharotomy. It's an escharotomy, a surgical
incision through the inelastic burned skin to
relieve the pressure and restore flow. This typically
happens after the first six hours of resuscitation,
but it has to be anticipated. We often focus
on the limbs, but you mentioned truncal compartment
syndrome. How does that manifest? Circumferential
burns to the chest can severely restrict chest
wall expansion. As edema progresses, the patient
requires greater force to inflate the lungs,
leading to increased peak inspiratory pressures,
decreased tidal volumes, and respiratory distress,
even with an endotracheal tube in place. And
that requires a chest esverotomy. A prompt one?
Yes. Similarly, circumferential abdominal burns
can lead to abdominal compartment syndrome, causing
hemodynamic instability and reduced renal perfusion,
requiring an abdominal escharotomy. Before we
leave this section, let's revisit pain management
and sedation. You cautioned against treating
restlessness solely as pain. Restlessness is
a nonspecific sign that demands a critical reassessment
of the ABCs. It can be a sign of hypoxemia, hypoxia,
or hypovolemia. You must ensure resuscitation
and oxygenation are optimized first. Once those
are ruled out, then you address the pain. And
how should analgesics be administered? Analgesics
and sedatives must be administered intravenously
only in small, frequent doses. Why the strict
IV -only rule? because absorption of medications
given intramuscularly or subcutaneously is unpredictable
and delayed in the presence of massive soft tissue
edema and shock. As resuscitation progresses
and perfusion returns, those accumulated doses
can be suddenly released, leading to a massive
overdose and respiratory depression. Four administration
ensures rapid onset, predictable dosing, and
tight control. Finally, wound care basics for
the emergency room. What are the essential immediate
rules? Never apply cold water or cold compresses
to extensive burns. That means burns greater
than 10 % TBSA, because this dramatically increases
the risk of severe hypothermia, which is catastrophic
to the patient. OK. Also, do not break intact
blisters. They function as a temporary sterile
biological dressing. Clean dirty wounds gently
with sterile saline and protect all fresh burns
from environmental contamination universal precautions,
including gloves and gowns for all caregivers,
are mandatory. What about the common temptation
to start systemic antibiotics immediately? Prophylactic
systemic antibiotics are not indicated in the
early post -burn period. They don't prevent subsequent
infection and they only serve to select for resistant
organisms. Antibiotics should be reserved strictly
for documented or strongly suspected infection.
And again, always determine and manage the patient's
tetanus immunization status. Let's pivot to the
injury patterns that break the conventional rules.
First, a deeper dive into chemical burns. We
established that alkalis are more dangerous due
to liquefaction necrosis. What are the key management
pitfalls specific to chemical exposure? The primary
pitfall is the attempt to neutralize the agent.
do not use neutralizing agents. The chemical
reaction itself is exothermic. It produces heat,
and that heat will inflict a secondary thermal
injury, which worsens the tissue damage caused
by the primary chemical. We rely entirely on
massive, sustained dilution with warmed water
or saline. And the specific detail for ocular
injuries involving alkali. Alkaline brings to
the eye are true emergencies because they penetrate
so rapidly and cause devastating, often permanent,
injury. They require continuous irrigation for
the first eight hours, often requiring specialized
equipment to maintain constant flushing. What
if the chemical is unknown or if there is a risk
of systemic toxicity? For unfamiliar compounds,
especially in industrial settings, the first
action after initiating irrigation is to obtain
the material safety data sheet, or MSDS. It outlines
specific risks, toxicity, and necessary decontamination
procedures. And always contact a regional poison
control center. They are invaluable resources
for managing systemic absorption risks. Next,
electrical burns. These are the most deceptive
injuries where the skin may look almost normal,
but there's massive internal damage hidden. Electrical
injuries defy standard assessment. The current
travels through structures with the lowest resistance
nerves, blood vessels, and muscle. This causes
deep muscle necrosis, often remote from the small
surface entry and exit wounds. The current also
causes intense vasospasm and thrombosis in the
microvasculature, leading to progressive tissue
ischemia. What about the muscle contractions?
A high alert sign is the titanic, forced muscle
contraction that occurs upon contact. What does
that forced contraction lead to, clinically?
