Burn

A burn is an injury caused by heat, cold, electricity, chemicals, light, radiation, or

friction. Statistically, it is the second highest unintentional cost of human life behind
automobile accidents. Burns can be highly variable in terms of the tissue affected, the
severity, and resultant complications. Muscle, bone, blood vessel, and epidermal tissue
can all be damaged with subsequent pain due to profound injury to nerve endings.
Depending on the location affected and the degree of severity, a burn victim may
experience a wide number of potentially fatal complications including shock, infection,
electrolyte imbalance and respiratory distress. Beyond physical complications, burns can
also result in severe psychological and emotional distress due to scarring and deformity.

Contents
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• 1 Classification by degree
• 2 Other classifications
• 3 Causes of burns
o 3.1 Scalding
o 3.2 Cold burn
• 4 Management

Classification by degree
The most common system of classifying burns categorizes them as first-, second-, or
third-degree. Sometimes this is extended to include a fourth or even up to a sixth degree,
but most burns are first- to third-degree, with the higher-degree burns typically being
used to classify burns post-mortem. The following are brief descriptions of these classes:

• First-degree burns are usually limited to redness (erythema), a white plaque and
minor pain at the site of injury. These burns only involve the epidermis.
• Second-degree burns manifest as erythema with superficial blistering of the skin,
and can involve more or less pain depending on the level of nerve involvement.
Second-degree burns involve the superficial (papillary) dermis and may also
involve the deep (reticular) dermis layer.
• Third-degree burns occur when most of the epidermis is lost with damaged to
underlying ligaments, tendons and muscle. Burn victims will exhibit charring of
the skin, and sometimes hard eschars will be present. An eschar is a scab that has
separated from the unaffected part of the body. These types of burns are often
considered painless, because nerve endings have been destroyed in the burned
area. Hair follicles and sweat glands may also be lost due to complete destruction
 of the dermis. Third degree burns result in scarring and may be fatal if the
affected area is significantly large.
• Fourth-degree burns damage bone tissue and may result in a condition called
compartment syndrome, which threatens the life of the limb.
• Fifth-degree burns are burns in which most of the hypodermis is lost, charring
and exposing the muscle underneath. Sometimes, fifth-degree burns can be fatal.
• Sixth-degree burns, the most severe form, are burn types in which almost all the
muscle tissue in the area is destroyed, leaving almost nothing but charred bone.
Often, sixth-degree burns are deadly.

Other classifications
A newer classification of "Superficial Thickness", "Partial Thickness" (which is divided
into superficial and deep categories) and "Full Thickness" relates more precisely to the
epidermis, dermis and subcutaneous layers of skin and is used to guide treatment and
predict outcome.

Table 1. A description of the traditional and current classifications of burns.

Traditional
Nomenclature Depth Clinical findings
nomenclature

Superficial Erythema, minor pain, lack

First-degree Epidermis involvement
thickness of blisters

Partial thickness Superficial (papillary) Blisters, clear fluid, and

Second-degree
— superficial dermis pain

Whiter appearance, with

Partial thickness decreased pain. Difficult to
Second-degree Deep (reticular) dermis
— deep distinguish from full
thickness

Dermis and underlying Hard, leather-like eschar,

Third- or fourth-
Full thickness tissue and possibly purple fluid, no sensation
degree
fascia, bone, or muscle (insensate)

Main article: Total body surface area

Burns can also be assessed in terms of total body surface area (TBSA), which is the
percentage affected by partial thickness or full thickness burns (superficial thickness
burns are not counted). The rule of nines is used as a quick and useful way to estimate the
affected TBSA.

Causes of burns
Burns may be caused by a wide variety of substances and external sources such as
exposure to chemicals, friction, electricity, radiation, and extreme temperatures, both hot
and cold.

Most chemicals (but not all) that can cause moderate to severe chemical burns are strong
acids or bases.[6] Chemical burns are usually caused by caustic chemical compounds, such
as sodium hydroxide, silver nitrate, and more serious compounds (such as sulfuric acid
and Nitric acid).[7] Hydrofluoric acid can cause damage down to the bone and its burns
are sometimes not immediately evident.

