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Burn


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Associate Editor-in-Chief: Eman Alademi, M.D.[3]

Keywords and : Fluid rescuscitation, Stress ulcers, Inhalation injury, Burn wound care, Skin substitutes, Electric injury, Hypermetabolis, Nutrition

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Eman Alademi, M.D.[2]

Overview

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

Historical Perspective

The first case of burns injury was discovered from more than 3,500 years ago. French barber-surgeon Ambroise Paré was the first to describe different degrees of burns in the 1500s. For many decades after original description, there was little progress in defining the pathogenesis of burns occurred and different treatment. In the 1900’s, it was found that the development of modern burn care began by Arabian physician his name Rhazes, at about the ninth century. In 1940’s major advances procedure was acknowledged(skin graft). to improve the body structure and early wound healing of patients. The term was subsequently formally adopted in medical nomenclature to describe individuals of all ages with a characteristic common symptom pattern, disease causes, and treatment.

Classification

Burns may be classified according to severity into first, second and third degree burn injury. It may also be classified based on superficial and deep categories into “Superficial Thickness” , “Partial Thickness” of burns.

Pathophysiology

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

Causes

Burn injury may be caused by chemicals, friction, electricity, radiation, extreme temperatures(hot and cold) and Inhalation injury in burns.

Differentiating (Disease name) from other Conditions

Epidemiology and Demographics

Burn injuries is the most frequently observed form of scald (thermal) injuries, and it typically develops in Children, younger children and younger patients. An estimated 1,344,100 fires Americans of all ages have burn injuries. An estimated patients aged 20 and 30 years are the most prevalent age group . Burn injuries has been known to affect females more than males. people of low and middle income and people in low-income countries are more likely to develop burn injuries than older whites. Pulmonary complications following burns and inhalation injury are responsible for up to 77 percent of the deaths.

Risk Factors

Natural History, Complications and Prognosis

Burns injuries is a common condition that involves complications such as the disability . If left untreated, progresses from early stage of burn to advanced skin scar and contraction. Common complications of burns injuries include infection, bedsores, post-burn seizures, hypertrophic scars and keloids, Respiratory complications, systemic complications. There is a cure for burns injuries and the treatment focuses on the stage of the burn( size and depth) so fluid resuscitation, wound excision, grafting and coverage, infection control and nutritional support can be part of the management of the burn injuries.

Diagnosis

History and Symptoms

Although each patient experiences burn injury in a unique way, there are many common symptoms. The symptoms of burn we can divided it in to two types, skin and airways symptoms.


Physical Examination

Patients with burn injury usually appear as burned(injury) skin . When a doctor or physician has been admitted burned patient, the diagnosis is usually known by physical examination of the patient. Physical examination of burn injury consists of a thorough of thickness and total body surface area of the patient body. Patient may be have burn on his head, neck, arm, leg, Anterior trunk,Posterior trunk, and genitalia.


Laboratory Findings

There are no specific diagnostic laboratory findings associated with burn injury. However, laboratory findings are done to the estimate the severity of the burn and the symptoms. These include CBC analysis like increase WBC for infection and inflammation , RBC decrease due to trauma of the burn, high hematocrit, because of lost a lot of fluid from leaky blood vessels. BUN reflects kidney damage, decrease total Protein, albumin, and globulin values (proteins have been lost through damaged blood vessels).


Electrocardiogram

ECG has minimal diagnostic value in diagnosing burns but plays a role in diagnosing concurrent conduction abnormalities and monitoring side effects of sever and electrical weapons . Electrocardiogram of a patient with acute burn injury may show prolonged QT and sinus tachycardia .Fatal cardiac arrest by electrical weapons .


Chest X Ray

Echocardiography or Ultrasound

Other Imaging Findings

CT scan of the burn may be helpful in the diagnosis of burn injury. Findings include skin thickening, subcutaneous soft tissue, and The deep fascia and underlying muscle layer. Computed tomography (CT) the chest evaluate the lungs for inhalation injury and smoke inhalation

Treatment

Medical Therapy

Surgery

Prevention

Education, engineering, and enforcement are often recommended as both a possible prevention and a sensible way of managing the burn injury. Combination of prevention and care strategies have made progress reducing the incidence of burn injuries and burn severity and lowering rates of burn death and length of hospital stay.


References

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor-In-Chief: Eman Alademi, M.D.[2]


Overview

The first case of burns injury was discovered from more than 3,500 years ago. French barber-surgeon Ambroise Paré was the first to describe different degrees of burns in the 1500s. For many decades after original description, there was little progress in defining the pathogenesis of burns occurred and different treatment. In the 1900’s, it was found that the development of modern burn care began by Arabian physician his name Rhazes, at about the ninth century. In 1940’s major advances procedure was acknowledged(skin graft). to improve the body structure and early wound healing of patients. The term was subsequently formally adopted in medical nomenclature to describe individuals of all ages with a characteristic common symptom pattern, disease causes, and treatment.

Historical Perspective

Burns injury was discovered from more than 3,500 years ago, since the people use the fire either to prepare the food or to warm themselves.

