Materiały źródłowe

• #1 Chemical Burns – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499888/

  Healthcare professionals should understand chemical burns from exposure to acids (pH less than 7), alkalis (pH greater than 7), and irritants to recognize, manage and care for these common types of injury. […] Chemical burns cause damage as a result of irritant properties, acidity/alkalinity, concentration, form, amount of contact, the length of exposure, and location of contact. For example, contact with a mucosal surface such as the eye is likely to cause earlier and more extensive damage than contact with intact skin where there may be some barrier protection. After inadvertent or intentional ingestion, there will be prompt contact with the mucosal surface and both direct and absorptive toxicity. […] After exposure to an alkaline agent, the -OH moiety causes injury due to liquefaction necrosis, which leads to often irreversible changes in the protein matrix. Additionally, there is vascular damage that can create a local or systemic effect.

• #2 Chemical Burns: Types, Complications, & Management

  https://www.theplasticsfella.com/chemical-burns/

  The most common chemical burns are acids and alkalis. This article details their mechanisms, clinical features, and management. […] Chemical burns can be broadly categorised into 4 main groups: acids, burns, organic solvents, and inorganic solvents. They differ in their pathophysiology, clinical progression, and potential complications. […] The degree of chemical burn is dependent upon the following variables: Type and extent of exposure (skin, mucosa, inhalation), Type of chemical agent and its mechanism of action, Quantity, strength, or concentration of agent. […] Unlike thermal burns, chemical burns will continue their tissue destruction until inactivated by a neutralising agent. […] Each chemical has its own mechanism of burn. As a result, each chemical can often have a specific set of secondary clinical presentations. […] Chemical burns are generally treated with prompt and constant water irrigation with some exceptions. […] In addition to the above management, hydrofluoric acid requires neutralisation with calcium gluconate to inactivate free fluoride ions.

• #3 The chemical burns – Ouvry – CBRN Protective System

  https://ouvry.com/en/the-chemical-burns/

  Chemical burns are rare (1-2% of burns) and most often ocular (50% of chemical burns), but unlike a thermal burn, chemical burns continue to evolve until they are chemically neutralized. […] The severity of a chemical burn is directly related to: the nature of the product (penetrating power and mode of action); the amount of product; the concentration of the product used; the duration of contact between the skin and the chemical; the nature of the exposed tissue; the eye is more fragile than the skin; toxicity by absorption by a mucosa is very important. […] Six mechanisms predominate: oxidation-reduction, the chemical causes cell destruction; desiccation, dehydration processes; the exothermic reaction causes thermal burning; saponification of fats, skin lysis due to alteration of fatty elements; coagulation of proteins, liquefaction of proteins.

• #4 Chemical Burns – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK499888/

  Acidic agents cause coagulation necrosis, which leads to cytotoxicity. Additionally, there are mucosal or skin changes that may prevent further toxicity and limit absorption. […] Overall, alkaline agents are more toxic than acidic agents, due to the irreversible changes in protein and tissue damage.

• #5 Chemical Burns: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/769336-overview

  Chemical burns can be caused by acids or bases that come into contact with tissue. Acids are defined as proton donors (H+), and bases are defined as proton acceptors (OH-). Bases also are known as alkalis. Both acids and bases can be defined as caustics, which cause significant tissue damage on contact. The strength of an acid is defined by how easily it gives up the proton; the strength of a base is determined by how avidly it binds the proton. The strength of acids and bases is defined by using the pH scale, which ranges from 1-14 and is logarithmic. A strong acid has a pH of 1, and a strong base has a pH of 14. A pH of 7 is neutral. […] Most acids produce a coagulation necrosis by denaturing proteins, forming a coagulum (eg, eschar) that limits the penetration of the acid. Bases typically produce a more severe injury known as liquefaction necrosis. This involves denaturing of proteins as well as saponification of fats, which does not limit tissue penetration. Hydrofluoric acid is somewhat different from other acids in that it produces a liquefaction necrosis.

• #6 Chemical burns

  https://dermnetnz.org/topics/chemical-burn

  Chemical burn is a burn to internal or external organs of the body caused by a corrosive or caustic chemical substance that is a strong acid or base (also known as alkali). […] The main cause of chemical burn is contact with strong acids or bases. […] A very strong acid has a pH of 1 and may cause a severe burn. […] A very strong base has a pH of 14 and may also cause a severe burn. […] Some signs and symptoms of chemical burns include: Formation of black dead skin (eschar) this occurs particularly with acid chemical burns as they produce a coagulation necrosis by denaturing proteins. […] Deep tissue injury to the skin is caused by alkali chemical burns, as they produce a liquefaction necrosis that involves denaturing of proteins as well as saponification of fats. […] In severe chemical burns where the agent has been swallowed, inhaled or absorbed into the bloodstream, the following systemic symptoms may occur.