Electrical burns are generally caused by an exogenous electric shock, such as being
struck by lightning or defibrillated or cardioverted without a conductive gel. The internal
injuries sustained may be disproportionate to the size of the burns seen, and the extent of
the damage is not always obvious. Such injuries may lead to cardiac arrhythmias, cardiac
arrest, and unexpected falls with resultant fractures.

Radiation burns may be caused by protracted and overexposure to UV light (as from the
sun), tanning booths, radiation therapy (as patients who are undergoing cancer therapy),
sunlamps, and X-rays. By far the most common burn associated with radiation is sun
exposure, specifically two wavelengths of light UVA, and UVB, the latter being the more
dangerous of the two. Tanning booths also emit these wavelengths and may cause similar
damage to the skin such as irritation, redness, swelling, and inflammation. More severe
cases of sun burn result in what is known as sun poisoning.

Scalding is a specific type of burning that is caused by hot fluids or gases. They most
commonly occur in the home from exposure to high temperature tap water.[10] Steam is a
common gas that causes scalds. The injury is usually regional and usually does not cause
death. More damage can be caused if hot liquids enter an orifice. However, deaths have
occurred in more unusual circumstances, such as when people have accidentally broken a
steam pipe. The demographics that are of the highest risk to suffering from scalding are
young children, with their delicate skin, and the elderly over 65 years of age.
Cold burn

A cold burn (see frostbite) is a kind of burn which arises when the skin is in contact with
a low-temperature body. They can be caused by prolonged contact with moderately cold
bodies (snow and cold air for instance) or brief contact with very cold bodies such as dry
ice, liquid helium, liquid nitrogen, or canned air. In such a case, the heat transfers from
the skin and organs to the external cold body. The effects are very similar to that of a burn
caused by extreme heat. The remedy is also the same. For a minor cold burn, it is
advisable to keep the injured organ under a flow of water of comfortable temperature.
This will allow heat to transfer slowly from the water to the organs.

Management
A local anesthetic is usually sufficient in managing pain of minor first-degree and second-
degree burns. However, systemic anti-inflammatory drugs such as naproxen may be
effective in mitigating pain and swelling. Additionally, topical antibiotics such as
Mycitracin are useful in preventing infection to the damaged area.[11] Lidocaine can be
administered to the spot of injury and will generally negate most of the pain. Regardless
of the cause, the first step in managing a person with a burn is to stop the burning process
at the source. For instance, with dry powder burns, the powder should be brushed off
first. With other burns, such as those caused by exposure to chemicals, the affected area
should be rinsed throughly with a large amount of clean water to remove the caustic agent
and any foreign bodies. Cold water should not be applied to a person with extensive
burns, however, as it may compromise the burn victim's temperature status.

If the patient was involved in a fire accident, then it must be assumed that he or she has
sustained inhalation injury until proven otherwise, and treatment should be managed
accordingly. At this stage of management, it is also critical to assess the airway status.
Any hint of burn injury to the lungs (e.g. through smoke inhalation) is considered a
medical emergency. Survival and outcome of severe burn injuries is remarkably
improved if the patient is treated in a specialized burn center/unit rather than a hospital.
Serious burns, especially if they cover large areas of the body, can result in death.

Once the burning process has been stopped, the patient should be volume resuscitated
according to the Parkland formula, since such injuries can disturb a person's osmotic
balance. This formula dictates the amount of Lactated Ringer's solution to deliver in the
first twenty four hours after time of injury. This formula excludes first and most second
degree burns. Half of the fluid should be given in the first eight hours post injury and the
rest in the subsequent sixteen hours. The formula is a guide only and infusions must be
tailored to urine output and central venous pressure. Inadequate fluid resuscitation causes
renal failure and death.
Shock
Shock is a serious, often life-threatening medical condition where insufficient blood flow
reaches the body tissues. As blood is the body's carrier of oxygen and nutrients,
insufficient flow leads to a deficiency in these components, which are necessary for
proper tissue functioning. The process affected, where blood enters the tissues, is called
perfusion and this process not occurring properly causes a hypoperfusional (hypo =
below) state.