  • many types of treating records during the centuries, Egyptians treated burns by incantations and a mixture of gum, goat’s hair, and milk from a woman who had given birth to a son[1].
  • In the 1500 BCE (years before Christ) Smith papyrus reports of some type of linen strips soaked in an oily preparation ( honey and the salve of resin)[2].
    • (1) Celsus described treatment with a honey and bran, and then cork and ashes(wine and myrrh) documented to 100 CE.
    • (2) Pliny the Elder wondered if it would not be better to allow burns to remain exposed to the open air rather than covering them with grease.
  • Paulus of Aegina, a Byzantine of the seventh century A.D. whose writings reflected Greco-Roman thought, used various emollient preparations.
  • In the 1940s, the importance of early excision and skin grafting was acknowledged, and around the same time, fluid resuscitation and formulas to guide it were developed. In the 1970s, researchers demonstrated the significance of the hypermetabolic state that follows large burns [4][5][6][7].


References

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Eman Alademi, M.D.[2]


Overview

Burns may be classified according to severity into first, second and third degree burn injury. It may also be classified based on superficial and deep categories into “Superficial Thickness” , “Partial Thickness” of burns.

Classification

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:[1]The basis of burn classification is depth. When examining a burn, there are four components needed to assess depth: appearance, blanching to pressure, pain, and sensation.[2] Burns can be categorized by thickness according to the American Burn Criteria using those four elements. Burn injuries tend to be a dynamic process. Some burns, especially partial-thickness, may progress over 2 to 4 days, peaking at day 3.[3]

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.[5]

Table 1. A Description of the Traditional and Current Classifications of Burns

Template:Bgcolor-gold |Nomenclature Template:Bgcolor-gold |Traditional nomenclature Template:Bgcolor-gold |Depth Template:Bgcolor-gold |Clinical findings
Superficial thickness First-degree Epidermis involvement Erythema, minor pain, lack of blisters
Partial thickness — superficial Second-degree Superficial (papillary) dermis Blisters, clear fluid, and pain
Partial thickness — deep Second-degree Deep (reticular) dermis Whiter appearance, with decreased pain. Difficult to distinguish from full thickness
Full thickness Third- or fourth-degree Dermis and underlying tissue and possibly fascia, bone, or muscle Hard, leather-like eschar, purple fluid, no sensation (insensate)

Table 2. Scald Time (Hot Water)

Template:Bgcolor-gold |Temperature Template:Bgcolor-gold |Max duration until injury
155F (68.3C) 1 second
145F (62.9C) 3 seconds
135F (57.2C) 10 seconds
130F (54.4C) 30 seconds
125F (51.6C) 2 minutes
120F (48.8C) 5 minutes

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.

Table 3. Rule of Nines for Assessment of Total Body Surface Area Affected by a Burn – Adult
Template:Bgcolor-gold |Anatomic Structure Template:Bgcolor-gold |Surface Area
Head 9%
Anterior Torso 18%
Posterior Torso 18%
Each Leg 18%
Each Arm 9%
Perineum 1%
Table 4. Rule of Nines for Assessment of Total Body Surface Area Affected by a Burn – Infant
Template:Bgcolor-gold |Anatomic Structure Template:Bgcolor-gold |Surface Area
Head 18%
Anterior Torso 18%
Posterior Torso 18%
Each Leg 14%
Each Arm 9%
Perineum 1%

References

  1. Mertens DM, Jenkins ME, Warden GD (June 1997). “Outpatient burn management”. Nurs Clin North Am. 32 (2): 343–64. PMID 9115481.
  2. Toussaint J, Singer AJ (2014) The evaluation and management of thermal injuries: 2014 update. Clin Exp Emerg Med 1 (1):8-18. DOI:10.15441/ceem.14.029 PMID: 27752547 PMCID: PMC5052819 DOI: 10.15441/cee PMID: 27752547 PMCID: PMC5052819 DOI: 10.15441/cee
  3. 3.0 3.1 3.2 Evers LH, Bhavsar D, Mailänder P (2010) The biology of burn injury. Exp Dermatol 19 (9):777-83. DOI:10.1111/j.1600-0625.2010.01105.x PMID: 20629737 DOI: 10.1111/j.1600-0625.2010.01105 PMID: 20629737 DOI: 10.1111/j.1600-0625.2010.01105
  4. 4.0 4.1 Tolles J (2018) Emergency department management of patients with thermal burns. Emerg Med Pract 20 (2):1-24. PMID: 29369586 PMID: 29369586
  5. Evers LH, Bhavsar D, Mailänder P (September 2010). “The biology of burn injury”. Exp Dermatol. 19 (9): 777–83. doi:10.1111/j.1600-0625.2010.01105.x. PMID 20629737.

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Eman Alademi, M.D.[2]


Overview

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

Pathophysiology

Burns is the result of damage to the skin involving the two main layers – the thin, outer epidermis and the thicker, deeper dermis by a temperatures greater than 44 °C (111 °F), leads to cell and tissue damage because of breaking down of the cells proteins then start losing their three-dimensional shape. Burn caused by[1][2]:

  • Electrical injuries (can be deceiving with small entry and exit wounds, however, there may be extensive internal organ injury or associated traumatic injuries).
• Obvious pattern from cigarettes, lighters, irons
• Burns to soles, palms, genitalia, buttocks, perineum
• Symmetrical burns of uniform depth
• No splash marks in a scald injury. A child falling into a bath will splash; one that is placed into it may not
• Restraint injuries on upper limbs
• Is there sparing of flexion creases—that is, was child in fetal position (position of protection) when burnt? Does this correlate to a “tide line” of scald—that is, if child is put into a fetal position, do the burns line up?
• “Doughnut sign,” an area of spared skin surrounded by scald. If a child is forcibly held down in a bath of hot water, the part in contact with the bottom of the bath will not burn, but the tissue around will
• Other signs of physical abuse—bruises of varied age, poorly kempt, lack of compliance with health care (such as no immunisations)


Most burns are small and superficial causing only local injuries, However, burns can be larger and deeper, and patients can also have a systemic response to severe burns[5][6]

Local response

The three zones of a burn were described by Jackson in 1947.