• #7 Chemical burns – pathophysiology and treatment – handout | PDF

  https://www.slideshare.net/slideshow/chemical-burns-pathophysiology-and-treatment-handout-25126187/25126187

  Mechanisms of action (1) Oxidation: The protein denaturation is caused by inserting an oxygen, sulphur, or halogen atom to viable body proteins. E.g. sodium hypochlorite, potassium permanganate, and chromic acid. (2) Reduction: Reducing agents act by binding free electrons in tissue proteins. Heat from exothermic reaction may cause a mixed picture. E.g. hydrochloric acid, nitric acid and alkyl mercuric compounds. (3) Corrosion: Corrosive agents cause protein denaturation on contact. Produce a soft eschar, which may progress to shallow ulceration. E.g. phenols, sodium hypochlorite, and white phosphorous. (4) Protoplasmic poisons: Produce their effects by causing the formation of esters with proteins or by binding or inhibiting calcium or other organic ions necessary for tissue viability and function. E.g. ester formers: formic and acetic acids, inhibitors: oxalic and hydrofluoric acids. (5) Vesicants: produce ischemia with anoxic necrosis at the site of contact. Characterized to produce cutaneous blisters. E.g. mustard gas, dimethyl sulfoxide (DMSO), and Lewisite. (6) Desiccants: cause damage by dehydration of tissues. Often exacerbated by heat production due to exothermic reactions. E.g. sulphuric and muriatic (concentrated hydrochloric) acids.

• #8 Ophthalmologic Approach to Chemical Burns: Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/1215950-overview

  Chemical injuries to the eye constitute a critical ophthalmic emergency, demanding immediate and decisive action. […] The severity of this injury is related to chemical composition, pH, volume, concentration, duration of exposure, and the degree of penetration of the chemical. The mechanism of injury differs slightly between acids and alkali. […] Acids dissociate into hydrogen ions in the cornea. This usually occurs when a strong acid has a pH of less than 4. The hydrogen molecule damages the ocular surface by altering the pH, whereas the anion causes protein denaturation, precipitation, and coagulation. Protein coagulation creates a barrier and thus generally prevents deeper penetration of acids and is responsible for the ground glass appearance of the corneal stroma following acid injury.

• #9 Chemical Eye Injuries from Acids – Insight Vision Center Optometry

  https://www.insightvisionoc.com/uncategorized/chemical-eye-injuries-from-acids/

  Experiencing a chemical eye injury can be distressing and potentially harmful, especially if acids are involved. These injuries are often caused by everyday household items such as cleaning agents, car batteries, and even swimming pool acid washes. While acids generally cause less damage than alkali substances, they can still lead to serious harm if not treated promptly. […] Acidic injuries, while generally less severe than alkali burns, cause damage through the coagulation and denaturation of corneal proteins. Upon contact, acids typically form a coagulated protein barrier in the eye, which limits their penetration past superficial layers. […] Common acids that cause ocular injuries include hydrochloric acid (found in pool cleaners) and sulfuric acid (used in car batteries). Unlike alkali burns, acids primarily affect the corneal surface creating a ground-glass appearance and generally do not penetrate into deeper eye tissues.

• #10 Chemical burns acid or alkali, what’s the difference? | Eye

  https://www.nature.com/articles/s41433-019-0735-1

  Acid and alkali injuries have traditionally been assigned clearly defined pathophysiological pathways by which injury and tissue damage occurs but in severe cases the outcome is equally devastating. Acids usually causes tissue coagulation and shrinking of collagen fibres. Ocular surface tissue proteins bind to acid molecules neutralizing the acid and causing coagulative necrosis. The coagulum acts as a barrier preventing further penetration of the acid, theoretically limiting its damaging effect […] Alkali burns that represent two third of chemical burns worldwide, cause hydrophilic and lipophilic degeneration. Saponification of the fatty acids of cell membrane causes rapid penetration of the alkali into the cells. With hydrolysis of the interfibrillar glycosaminoglycans and shrinking of the collagen fibrils, the tissue becomes more susceptible to enzymatic degradation with further penetration of the alkali into the ocular tissue.