Medical shock must not be confused with the emotional state, and the two are not related.
Medical shock is a life-threatening medical emergency and one of the leading causes of
death for critically ill people. This primary cause may lead to many other medical
emergencies, such as hypoxia (a lack of oxygen in the body tissues) or cardiac arrest (the
heart stopping).

Shock can have a number of effects, all with similar outcomes, but all relate to a problem
with the body's circulatory system.

Contents
• 1 Stages of shock
• 2 Types of shock
• 3 Signs and symptoms
• 4 Treatment
o 4.1 Hypovolaemic shock
o 4.2 Cardiogenic shock
o 4.3 Distributive shock
o 4.4 Obstructive shock
o 4.5 Endocrine shock
• 5 Prognosis
• 6 Notes
Stages of shock

Effects of inadequate perfusion on cell function.

There are four stages of shock.

Initial
During this stage, the hypoperfusional state causes hypoxia, leading to the
mitochondria being unable to produce adenosine triphosphate. Due to this lack of
oxygen, the cell membranes become damaged, they become leaky to extra-
cellular fluid, and the cells perform anaerobic respiration. This causes a build-up
of lactic and pyruvic acid which results in systemic metabolic acidosis. The
process of removing these compounds from the cells by the liver requires oxygen,
which is absent.
Compensatory (Compensating)
This stage is characterised by the body employing physiological mechanisms,
including neural, hormonal and bio-chemical mechanisms in an attempt to reverse
the condition. As a result of the acidosis, the person will begin to hyperventilate in
order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the
blood and by removing it the body is attempting to raise the pH of the blood. The
baroreceptors in the arteries detect the resulting hypotension, and cause the
release of adrenaline and noradrenaline. Noradrenaline causes predominately
vasoconstriction with a mild increase in heart rate, whereas adrenaline
predominately causes an increase in heart rate with a small effect on the vascular
tone; the combined effect results in an increase in blood pressure. Renin-
angiotensin axis is activated and arginine vasopressin is released to conserve fluid
via the kidneys. Also, these hormones cause the vasoconstriction of the kidneys,
gastrointestinal tract, and other organs to divert blood to the heart, lungs and
brain. The lack of blood to the renal system causes the characteristic low urine
production. However the effects of the Renin-angiotensin axis take time and are
of little importance to the immediate homeostatic mediation of shock.
Progressive (Decompensating)
Should the cause of the crisis not be successfully treated, the shock will proceed
to the progressive stage and the compensatory mechanisms begin to fail. Due to
the decreased perfusion of the cells, sodium ions build up within while potassium
ions leak out. As anaerobic metabolism continues, increasing the body's metabolic
acidosis, the arteriolar and precapillary sphincters constrict such that blood
remains in the capillaries. Due to this, the hydrostatic pressure will increase and,
combined with histamine release, this will lead to leakage of fluid and protein into
the surrounding tissues. As this fluid is lost, the blood concentration and viscosity
increase, causing sludging of the micro-circulation. The prolonged
vasoconstriction will also cause the vital organs to be compromised due to
reduced perfusion.
Refractory
At this stage, the vital organs have failed and the shock can no longer be reversed.
Brain damage and cell death have occurred. Death will occur imminently.

Shock is a complex and continuous condition and there is no sudden transition from one
stage to the next.

Types of shock
In 1972 Hinshaw and Cox suggested the following classification which is still used today.
It uses four types of shock: hypovolaemic, cardiogenic, distributive and obstructive
shock:

Hypovolemic shock - This is the most common type of shock and based on insufficient
circulating volume. Its primary cause is loss of fluid from the circulation from either an
internal or external source. An internal source may be haemorrhage. External causes may
include extensive bleeding, high output fistulae or severe burns.