It frequently causes secondary trauma, especially
fractures. We must always examine for spinal
and long bone fractures. And the high muscle
activity is what drives the major life -threatening
risk. Of bone myelosis. Okay, let's focus on
that musculoskeletal and renal risk. Electricity
causes massive tissue breakdown, flooding the
system with myoglobin. How do we manage this,
and how does it change our fluid strategy? Myoglobin,
if it's allowed to concentrate, precipitates
in the renal tubules, leading to acute renal
failure. So we must institute aggressive fluid
resuscitation immediately to flush the kidneys.
You assume hemochromogens are present if the
patient's urine is dark red or brown even before
you get lab confirmation. And this demands a
significant change in the fluid resuscitation
math. A critical change. For electrical burn
injury, the standard Parkland or consensus formula
is replaced. We start resuscitation immediately
at 4 mL times kilojoules times percent TBSA LR.
That's an increase of 50 to 100 percent over
the standard formula, specifically to prevent
renal failure. And the target urine output changes
dramatically as well. The goal is no longer 30
to 50 mL per hour. The immediate high -volume
urine output target modification is to aim for
100 mL per hour in a adults and 1 to 1 .5 ml
per kilo per hour in children. This high output
rate must be maintained until the urine visibly
clears of pigmentation. Only once the urine is
pale and clear do you titrate the IV fluid down
to the standard burn rate of 0 .5 ml per kilo
per hour. And we also often consult the burn
unit before using alkalinizing agents like bicarbonate
or mannitol as their use is debated and complex.
to extremely sticky thermal injury, tar burns.
How do you safely remove molten tar, which can
adhere and maintain extremely high temperatures?
Tar is a thick, highly adhesive substance that
can burn at temperatures up to 450 degrees Fahrenheit.
The first step is rapid cooling, often with water,
to stop the heat transfer. But attempting mechanical
removal will cause severe pain and deeper trauma.
There was a solution. The simple, elegant solution
is using a substance that dissolves the tar without
harming the injured skin. mineral oil or a non
-petroleum -based antibiotic ointment. You apply
it liberally, it's inert, and it allows the tar
to gradually dissolve and be gently peeled away
without inflicting further mechanical damage.
Finally, we have to address suspicious injury
patterns indicating potential abuse, especially
in the most vulnerable populations, children
and the elderly. What patterns should always
raise clinical suspicion? We have to maintain
a high index of suspicion and objectively document
the pattern of injury. You look for patterns
that are inconsistent with the history provided.
For instance, burns with clear sharp edges or
circular burns often suggest contact with a specific
hot object like a cigarette, an iron, or a heating
element. What about immersion burns? Those are
often highly suggestive of non -accidental trauma.
Immersion burns, especially scald injuries, leave
distinct patterns. In children, burns on the
soles of the feet or the buttocks, or a stocking
glove pattern where the extremity is uniformly
burned with clear lines of demarcation, suggest
the child was forcefully immersed in hot water.
As opposed to an accident. Right. A child falling
into hot water naturally attempts to step out
or splash, which leads to a non -uniform pattern.
A uniform, deep, and symmetric burn strongly
suggest forced, non -accidental immersion. For
elderly patients, similar posterior lower extremity
or buttocks burns may suggest intentional neglect
or placement into water that was too hot. The
mechanism provided by the caregiver must match
the documented injury pattern. Shifting to the
opposite end of the spectrum, cold injury. While
it's a different mechanism, the outcome tissue
anoxia and necrosis is the same. Let's distinguish
between the two major types of local cold injury.
We have frostbite, which involves actual tissue
freezing. Ice crystals form. They mechanically
injure cells and cause massive microvascular
occlusion and subsequent tissue death. It's classified
by depth, similar to burns, from superficial
first degree to deep fourth degree involving
muscle and bone. And the other type. Then we
have non -freezing injury, often called French
foot or immersion foot. And what causes that?