• #11 Chemical (Alkali and Acid) Injury of the Conjunctiva and Cornea – EyeWiki

  https://eyewiki.org/Chemical_(Alkali_and_Acid)_Injury_of_the_Conjunctiva_and_Cornea

  Chemical (alkali and acid) injury of the conjunctiva and cornea is a true ocular emergency and requires immediate intervention. Chemical injuries to the eye can produce extensive damage to the ocular surface and anterior segment leading to visual impairment and disfigurement. Early recognition and treatment ensures the best possible outcome for this potentially blinding condition. […] Alkali agents are lipophilic and therefore penetrate tissues more rapidly than acids. They saponify the fatty acids of cell membranes, penetrate the corneal stroma, and destroy proteoglycan ground substance and collagen bundles. The damaged tissues then secrete proteolytic enzymes, which lead to further damage. […] Acids are generally less harmful than alkali substances. They cause damage by denaturing and precipitating proteins in the tissues they contact. The coagulated proteins act as a barrier to prevent further penetration (unlike alkali injuries). The one exception to this is hydrofluoric acid, where the fluoride ion rapidly penetrates the thickness of the cornea and causes significant anterior segment destruction.

• #12 Glaucoma Associated With Chemical Burns – Glaucoma Today

  https://glaucomatoday.com/articles/2012-may-june/glaucoma-associated-with-chemical-burns

  Chemically burned eyes often develop multiple ocular diseases, including opaque corneas, ocular surface derangements, cataract, and uveitis. The most important preventable complication is glaucoma, however, which occurs in up to 75% of eyes with severe chemical burns. The severity of damage from a chemical burn varies with the type and concentration of the causative agent and with exposure time. Acids denature, precipitate, and coagulate corneal proteins. By acting as a barrier, protein coagulation helps to prevent the chemicals’ penetration into deeper structures. Thus, acid burns tend to be less severe than other chemical burns. The single exception is hydrofluoric acid (found in antirust solutions), which may rapidly penetrate the cornea and anterior chamber. Alkalis are lipophilic, and they penetrate ocular tissues more deeply and more rapidly than acids. Alkalis quickly enter ocular surface cells, producing a saponification reaction. During the inflammatory response, damaged cells secrete proteolytic enzymes, causing further surrounding damage. Strong alkalis can reach the anterior chamber and damage the lens, iris, trabecular meshwork (TM), and ciliary body in as little as 5 to 15 minutes. Overall, the pattern of IOP alterations is complex. A rapid, acute rise may result from collagen shrinkage and contraction and from increased uveal blood flow. This increase may be followed by a return to normal IOP or hypotony (due to ciliary body damage) and then a sustained elevation of IOP. Long-term glaucoma may be caused by multiple mechanisms, including pupillary block, an accumulation of inflammatory debris in the TM, and direct damage to the TM. Chronic and subacute inflammation also contribute. Not only can the primary insult cause glaucoma, but necessary treatments can cause or worsen the disease. The standard of care for a chemical injury demands the long-term use of topical steroids. Multiple surgeries can also necessitate months of topical and/or oral steroids and possibly a peribulbar and/or intravitreal steroid. Steroid treatment can cause glaucoma. In addition, multiple surgeries may damage the TM or cause progressive angle closure. Finally, trauma and scarring from limbal stem cell surgery may impair episcleral venous outflow. After chemical burns, physicians’ attention focuses on the cornea, and glaucoma is a secondary consideration. IOP spikes may be missed, and glaucoma is frequently overlooked entirely. This disease, however, is the single most important factor limiting patients’ visual outcomes. The treatment of elevated IOP must be a priority in the early phase of managing a chemical burn through the initiation of generously administered glaucoma drops. If the disease progresses on maximal medical therapy, tube shunts and/or cyclophotocoagulation are necessary. Trabeculectomy is fraught with potential complications. Chronic, subacute inflammation may also severely shorten the lifespan of the bleb. Physicians continue to underestimate the danger of IOP spikes and the potential for long-term glaucomatous damage after an ocular chemical burn. Data have suggested a 22% incidence of secondary glaucoma in patients with severe chemical burns, but disturbingly, 75% of the patients in a study by Cade et al had advanced glaucoma prior to vision rehabilitation surgery. Despite the heroic efforts of doctors and patients alike, visual rehabilitation surgery is futile if glaucoma goes unrecognized or undertreated.