• Cardiogenic shock - This type of shock is caused by the failure of the heart to
pump effectively. This can be due to damage to the heart muscle, most often from
a large myocardial infarction. Other causes of cardiogenic shock include
arrhythmias, cardiomyopathy, congestive heart failure (CHF), contusio cordis or
cardiac valve problems.
• Distributive shock - As in hypovolaemic shock there is an insufficient
intravascular volume of blood. This form of "relative" hypovolaemia is the result
of dilation of blood vessels which diminishes systemic vascular resistance.
Examples of this form of shock are:
o Septic shock - This is caused by an overwhelming infection leading to
vasodilation, such as by Gram negative bacteria i.e. Escherichia coli,
Proteus species, Klebsiella pneumoniae which release an endotoxin which
produces adverse biochemical, immunological and occasionally
neurological effects which are harmful to the body. Gram-positive cocci,
such as pneumococci and streptococci, and certain fungi as well as Gram-
positive bacterial toxins produce a similar syndrome.
o Anaphylactic shock - Caused by a severe anaphylactic reaction to an
allergen, antigen, drug or foreign protein causing the release of histamine
which causes widespread vasodilation, leading to hypotension and
increased capillary permeability.
o Neurogenic shock - Neurogenic shock is the rarest form of shock. It is
caused by trauma to the spinal cord resulting in the sudden loss of
autonomic and motor reflexes below the injury level. Without stimulation
by sympathetic nervous system the vessel walls relax uncontrolled,
resulting in a sudden decrease in peripheral vascular resistance, leading to
vasodilation and hypotension.
 • Obstructive shock - In this situation the flow of blood is obstructed which
impedes circulation and can result in circulatory arrest. Several conditions result
in this form of shock.
o Cardiac tamponade in which blood in the pericardium prevents inflow of
blood into the heart (venous return). Constrictive pericarditis, in which the
pericardium shrinks and hardens, is similar in presentation.
o Tension pneumothorax. Through increased intrathoracic pressure,
bloodflow to the heart is prevented (venous return).
o Massive pulmonary embolism is the result of a thromboembolic incident
in the bloodvessels of the lungs and hinders the return of blood to the
heart.
o Aortic stenosis hinders circulation by obstructing the ventricular outflow
tract

Recently a fifth form of shock has been introduced:

• Endocrine shock based on endocrine disturbances.

o Hypothyroidism, in critically ill patients, reduces cardiac output and can
lead to hypotension and respiratory insufficiency.
o Thyrotoxicosis may induce a reversible cardiomyopathy.
o Acute adrenal insufficiency is frequently the result of discontinuing
corticosteroid treatment without tapering the dosage. However, surgery
and intercurrent disease in patients on corticosteroid therapy without
adjusting the dosage to accommodate for increased requirements may also
result in this condition.
o Relative adrenal insufficiency in critically ill patients where present
hormone levels are insufficient to meet the higher demands
Signs and symptoms
• Hypovolemic shock
o Anxiety, restlessness, altered mental state due to decreased cerebral
perfusion and subsequent hypoxia.
o Hypotension due to decrease in circulatory volume.
o A rapid, weak, thready pulse due to decreased blood flow combined with
tachycardia.
o Cool, clammy skin due to vasoconstriction and stimulation of
vasoconstriction.
o Rapid and shallow respirations due to sympathetic nervous system
stimulation and acidosis.
o Hypothermia due to decreased perfusion and evaporation of sweat.
o Thirst and dry mouth, due to fluid depletion.
o Fatigue due to inadequate oxygenation.
o Cold and mottled skin (cutis marmorata), especially extremities, due to
insufficient perfusion of the skin.
o Distracted look in the eyes or staring into space, often with pupils dilated.
• Cardiogenic shock, similar to hypovolaemic shock but in addition:
o Distended jugular veins due to increased jugular venous pressure.
o Absent pulse due to tachyarrhythmia.
• Obstructive shock, similar to hypovolaemic shock but in addition:
o Distended jugular veins due to increased jugular venous pressure.
o Pulsus paradoxus in case of tamponade
• Septic shock, similar to hypovolaemic shock except in the first stages:
o Pyrexia and fever, or hyperthermia, due to overwhelming bacterial
infection.
o Vasodilation and increased cardiac output due to sepsis.
• Neurogenic shock, similar to hypovolaemic shock except in the skin's
characteristics. In neurogenic shock, the skin is warm and dry.
• Anaphylactic shock
o Skin eruptions and large welts.
o Localised edema, especially around the face.
o Weak and rapid pulse.
o Breathlessness and cough due to narrowing of airways and swelling of the
throat.