Zone of coagulation—This occurs at the point of maximum damage. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins.

Zone of stasis—The surrounding zone of stasis is characterized by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The main aim of burns resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults—such as prolonged hypotension, infection, or edema—can convert this zone into an area of complete tissue loss.

Zone of hyperemia—In this outermost zone tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion.

These three zones of a burn are three dimensional, and loss of tissue in the zone of stasis will lead to the wound deepening as well as widening.

Systemic response

The increase of the catecholamines and cortisol,or The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 30% of total body surface area and the site of injury lead to:

  1. Cardiovascular system changes—Capillary permeability is increased, leading to loss of intravascular proteins and fluids into the interstitial compartment. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased, possibly due to release of tumor necrosis factor α (TNFα). These change[7][8]s, coupled with fluid loss from the burn wound,[9] result in systemic hypotension and end organ hypoperfusion because of Increased levels of catecholamines. and a fast heart rate[10]
  2. Renal system changes—kidney failure because of the Poor blood flow to organs.[11]
  3. Respiratory system changes—Inflammatory mediators cause bronchoconstriction, and in severe burns adult respiratory distress syndrome can occur.
  4. Gastrointestinal system changes— stomach ulcers because of the Poor blood flow to organs.[12][13][14][15][16][17]
  5. Skin[18][19][20][21]
  6. Immune system changes—Non-specific down regulation of the immune response occurs, affecting both cell mediated and humeral pathway[22][23][24].[25][26]
  7. Metabolic changes—The basal metabolic rate increases up (hypermetabolic) to three times its original rate because of Increased levels of catecholamines and cortisol . This, coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity. Immunological[27][28][29]
  8. Increased leakage of fluid from the capillaries, and subsequent tissue edema. This causes overall blood volume loss, with the remaining blood suffering significant plasma loss, making the blood more concentrated.[30]




Gross Pathology

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Trachea, thermal burn smoke inhalation
Lung, thermal burn smoke inhalation
Ischemia: Gross natural color close-up of liver with shock necrosis and a large area of necrosis beneath capsule quite good burn sepsis DIC
Small intestine: Ischemia: Gross natural color frankly gangrenous gut shown rather close-up excellent example burn sepsis DIC
Kidney: Bilateral Cortical Necrosis: Gross natural color excellent gross example showing capsular and cut surfaces burn case
Kidney: Acute Tubular Necrosis: Gross good example swollen cortex secondary to body burn
Kidney: Acute Pyelonephritis: Gross cut surface obvious abscesses burn case with Pseudomonas sepsis
Brain: Bacterial Meningitis: Gross base of frontal lobes well shown meningitis burn case with Pseudomonas sepsis
Stomach: Curlings Ulcers: Gross natural color multiple superficial mucosal ulcers well shown in fundus and prepyloric area in lesser curvature. A good example of burn patient
Thyroid: Fibrosis: Gross natural color cross section into fibrotic and apparently contracted gland can be used as an example of burned out thyroiditis or what we used to call Riedels struma
