• #13 Ocular Chemical Burns | 5-Minute Clinical Consult

  https://www.unboundmedicine.com/5minute/view/5-Minute-Clinical-Consult/116411/all/Ocular_Chemical_Burns?q=Bradycardia

  Chemical exposure to the eye can result in rapid, devastating, and permanent damage and is one of the true emergencies in ophthalmology. […] Alkali burns: more severe; alkaline compounds are lipophilic and penetrate rapidly into eye tissue; saponification of cell membranes leads to necrosis and may cause injury to lids, conjunctiva, cornea, sclera, iris, and lens. […] Acid burns: less severe; associated anions from acidic compounds cause protein denaturation, creating a barrier to further acid penetration (hydrofluoric acid is an exception to this rule; see below). Injury is often limited to lids, conjunctiva, and cornea. […] Hydroxide causes saponification of fatty acids in cell membranes, leading to cell death. […] Anion leads to protein denaturing and protective barrier formation by coagulation necrosis forming an eschar. This more superficial mechanism of injury reduces further tissue penetration but may lead to more prominent scarring.

• #14 Rare chemical burns: Review of the Literature

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7949277/

  Hydrofluoric acid is particularly dangerous because of its double action mechanism. In addition to the acidic corrosive effect, fluoride ions penetrate deeply into the tissues and react with calcium and magnesium to cause multiple local and systemic effects. HF activity is proportional to the size of the damage caused. This is because of the shifts of potassium in intracellular compartment, which leads to ongoing nerve depolarization. Other local effects include slow healing wounds and osteolysis. Systemic hypocalcemia and resulting hyperkalemia may cause myocardial arrhythmia. Hypocalcemia may develop even with 1% total body surface area exposure in concentrated HF. […] As a result, although chemical burns vary according to their types, they generally cause deep burns. Although they appear to affect superficially initially, they may cause a larger scar and bad appearance in their final form. In the early period, the removal of the substance and neutralisation with water is the most important step in the treatment. In addition, the metabolic and systemic effects that may develop with absorption should be considered.

• #14 Rare chemical burns: Review of the Literature

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7949277/

  There are many chemicals that can cause burns. Although they are generally acidic and basic in nature, there are more than one million known chemical compounds, of which 300 have been declared highly hazardous chemical substances by the National Fire Protection Society. Chemical burns account for approximately 10.7% of all burn injuries and 30% of deaths because of burns. Chemicals can be classified as acid, alkali, organic, and inorganic compounds. Acids act by denaturing and coagulating proteins. Alkaline burns cause deeper burns than acid burns. […] Acids act by denaturing and coagulating proteins. Alkaline burns cause deeper burns than acid burns. Alkaline compounds saponification on the surface epithelium of the skin and laxity causes necrosis. Organic solutions cause injury by dissolving the lipid membrane, leading to disruption of physiological processes. Inorganic solutions cause injury through denaturation mechanisms.

• #15 Topical chemical burns: Initial evaluation and management – UpToDateChemical_burns.htm

  https://www.uptodate.com/contents/topical-chemical-burns-initial-evaluation-and-management/print

  The presence of dyspnea, cough, hoarseness, drooling, stridor, tachypnea, decreased breath sounds, wheezing, rales, rhonchi, or use of accessory respiratory muscles suggests a caustic chemical inhalation with upper airway or lung parenchymal edema or injury. […] Hydrofluoric acid penetrates quickly through the epidermal layer into the dermis and deeper. […] Hydrofluoric acid (HF) is a highly corrosive inorganic acid with numerous applications. […] Hydrofluoric acid burns cause intense pain and tissue destruction, as well as electrolyte abnormalities that may precipitate cardiac arrest. […] Hydrofluoric acid can cause both local injury and potentially fatal systemic toxicity from hypocalcemia, hypomagnesemia, and cardiac dysrhythmias. […] Hydrofluoric acid penetrates quickly through the epidermal layer into the dermis and deeper.

• #16 Occupational Hydrofluoric Acid Injury from Car and Truck Washing — Washington State, 2001–2013

  https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6432a4.htm

  Exposure to hydrofluoric acid (HF) causes corrosive chemical burns and potentially fatal systemic toxicity. […] HF can produce serious health effects through any exposure route. Exposure of HF solution to the eye can cause irritation as well as potentially permanent ocular damage. Tissue damage from skin contact occurs by two mechanisms. Free hydrogen ions can cause a corrosive burn, and free fluoride ions can cause local cellular destruction and penetrate the skin, causing muscle and bone necrosis. […] Systemically, fluoride toxicity by any route of exposure can cause fatal cardiac arrhythmias precipitated by hypocalcemia and hyperkalemia. […] Occupational exposure to HF-based wash solutions can result in chemical burns, disability, and death. HF’s potential to cause severe injury combined with the inherent challenge of relying on PPE to protect workers warrants efforts to identify less hazardous alternatives, which would provide the most effective means of prevention.