This results from prolonged exposure to wet conditions
and temperatures just above freezing, roughly
1 .6 to 10 degrees Celsius. There is no actual
freezing, but the cold, wet conditions cause
profound sustained vasoconstriction and direct
microvascular endothelial damage. This leads
to stasis and occlusion over time. What is the
clinical timeline for trench foot? The affected
part is initially cold, numb, and pale, but after
the exposure ends, during the rewarming and hypereomic
phase, usually 24 to 48 hours later, the patient
experiences this intense, almost unbearable,
painful burning and dysesthesia that's a key
clinical differentiator from frostbite. Now,
the acute management of frostbite, this is a
sequence where timing is everything, especially
concerning rewarming. The immediate rule of frostbite
is do not attempt rewarming if there's any chance
of refreezing. Thawing and then refreezing causes
massive irreversible tissue damage. If the patient
has to walk out of the environment or if transport
conditions are unstable, you keep the tissue
frozen until they reach a definitive warm care
environment. Once they are safe, what is the
precise controlled method for thawing? We use
rapid constant rewarming. The injured part is
placed into circulating water at a constant 40
degrees Celsius or 104 degrees Fahrenheit until
the tissue turns red and pliable, indicating
perfusion has returned. This typically takes
20 to 30 minutes. And the crucial do -nots during
this process. Do not use dry heat sources like
radiators or campfires. They cause uncontrolled,
unequal heating and increase the risk of a secondary
burn, especially since the tissue is insensate.
And crucially, do not rub, massage, or use friction
on the area. Why not? The tissue is extremely
fragile and friction will shred the already damaged
cell membranes. And since rewarming is excruciatingly
painful, adequate intravenous narcotic analgesia
is essential to allow the patient to tolerate
the necessary procedure. Rewarming a large frozen
area carries a systemic risk, which clinicians
have to monitor closely. Yes, this is the risk
of reperfusion syndrome. As frozen tissue thaws
and blood returns, locally accumulated waste
products, including high levels of potassium,
are suddenly released into the systemic circulation.
This risk requires careful cardiac monitoring
for dysrhythmias and monitoring of electrolytes
and blood gases for metabolic acidosis and hyperkalemia.
Let's discuss local wound care for frostbite.
particularly the blister management. Once it's
re -warmed, the tissue is protected by elevation
to limit swelling, often using a tent or a cradle
over the extremity to prevent pressure and friction.
Regarding blisters, we leave clear, non -hemorrhagic,
non -infected blisters intact. Why is that? They
act as a sterile biological dressing, promoting
underlying epithelialization. Hemorrhagic blisters,
which are dark and blood -filled, usually signify
a deeper, more severe injury and are often debrided.
Active management includes withholding all tobacco
products, as nicotine is a potent vasoconstrictor
that impairs microcirculatory flow, which is
already severely compromised. And the key distinction
in prognosis' timeline compared to a burn. This
is a major difference. Estimating the final depth
and extent of tissue death in frostbite is highly
inaccurate in the first few days. Final tissue
demarcation. That clear line between viable and
non -viable tissue takes weeks, sometimes months,
to fully develop. So surgery is delayed. It means
surgical intervention, such as amputation, is
rarely necessary in the acute phase unless a
life -threatening infection is present. This
protracted assessment period shifts the focus
heavily onto long -term supportive care and observation.
Finally, systemic hypothermia. This is a core
temperature below 36 degrees Celsius, and it
complicates all trauma, including burns and environmental
cool injury. Systemic hypothermia must be prevented
or aggressively treated. It profoundly worsens
coagulopathy, increases the risk of cardiac arrhythmias,
and impairs almost all organ system functions.
The nursing priority is limiting heat loss through
passive and active rewarming techniques. What
defines the difference between passive and active
rewarming? Passive rewarming is used for mild
hypothermia, so above 34 degrees Celsius. This
relies on the patient's own intact thermoregulatory
mechanism. We simply reduce heat loss using dry
clothing, blankets, and a warm environment. Active
rewarming is required for moderate and severe
hypothermia, so below 32 degrees Celsius. This
involves supplying external heat, such as warmed
5e fluids, applying warmed packs or heating devices
to areas of high vascular flow like the axilla
and groin, or in severe cases, using advanced
methods like warmed peritoneal lavage or circulatory
bypass. Okay, so the initial stabilization of
a complex injury often means preparing the patient
for transfer to a specialized burn center. Knowing
the American Burn Association, or ABA, transfer
criteria is essential triage knowledge that guides
resource allocation. These guidelines ensure
that complex injuries, which demand multidisciplinary
specialty care, receive it quickly. There are
10 specific categories that mandate transfer
to a burn center. Let's review those 10 categories
in detail, as this really forms the framework
for all initial treatment decisions. Okay. First,
any partial thickness burns greater than 10 %
TBSA in any age group. Second, burns involving
functional or cosmetic areas, the face, hands,
feet, genitalia, perineum burns over major joints.