Treatment

Modified and adapted from Alexander M.F., Fawcett J.N. and Runciman, P.N. (2004)
Nursing Practice. The Hospital and Home. The Adult. (2nd edition) Edinburgh: Churchill
Livingstone
In the early stages, shock requires immediate intervention to preserve life. Therefore, the
early recognition and treatment depends on the transfer to a hospital.

The management of shock requires immediate intervention, even before a diagnosis is

made. Re-establishing perfusion to the organs is the primary goal through restoring and
maintaining the blood circulating volume ensuring oxygenation and blood pressure are
adequate, achieving and maintaining effective cardiac function, and preventing
complications. Patients attending with the symptoms of shock will have, regardless of the
type of shock, their airway managed and oxygen therapy initiated. In case of respiratory
insufficiency (i.e. diminished levels of consciousness, hyperventilation due to acid-base
disturbances or pneumonia) intubation and mechanical ventilation may be necessary. A
paramedic may intubate in emergencies outside the hospital, whereas a patient with
respiratory insufficiency in-hospital will be intubated usually by a physician.

The aim of these acts is to ensure survival during the transportation to the hospital; they
do not cure the cause of the shock. Specific treatment depends on the cause.

A compromise must be found between:

• raising the blood pressure to be able to transport "safely" (when the blood
pressure is too low, any motion can lower the heart and brain perfusion, and thus
cause death);
• respecting the golden hour. If surgery is required, it should be performed within
the first hour to maximise the patient's chance of survival.

This is the stay and play versus the load and go debate.

Hypovolaemic shock

In hypovolaemic shock, caused by bleeding, it is necessary to immediately control the

bleeding and restore the victim's blood volume by giving infusions of balanced salt
solutions. Blood transfusions are necessary for loss of large amounts of blood (e.g.
greater than 20% of blood volume), but can be avoided in smaller and slower losses.
Hypovolaemia due to burns, diarrhoea, vomiting, etc. is treated with infusions of
electrolyte solutions that balance the nature of the fluid lost. Sodium is essential to keep
the fluid infused in the extracellular and intravascular space whilst preventing water
intoxication and brain swelling. Metabolic acidosis (mainly due to lactic acid)
accumulates as a result of poor delivery of oxygen to the tissues, and mirrors the severity
of the shock. It is best treated by rapidly restoring intravascular volume and perfusion as
above. Inotropic and vasoconstrictive drugs should be avoided, as they may interfere in
knowing blood volume has returned to normal.

Regardless of the cause, the restoration of the circulating volume is priority. As soon as
the airway is maintained and oxygen administered the next step is to commence
replacement of fluids via the intravenous route.
Opinion varies on the type of fluid used in shock. The most common are:

• Crystalloids - Such as sodium chloride (0.9%), or Hartmann's solution (Ringer's

lactate). Dextrose solutions which contain free water are less effective at re-
establishing circulating volume, and promote hyperglycaemia.
• Colloids - For example, synthetic albumin (Dextran™), polygeline
(Haemaccel™), succunylated gelatin (Gelofusine™) and hetastarch (Hepsan™).
Colloids are, in general, much more expensive than crystalloid solutions and have
not conclusively been shown to be of any benefit in the initial treatment of shock.
• Combination - Some clinicians argue that individually, colloids and crystalloids
can further exacerbate the problem and suggest the combination of crystalloid and
colloid solutions.
• Blood - Essential in severe haemorrhagic shock, often pre-warmed and rapidly
infused.