References

  1. Stiles K (July 2018). “Emergency management of burns: part 2”. Emerg Nurse. 26 (2): 36–41. PMID 30095874.
  2. “Burn Evaluation And Management – StatPearls – NCBI Bookshelf”.
  3. Hettiaratchy S, Dziewulski P (2004) ABC of burns: pathophysiology and types of burns. BMJ 328 (7453):1427-9. DOI:10.1136/bmj.328.7453.1427 PMID: 15191982 PMID: 15191982
  4. “Pathophysiology and Current Management of Burn Injury : Advances in Skin & Wound Care”.
  5. “ABC of burns: Pathophysiology and types of burns”.
  6. Rojas Y, Finnerty CC, Radhakrishnan RS, Herndon DN (December 2012). “Burns: an update on current pharmacotherapy”. Expert Opin Pharmacother. 13 (17): 2485–94. doi:10.1517/14656566.2012.738195. PMC 3576016. PMID 23121414.
  7. Jeschke MG, Patsouris D, Stanojcic M, Abdullahi A, Rehou S, Pinto R; et al. (2015). “Pathophysiologic Response to Burns in the Elderly”. EBioMedicine. 2 (10): 1536–48. doi:10.1016/j.ebiom.2015.07.040. PMC 4634201. PMID 26629550.
  8. Rehou S, Shahrokhi S, Thai J, Stanojcic M, Jeschke MG (2019). “Acute Phase Response in Critically Ill Elderly Burn Patients”. Crit Care Med. 47 (2): 201–209. doi:10.1097/CCM.0000000000003516. PMID 30371519.
  9. Van de Veire NR, De Backer J, Ascoop AK, Middernacht B, Velghe A, Sutter JD (2006). “Echocardiographically estimated left ventricular end-diastolic and right ventricular systolic pressure in normotensive healthy individuals”. Int J Cardiovasc Imaging. 22 (5): 633–41. doi:10.1007/s10554-006-9082-y. PMID 16541230.
  10. Ogawa T, Spina RJ, Martin WH, Kohrt WM, Schechtman KB, Holloszy JO; et al. (1992). “Effects of aging, sex, and physical training on cardiovascular responses to exercise”. Circulation. 86 (2): 494–503. doi:10.1161/01.cir.86.2.494. PMID 1638717.
  11. Nyengaard JR, Bendtsen TF (1992). “Glomerular number and size in relation to age, kidney weight, and body surface in normal man”. Anat Rec. 232 (2): 194–201. doi:10.1002/ar.1092320205. PMID 1546799.
  12. Clayton NA, Nicholls CM, Blazquez K, Brownlow C, Maitz PK, Fisher OM; et al. (2018). “Dysphagia in older persons following severe burns: Burn location is irrelevant to risk of dysphagia and its complications in patients over 75 years”. Burns. 44 (8): 1997–2005. doi:10.1016/j.burns.2018.07.010. PMID 30107942.
  13. Pablo AM, Izaga MA, Alday LA (2003). “Assessment of nutritional status on hospital admission: nutritional scores”. Eur J Clin Nutr. 57 (7): 824–31. doi:10.1038/sj.ejcn.1601616. PMID 12821882.
  14. Gariballa SE, Sinclair AJ (1998). “Nutrition, ageing and ill health”. Br J Nutr. 80 (1): 7–23. doi:10.1017/s000711459800172x. PMID 9797639.
  15. Jeschke MG, Patsouris D, Stanojcic M, Abdullahi A, Rehou S, Pinto R; et al. (2015). “Pathophysiologic Response to Burns in the Elderly”. EBioMedicine. 2 (10): 1536–48. doi:10.1016/j.ebiom.2015.07.040. PMC 4634201. PMID 26629550.
  16. Rosenfeld RM, Schwartz SR, Cannon CR, Roland PS, Simon GR, Kumar KA; et al. (2014). “Clinical practice guideline: acute otitis externa”. Otolaryngol Head Neck Surg. 150 (1 Suppl): S1–S24. doi:10.1177/0194599813517083. PMID 24491310.
  17. Okaya T, Blanchard J, Schuster R, Kuboki S, Husted T, Caldwell CC; et al. (2005). “Age-dependent responses to hepatic ischemia/reperfusion injury”. Shock. 24 (5): 421–7. doi:10.1097/01.shk.0000181282.14050.11. PMID 16247327.
  18. Goodson WH, Hunt TK (1979). “Wound healing and aging”. J Invest Dermatol. 73 (1): 88–91. doi:10.1111/1523-1747.ep12532775. PMID 448182.
  19. Gosain A, DiPietro LA (2004). “Aging and wound healing”. World J Surg. 28 (3): 321–6. doi:10.1007/s00268-003-7397-6. PMID 14961191.
  20. Zouboulis CC, Makrantonaki E (2011). “Clinical aspects and molecular diagnostics of skin aging”. Clin Dermatol. 29 (1): 3–14. doi:10.1016/j.clindermatol.2010.07.001. PMID 21146726.
  21. Farage MA, Miller KW, Elsner P, Maibach HI (2013). “Characteristics of the Aging Skin”. Adv Wound Care (New Rochelle). 2 (1): 5–10. doi:10.1089/wound.2011.0356. PMC 3840548. PMID 24527317.
  22. Emami SA, Motevalian SA, Momeni M, Karimi H (2016). “The epidemiology of geriatric burns in Iran: A national burn registry-based study”. Burns. 42 (5): 1128–1132. doi:10.1016/j.burns.2016.03.011. PMID 27126815.
  23. Fitzwater J, Purdue GF, Hunt JL, O’Keefe GE (2003). “The risk factors and time course of sepsis and organ dysfunction after burn trauma”. J Trauma. 54 (5): 959–66. doi:10.1097/01.TA.0000029382.26295.AB. PMID 12777910.
  24. Frankel JH, Boe DM, Albright JM, O’Halloran EB, Carter SR, Davis CS; et al. (2018). “Age-related immune responses after burn and inhalation injury are associated with altered clinical outcomes”. Exp Gerontol. 105: 78–86. doi:10.1016/j.exger.2017.10.022. PMC 5871535. PMID 29080833.
  25. Jagger A, Shimojima Y, Goronzy JJ, Weyand CM (2014). “Regulatory T cells and the immune aging process: a mini-review”. Gerontology. 60 (2): 130–7. doi:10.1159/000355303. PMC 4878402. PMID 24296590.
  26. Franceschi C, Bonafè M, Valensin S, Olivieri F, De Luca M, Ottaviani E; et al. (2000). “Inflamm-aging. An evolutionary perspective on immunosenescence”. Ann N Y Acad Sci. 908: 244–54. doi:10.1111/j.1749-6632.2000.tb06651.x. PMID 10911963.
  27. Ward J, Phillips G, Radotra I, Smailes S, Dziewulski P, Zhang J; et al. (2018). “Frailty: an independent predictor of burns mortality following in-patient admission”. Burns. 44 (8): 1895–1902. doi:10.1016/j.burns.2018.09.022. PMID 30361081.
  28. Romanowski KS, Barsun A, Pamlieri TL, Greenhalgh DG, Sen S (2015). “Frailty score on admission predicts outcomes in elderly burn injury”. J Burn Care Res. 36 (1): 1–6. doi:10.1097/BCR.0000000000000190. PMID 25383979.
  29. Herndon DN, Tompkins RG (2004). “Support of the metabolic response to burn injury”. Lancet. 363 (9424): 1895–902. doi:10.1016/S0140-6736(04)16360-5. PMID 15183630.
  30. “Porth Pathophysiology: Concepts of Altered Health States – Charlotte Pooler – كتب Google”.