Third, all third degree or full thickness burns,
regardless of the TVSA size. Fourth, electrical
burns, including lightning injury due to the
high risk of hidden deep tissue damage. Fifth,
chemical burns due to the depth and systemic
risk. And sixth, inhalation injury. What about
comorbidities and associated trauma? Seventh,
any burn injury in patients with pre -existing
medical disorders that could complicate management,
prolong recovery, or increase mortality risk,
things like diabetes, severe car - cardiac disease
or chronic kidney disease. Eighth, any patient
with burns and concomitant trauma -like severe
fractures or a head injury, where the burn injury
itself poses the greatest threat to morbidity
or mortality. And the final two categories address
logistics and demographics. Ninth, burn children
in hospitals that lack qualified pediatric personnel
or equipment. And tenth, burn injury in patients
who will require special, social, emotional,
or rehabilitative intervention that cannot be
provided locally. If the patient meets these
criteria, the transfer procedure has to be executed
flawlessly. What are the key logistical and documentation
imperatives to ensure the receiving center can
continue optimal care? Documentation is absolutely
paramount. The sins of the transferring facility
often surface in the receiving facility's resuscitation
bay. The transfer must be coordinated with the
receiving burn center physician, not just the
charge nurse. A comprehensive burn or trauma
flow sheet must accompany the patient. What needs
to be on that flow sheet? It's required to detail
all baseline test results, sequential vital signs,
every single milliliter of fluid administered,
and the corresponding urinary output hour by
hour. That flow sheet is the blueprint for resuscitation.
It is. Without it, the receiving team has no
idea if the patient is over or under resuscitated,
and they can't accurately adjust the fluid rate.
A clear pictorial diagram of the burn area and
estimated depth is also essential. An airway
reassessment, again, is the constant pitfall,
especially during transport. Yes. Reassess the
airway frequently just before transfer. If the
patient has inhalation risk factors or has received
significant resuscitation fluid, the edema will
continue to develop, potentially causing obstruction
en route. If there is any question regarding
airway stability and the transport time is long,
proactive intubation before the transfer is mandatory
and should be discussed with the receiving facility.
And patient comfort. Yes. Finally, ensure the
patient is comfortable. Provide adequate analgesia
before dressing changes or manipulation, and
use non -adherent burn sheets to protect the
integrity of the wounds during the move. This
deep dive has really crystallized the complexity
of acute thermal and cold injury management.
If we had to isolate the most high -yield clinical
skill set from this entire discussion, it's arguably
that predictive capacity knowing when intervention
is required before the patient is overtly symptomatic.
That is the core takeaway. If you master early
airway assessment, specifically knowing those
ABLS intubation criteria, anticipating edema,
and recognizing the failure of the pulse oximeter,
and you combine that with the precise application
and hourly titration of the fluid resuscitation
formula, you have managed the vast majority of
life -threatening events in the first 24 hours.
Your job is defined by vigilance. The ultimate
lesson, it seems, connects the science back to
the patient. The unique continuous inflammatory
pathophysiology of a burn means that aggressive
nursing care is essentially this constant vigilant
effort to balance fluid loss against dangerous
edema. It's an ongoing negotiation with the body's
systemic response. and something to ponder as
you connect the pathophysiology to the human
element. We established that the final demarcation
between viable and non -viable tissue in frostbite
can take weeks or even months. So how does this
protracted assessment period fundamentally change
the psychological support and the expectation
management required when you're caring for a
frostbite patient compared to the rapid, acute,
and often decisive interventions required for
a critical thermal burn patient in those first
24 hours? That's a powerful thought on the intersection
of trauma care and long -term recovery. We hope
you feel more informed, more prepared, and more
confident in handling these critical scenarios.
We'll see you next time.