Vasoconstrictor agents have no role in the initial treatment of hemorrhagic shock, due to
their relative inefficacy in the setting of acidosis, and due to the fact that the body, in the
setting of hemorrhagic shock, is in an endogenously catecholaminergic state. Definitive
care and control of the hemorrhage is absolutely necessary, and should not be delayed.

Cardiogenic shock

In cardiogenic shock: depending on the type of myocardal infarction one can infuse fluids
or in shock refractory to infusing fluids, inotropic agents. Inotropic agents, which
enhance the heart's pumping capabilities, are used to improve the contractility and correct
the hypotension. Should that not suffice an intra-aortic balloon pump -which reduces
workload for the heart, and improves perfusion of the coronary arteries- can be
considered or a left ventricular assist device -which augments the pump-function of the
heart.

The main goals of the treatment of cardiogenic shock are the re-establishment of
circulation to the myocardium, minimising heart muscle damage and improving the
heart's effectiveness as a pump. This is most often performed by percutaneous coronary
intervention and insertion of a stent in the culprit coronary lesion or sometimes by cardiac
bypass.

Although this is a protection reaction, the shock itself will induce problems; the
circulatory system being less efficient, the body gets "exhausted" and finally, the blood
circulation and the breathing slow down and finally stop (cardiac arrest). The main way
to avoid this deadly consequence is to make the blood pressure rise again with

• fluid replacement with intravenous infusions;

• use of vasopressing drugs (e.g. to induce vasoconstriction);
• use of anti-shock trousers that compress the legs and concentrate the blood in the
vital organs (lungs, heart, brain).
 • use of blankets to keep the patient warm - metallic PET film emergency blankets
are used to reflect the patient's body heat back to the patient.

Distributive shock

In distributive shock caused by sepsis the infection is treated with antibiotics and
supportive care is given (i.e. inotropica, mechanical ventilation, renal function
replacement). Anaphylaxis is treated with adrenaline to stimulate cardiac performance
and corticosteroids to reduce the inflammatory response. In neurogenic shock because of
vasodilation in the legs, one of the most suggested treatments is placing the patient in the
Trendelenburg position, thereby elevating the legs and shunting blood back from the
periphery to the body's core. However, since bloodvessels are highly compliant, and
expand as result of the increased volume locally, this technique does not work. More
suitable would be the use of vasopressors.

Obstructive shock

In obstructive shock, the only therapy consists of removing the obstruction.

Pneumothorax or haemothorax is treated by inserting a chest tube, pulmonary embolism
requires thrombolysis (to reduce the size of the clot), or embolectomy (removal of the
thrombus), tamponade is treated by draining fluid from the pericardial space through
pericardiocentesis.

Endocrine shock

In endocrine shock the hormone disturbances are corrected. Hypothyroidism requires

supplementation by means of levothyroxine, in hyperthyroidism the production of
hormone by the thyroid is inhibited through thyreostatica, i.e. methimazole (Tapazole®)
or PTU (propylthiouracil). Adrenal insufficiency is treated by supplementing
corticosteroids.

Prognosis
The prognosis of shock depends on the underlying cause and the nature and extent of
concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily
treatable and respond well to medical therapy. Septic shock however, is a grave condition
and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is
even worse.

Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock

involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction
of the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood
in reinfused. In pigs and humans 1) this is not seen and cessation of bleeding and
restoration of blood volume is usually very effective; however 2) prolonged hypovolemia
and hypotension does carry a risk of respiratory and then cardiac arrest. Perfusion of the
brain may be the greatest danger during shock. Therefore urgent treatment (cessation of
bleeding, rapid restoration of circulating blood volume and ready respiratory support) is
essential for a good prognosis in hypovolemic shock.