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:Eman Alademi, M.D.[2]

Overview:

Burn injury may be caused by chemicals, friction, electricity, radiation, extreme temperatures(hot and cold) and Inhalation injury in burns.

Causes

Burns may be caused by a wide variety of substances and external sources such as exposure to chemicals[1]. friction, electricity, radiation, and extreme temperatures, both hot and cold.

Chemical Burns

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 [2]can cause damage down to the bone and its burns are sometimes not immediately evident.[3][4]

Electrical Burns

Electrical burns are generally caused by an exogenous electric shock, such as being struck by lightning[5][6][7][8]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

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[9], swelling, and inflammation. More severe cases of sun burn result in what is known as sun poisoning.

Scalding

Two day-old scald caused by boiling radiator fluid.

Scalding [10]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.[11][12]

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

Frostbitten hands

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 liquid discharged from an upside-down gas duster. 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.

Inhalation injury in burns:

pulmonary complications were common in burn patients, inhalational injury has now replaced these two causes as the main cause of mortality in burn patients. Inhalational injury by itself has been shown to be associated with pulmonary dysfunction for at least 6 months after the injury. Pulmonary complications in burn patients can arise from direct injury to the respiratory tract via the inhalation of heated air and chemicals released by combustion, and also iatrogenic factors such as fluid-overloading during resuscitation and lung damage by mechanical ventilation.

References

  1. Pruitt VM (2006). “Work-related burns”. Clin Occup Environ Med. 5 (2): 423–33, ix–x. doi:10.1016/j.coem.2005.11.002. PMID 16647659.
  2. Makarovsky I, Markel G, Dushnitsky T, Eisenkraft A (2008) Hydrogen fluoride–the protoplasmic poison. Isr Med Assoc J 10 (5):381-5. PMID: 18605366 PMID: 18605366
  3. Brent J (2013). “Water-based solutions are the best decontaminating fluids for dermal corrosive exposures: a mini review”. Clin Toxicol (Phila). 51 (8): 731–6. doi:10.3109/15563650.2013.838628. PMID 24003912.
  4. Hardwicke J, Hunter T, Staruch R, Moiemen N (2012) Chemical burns–an historical comparison and review of the literature. Burns 38 (3):383-7. DOI:10.1016/j.burns.2011.09.014 PMID: 22037150 DOI: 10.1016/j.burns.2011.09.014 PMID: 22037150 DOI: 10.1016/j.burns.2011.09.014
  5. Baxter CR, Waeckerle JF (1988). “Emergency treatment of burn injury”. Ann Emerg Med. 17 (12): 1305–15. doi:10.1016/s0196-0644(88)80356-1. PMID 3057947.
  6. Cooper MA (1984). “Electrical and lightning injuries”. Emerg Med Clin North Am. 2 (3): 489–501. PMID 6534739.
  7. Spies C, Trohman RG (2006). “Narrative review: Electrocution and life-threatening electrical injuries”. Ann Intern Med. 145 (7): 531–7. doi:10.7326/0003-4819-145-7-200610030-00011. PMID 17015871.
  8. Browne BJ, Gaasch WR (1992). “Electrical injuries and lightning”. Emerg Med Clin North Am. 10 (2): 211–29. PMID 1559466.
  9. Balk SJ, Council on Environmental Health. Section on Dermatology (2011) Ultraviolet radiation: a hazard to children and adolescents. Pediatrics 127 (3):e791-817. DOI:10.1542/peds.2010-3502 PMID: 21357345 DOI: 10.1542/peds.2010-3502 PMID: 21357345 DOI: 10.1542/peds.2010-3502
  10. Maguire S, Moynihan S, Mann M, Potokar T, Kemp AM (2008) A systematic review of the features that indicate intentional scalds in children. Burns 34 (8):1072-81. DOI:10.1016/j.burns.2008.02.011 PMID: 18538478 DOI: 10.1016/j.burns.2008.02.011 PMID: 18538478 DOI: 10.1016/j.burns.2008.02.011
  11. Baxter CR (1993). “Management of burn wounds”. Dermatol Clin. 11 (4): 709–14. PMID 8222354.
  12. Mertens DM, Jenkins ME, Warden GD (1997). “Outpatient burn management”. Nurs Clin North Am. 32 (2): 343–64. PMID 9115481.

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Epidemiology and Demographics

Editor-In-Chief: Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1][[2]] Associate Editor(s)-in-Chief:Eman Alademi, M.D.[3]

Overview

Burn injuries is the most frequently observed form of scald (thermal) injuries, and it typically develops in Children, younger children and younger patients. An estimated 1,344,100 fires Americans of all ages have burn injuries. An estimated patients aged 20 and 30 years are the most prevalent age group . Burn injuries has been known to affect females more than males. people of low and middle income and people in low-income countries are more likely to develop burn injuries than older whites. Pulmonary complications following burns and inhalation injury are responsible for up to 77 percent of the deaths.

