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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.
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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
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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.
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
Superficial thickness Partial thickness — superficial
Erythema, minor pain, lack of blisters Blisters, clear fluid, and pain
Superficial (papillary) dermis
Partial thickness — deep
Whiter appearance, with decreased pain. Difficult to Deep (reticular) dermis distinguish from full thickness
Dermis and underlying Hard, leather-like eschar, Third- or fourthtissue 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. 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). 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. 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.
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.
A local anesthetic is usually sufficient in managing pain of minor first-degree and seconddegree 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. 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 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.
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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 extracellular 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. Reninangiotensin 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 Grampositive 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.
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 reestablishing 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
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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.
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.
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