Epidemiology and Demographics

  • In the 10 years from 2008 to 2017, the incidence in the United States of burns is approximately 1,344,100 fires, resulting in deaths per 100,000 individuals with a case-fatality rate of 3190 civilian, 16,225 civilian injuries.
  • Patients of all age groups may develop burns injury, but flame and scale burns it’s commonly affects individuals Children and younger(children younger than five years old are more often injured with scald burns) than/older(More adults are injured with flame burns ). patients aged between 20 and 30 years are the most prevalent age group, representing 15 percent of cases [3]. Older adults are most likely to sustain a burn in the bathroom, followed by the kitchen[4] . Pediatric burns occur more commonly in the home (84 percent) when children are unsupervised (80 percent)[5][6] .
  • There is no racial predilection to burn injury.
  • Armed conflict increases the incidence of burns, as shown by a survey of burns in Baghdad that demonstrated a rise in incidence from 30 per 100,000 in 2003 to 117 per 100,000 after invasion[21]

References

  1. Stamm O, Latscha U, Janecek P, Campana A (1976) Development of a special electrode for continuous subcutaneous pH measurement in the infant scalp. Am J Obstet Gynecol 124 (2):193-5. DOI:10.1016/s0002-9378(16)33297-5 PMID: . 2012 Dec 15;380(9859):2095-128. doi: 10.1 Lancet . 2012 Dec 15;380(9859):2095-128. doi: 10.1
  2. 2.0 2.1 “Burn Evaluation And Management – StatPearls – NCBI Bookshelf”.
  3. GBD 2015 Mortality and Causes of Death Collaborators (2016) Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 388 (10053):1459-1544. DOI:10.1016/S0140-6736(16)31012-1 PMID: 27733281 PMID: 27733281
  4. Mabrouk A, Maher A, Nasser S (2003). “An epidemiologic study of elderly burn patients in Ain Shams University Burn Unit, Cairo, Egypt”. Burns. 29 (7): 687–90. doi:10.1016/s0305-4179(03)00071-8. PMID 14556726.
  5. Forjuoh SN (2006). “Burns in low- and middle-income countries: a review of available literature on descriptive epidemiology, risk factors, treatment, and prevention”. Burns. 32 (5): 529–37. doi:10.1016/j.burns.2006.04.002. PMID 16777340.
  6. Rossi LA, Braga EC, Barruffini RC, Carvalho EC (1998). “Childhood burn injuries: circumstances of occurrences and their prevention in Ribeirão Preto, Brazil”. Burns. 24 (5): 416–9. doi:10.1016/s0305-4179(98)00046-1. PMID 9725680.
  7. Ribeiro, Priscila S.; Jacobsen, Kathryn H.; Mathers, Colin D.; Garcia-Moreno, Claudia (2008). “Priorities for women’s health from the Global Burden of Disease study”. International Journal of Gynecology & Obstetrics. 102 (1): 82–90. doi:10.1016/j.ijgo.2008.01.025. ISSN 0020-7292.
  8. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators (2016) Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 388 (10053):1545-1602. DOI:10.1016/S0140-6736(16)31678-6 PMID: 27733282 PMID: 27733282
  9. Haagsma, Juanita A; Graetz, Nicholas; Bolliger, Ian; Naghavi, Mohsen; Higashi, Hideki; Mullany, Erin C; Abera, Semaw Ferede; Abraham, Jerry Puthenpurakal; Adofo, Koranteng; Alsharif, Ubai; Ameh, Emmanuel A; Ammar, Walid; Antonio, Carl Abelardo T; Barrero, Lope H; Bekele, Tolesa; Bose, Dipan; Brazinova, Alexandra; Catalá-López, Ferrán; Dandona, Lalit; Dandona, Rakhi; Dargan, Paul I; De Leo, Diego; Degenhardt, Louisa; Derrett, Sarah; Dharmaratne, Samath D; Driscoll, Tim R; Duan, Leilei; Petrovich Ermakov, Sergey; Farzadfar, Farshad; Feigin, Valery L; Franklin, Richard C; Gabbe, Belinda; Gosselin, Richard A; Hafezi-Nejad, Nima; Hamadeh, Randah Ribhi; Hijar, Martha; Hu, Guoqing; Jayaraman, Sudha P; Jiang, Guohong; Khader, Yousef Saleh; Khan, Ejaz Ahmad; Krishnaswami, Sanjay; Kulkarni, Chanda; Lecky, Fiona E; Leung, Ricky; Lunevicius, Raimundas; Lyons, Ronan Anthony; Majdan, Marek; Mason-Jones, Amanda J; Matzopoulos, Richard; Meaney, Peter A; Mekonnen, Wubegzier; Miller, Ted R; Mock, Charles N; Norman, Rosana E; Orozco, Ricardo; Polinder, Suzanne; Pourmalek, Farshad; Rahimi-Movaghar, Vafa; Refaat, Amany; Rojas-Rueda, David; Roy, Nobhojit; Schwebel, David C; Shaheen, Amira; Shahraz, Saeid; Skirbekk, Vegard; Søreide, Kjetil; Soshnikov, Sergey; Stein, Dan J; Sykes, Bryan L; Tabb, Karen M; Temesgen, Awoke Misganaw; Tenkorang, Eric Yeboah; Theadom, Alice M; Tran, Bach Xuan; Vasankari, Tommi J; Vavilala, Monica S; Vlassov, Vasiliy Victorovich; Woldeyohannes, Solomon Meseret; Yip, Paul; Yonemoto, Naohiro; Younis, Mustafa Z; Yu, Chuanhua; Murray, Christopher J L; Vos, Theo; Balalla, Shivanthi; Phillips, Michael R (2016). “The global burden of injury: incidence, mortality, disability-adjusted life years and time trends from the Global Burden of Disease study 2013”. Injury Prevention. 22 (1): 3–18. doi:10.1136/injuryprev-2015-041616. ISSN 1353-8047.
  10. Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V | display-authors=etal (2012) Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 380 (9859):2095-128. DOI:10.1016/S0140-6736(12)61728-0 PMID: 23245604 DOI: 10.1016/S0140-6736(12)61728-0 PMID: 23245604 DOI: 10.1016/S0140-6736(12)61728-0
  11. Rossi LA, Braga EC, Barruffini RC, Carvalho EC (1998). “Childhood burn injuries: circumstances of occurrences and their prevention in Ribeirão Preto, Brazil”. Burns. 24 (5): 416–9. doi:10.1016/s0305-4179(98)00046-1. PMID 9725680.
  12. Forjuoh SN (1998). “The mechanisms, intensity of treatment, and outcomes of hospitalized burns: issues for prevention”. J Burn Care Rehabil. 19 (5): 456–60. PMID 9789183.
  13. Forjuoh SN (1998). “The mechanisms, intensity of treatment, and outcomes of hospitalized burns: issues for prevention”. J Burn Care Rehabil. 19 (5): 456–60. PMID 9789183.
  14. Híjar-Medina MC, Tapia-Yáñez JR, Lozano-Ascencio R, López-López MV (1992). “[Home accidents in children less than 10 years of age: causes and consequences]”. Salud Publica Mex. 34 (6): 615–25. PMID 1475697.
  15. Sanghavi P, Bhalla K, Das V (2009). “Fire-related deaths in India in 2001: a retrospective analysis of data”. Lancet. 373 (9671): 1282–8. doi:10.1016/S0140-6736(09)60235-X. PMID 19250664.
  16. Ryan CM, Schoenfeld DA, Thorpe WP, Sheridan RL, Cassem EH, Tompkins RG (1998). “Objective estimates of the probability of death from burn injuries”. N Engl J Med. 338 (6): 362–6. doi:10.1056/NEJM199802053380604. PMID 9449729 PMID: 9449729 Check |pmid= value (help).
  17. Darling GE, Keresteci MA, Ibañez D, Pugash RA, Peters WJ, Neligan PC (1996). “Pulmonary complications in inhalation injuries with associated cutaneous burn”. J Trauma. 40 (1): 83–9. doi:10.1097/00005373-199601000-00016. PMID 8577005.
  18. Carr JA, Phillips BD, Bowling WM (2009). “The utility of bronchoscopy after inhalation injury complicated by pneumonia in burn patients: results from the National Burn Repository”. J Burn Care Res. 30 (6): 967–74. doi:10.1097/BCR.0b013e3181bfb77b. PMID 19826269.
  19. Guo F, Chen XL, Wang YJ, Wang F, Chen XY, Sun YX (2009). “Management of burns of over 80% of total body surface area: a comparative study”. Burns. 35 (2): 210–4. doi:10.1016/j.burns.2008.05.021. PMID 18786768.
  20. Shirani KZ, Pruitt BA, Mason AD (1987). “The influence of inhalation injury and pneumonia on burn mortality”. Ann Surg. 205 (1): 82–7. doi:10.1097/00000658-198701000-00015. PMC 1492872. PMID 3800465.
  21. Stewart BT, Lafta R, Esa Al Shatari SA, Cherewick M, Burnham G, Hagopian A; et al. (2016). “Burns in Baghdad from 2003 to 2014: Results of a randomized household cluster survey”. Burns. 42 (1): 48–55. doi:10.1016/j.burns.2015.10.002. PMC 4724468. PMID 26526376.

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Natural History, Complications and Prognosis


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Eman Alademi, M.D.[2]


Overview

Burns injuries is a common condition that involves complications such as the disability . If left untreated, progresses from early stage of burn to advanced skin scar and contraction. Common complications of burns injuries include infection, bedsores, post-burn seizures, hypertrophic scars and keloids, Respiratory complications, systemic complications. There is a cure for burns injuries and the treatment focuses on the stage of the burn( size and depth) so fluid resuscitation, wound excision, grafting and coverage, infection control and nutritional support can be part of the management of the burn injuries.

Natural History

Patients with burn injury If left untreated[1], may progress to develop[2]:


  • infection and sepsis“: burn infection, Wound-associated inflammation is limited by immediate debridement of devitalized tissue and tangential excision of burn tissue and wound closure, primarily by skin grafts, within 48 hours of a full-thickness burn[3][4]. ( “Hypermetabolic response to moderate-to-severe burn injury and management”, section on ‘Early excision and grafting’ and “Burn wound)

In general, the burn wound or lungs are the most likely sites for an infection in the severely burned patient that subsequently develops MODS[12][13]. The release of endotoxins and/or exotoxins from an infective process initiates a cascade of inflammatory mediators that leads to organ damage and ultimately organ failure. Targeting the different cascade systems involved in the pathogenesis of burn-induced MODS is often not a feasible option[14].

Prevention:

Prevention of sepsis from burn wound infection is the most promising approach and illustrated by:

1. physiologically: such as the recognition of the importance of burn surface area, infection control and nutritional support and skin grafting and coverage,, [15]However, this was not reflected in improving survival and many patients still died of shock and infection

2.psychologically.[16]



Prognosis

Prognosis is generally depend on the etiological characteristics of the different age groups that should be considered for prevention. BI can be a reliable index of prognosis in severely burned patients. The results of the study showed that a large BI, elderly age, delayed admission after injury and combined inhalation injury are the main risk factors for extensively burned patients. [17][18][19].


References

  1. Janzekovic Z (1975). “The burn wound from the surgical point of view”. J Trauma. 15 (1): 42–62. PMID 1090743.
  2. “Fiona Wood | Australian surgeon | Britannica”.
  3. Janzekovic Z (January 1975). “The burn wound from the surgical point of view”. J Trauma. 15 (1): 42–62. PMID 1090743.
  4. Chan BP, Kochevar IE, Redmond RW (November 2002). “Enhancement of porcine skin graft adherence using a light-activated process”. J Surg Res. 108 (1): 77–84. doi:10.1006/jsre.2002.6516. PMID 12443718.
  5. A review of the complications of burns, their origin and importance for illness and death – Abstract J Trauma. 1979 May;19(5):358-69. Accessed February 27, 2008
  6. Sevitt S, Schmoldt A, Benthe HF, Haberland G, Ward CW, Thompson HC, Eisenstein TK, Schmoldt A, Benthe HF, Haberland G (May 1979). “A review of the complications of burns, their origin and importance for illness and death”. J Trauma. 19 (5): 358–69. doi:10.1097/00005373-197905000-00010. PMC 420673. PMID 448773.
  7. Janzekovic Z (1975). “The burn wound from the surgical point of view”. J Trauma. 15 (1): 42–62. PMID 1090743.
  8. Greenhalgh DG, Saffle JR, Holmes JH, Gamelli RL, Palmieri TL, Horton JW; et al. (2007). “American Burn Association consensus conference to define sepsis and infection in burns”. J Burn Care Res. 28 (6): 776–90. doi:10.1097/BCR.0b013e3181599bc9. PMID 17925660 DOI: 10.1097/BCR.0b013e3181599bc9 A PMID: 17925660 DOI: 10.1097/BCR.0b013e3181599bc9 A Check |pmid= value (help).
  9. Cumming J, Purdue GF, Hunt JL, O’Keefe GE (2001). “Objective estimates of the incidence and consequences of multiple organ dysfunction and sepsis after burn trauma”. J Trauma. 50 (3): 510–5. doi:10.1097/00005373-200103000-00016. PMID 11265031.
  10. Meakins JL (1990). “Etiology of multiple organ failure”. J Trauma. 30 (12 Suppl): S165–8. doi:10.1097/00005373-199012001-00033. PMID 2254977 DOI: 10.1097/00005373-199012001-0003 PMID: 2254977 DOI: 10.1097/00005373-199012001-0003 Check |pmid= value (help).
  11. Williams FN, Herndon DN, Hawkins HK, Lee JO, Cox RA, Kulp GA; et al. (2009). “The leading causes of death after burn injury in a single pediatric burn center”. Crit Care. 13 (6): R183. doi:10.1186/cc8170. PMC 2811947. PMID 19919684.
  12. Herndon DN, Tompkins RG (2004). “Support of the metabolic response to burn injury”. Lancet. 363 (9424): 1895–902. doi:10.1016/S0140-6736(04)16360-5. PMID 15183630.
  13. McCowen KC, Malhotra A, Bistrian BR (2001). “Stress-induced hyperglycemia”. Crit Care Clin. 17 (1): 107–24. doi:10.1016/s0749-0704(05)70154-8. PMID 11219223.
  14. “Burn-Induced Coagulopathies: a Comprehensive Review”.
  15. Herndon DN, Tompkins RG (June 2004). “Support of the metabolic response to burn injury”. Lancet. 363 (9424): 1895–902. doi:10.1016/S0140-6736(04)16360-5. PMID 15183630.
  16. “History of burns: The past, present and the future | Burns & Trauma | Full Text”.
  17. Cheng W, Shen C, Zhao D, Zhang H, Tu J, Yuan Z, Song G, Liu M, Li D, Shang Y, Qin B, Schmoldt A, Benthe HF, Haberland G, Tarentino AL, Maley F, Kidder GW, Montgomery CW, Moroi K, Sato T, Moroi K, Sato T (May 2019). “The epidemiology and prognosis of patients with massive burns: A multicenter study of 2483 cases”. Burns. 45 (3): 705–716. doi:10.1016/j.burns.2018.08.008. PMID 30837206.
  18. Mann R, Heimbach D, Claeyssens M, Henrissat B (October 1996). “Prognosis and treatment of burns”. West. J. Med. 165 (4): 215–20. doi:10.1002/pro.5560011008. PMC 1303748. PMID 8987427.
  19. Colohan SM, Schmoldt A, Benthe HF, Haberland G, Ward CW, Järvisalo J, Saris NE, Palmer GC, Manian AA, Wiesmann UN, DiDonato S, Herschkowitz NN, Bauer C (September 1975). “Predicting prognosis in thermal burns with associated inhalational injury: a systematic review of prognostic factors in adult burn victims”. J Burn Care Res. 31 (4): 529–39. doi:10.1097/BCR.0b013e3181e4d680. PMID 20523229.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-ray |CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

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