• #17 Hydrofluoric Acid Injuries and Illness for First Responders | Tactical and Law Enforcement Medicine

  https://www.acep.org/talem/newsroom/mar2021/hydrofluoric-acid-injuries-and-illness-for-first-responders

  HF acid toxicity can occur via contact with skin or eyes, inhalation, or ingestion. All of these initial contacts can lead to severe local and systemic effects. […] Toxicity results from the weak HF acid penetrating deep into the skin and underlying tissue before dissociating into hydrogen and fluoride ions, allowing fluoride anions into fascia, muscle, bone and the circulatory system. […] Fluoride ions are believed to be directly toxic to myocardial cells by inhibiting adenylate cyclase. […] Locally, fluoride ions are thought to directly inhibit Na+/K+ pumps, which creates local hyperkalemia with resultant neuronal depolarization and significant pain. […] HF causes local injury via two primary mechanisms: as an immediate burn and as a delayed burn with skin penetration. […] At high HF concentrations (50%), the hydrogen ion causes a corrosive burn similar to other acid burns, with immediate visible tissue damage.

• #18 Take a look at the Recent articles

  https://oatext.com/Chemical-burn-caused-by-high-concentration-hydrofluoric-acid-a-case-that-followed-a-lethal-course.php

  A review of several journals of emergency medicine showed that patients exposed to high-concentration HFA died from fatal arrhythmia within 1 hr in many reported cases. […] Exposure to high concentrations of HFA is potentially lethal, but the potential risks are not sufficiently recognized. It is necessary to educate both employees and employers about the corrosive nature of HFA and the risks of exposure to HFA. Further, it is necessary to establish an effective emergency manual to prevent future industry accidents resembling this case.

• #18 Take a look at the Recent articles

  https://oatext.com/Chemical-burn-caused-by-high-concentration-hydrofluoric-acid-a-case-that-followed-a-lethal-course.php

  Chemical burns from Hydrofluoric Acid (HFA) are poorly recognized, even though we sometimes encounter patients affected by these burns. HFA can cause lethal arrhythmia due to hypocalcemia and hypomagnesemia, particularly in cases of high-concentration HFA exposure. […] Hydrofluoric acid (HFA) is widely used in both domestic and industrial materials for cleaning glass, metal, and brick. HFA can cause intractable arrhythmia induced by hypocalcemia, hypomagnesemia, and hyperkalemia, resulting in death. Despite its hazardous nature, the risk of HFA burns is not well recognized, even to those who handle this material. […] The degree of tissue damage is dependent on the concentration and the involved area. Tissue damage by HFA is caused via two distinct mechanisms. First, damage caused by hydrogen ions produces corrosive burns. Second, fluoride ions have a highly lipophilic nature and penetrate tissues deeply, leading to tissue necrosis. The liberated fluorine ions enter the cells and bind calcium and magnesium, causing hypocalcemia and hypomagnesemia. The formation of calcium fluoride (CaF2) crystals causes a fall in the serum calcium concentration, resulting in pain and cramping. The potassium channel is forced open by calcium-dependent inhibition on Na+/K+-ATPase, which causes hyperkalemia. Myocardial adenylate cyclase is activated by fluoride ions, which increases cAMP and stimulates the myocardium, inducing refractory and fatal arrhythmia.

• #19 Cutaneous chemical burns: assessment and early management

  https://www.racgp.org.au/afp/2015/march/cutaneous-chemical-burns-assessment-and-early-mana

  The pathological end result of chemical burns, regardless of the type of chemical, is consistent with changes occurring during thermal burns. The external toxic stimulus causes denaturation of biological proteins and thus renders them physiologically inactive. This inactivation of essential proteins results in cell death. Thermal burns tend to cause rapid coagulation of protein due to protein crosslinking. By contrast, chemical burns cause denaturation of physiological proteins through six different processes including reduction, oxidation, corrosion, vesication, dessication and protoplasmic poisoning. It should be noted that many chemicals cause injury through combinations of these processes. […] Chemical agents can also be classified on the basis of the induced chemical reaction that the agent initiates. Such classification may be useful for consideration of early management options. Chemical agents may be classified into one of these categories despite slight variations in the resulting clinical sequelae.

• #19 Cutaneous chemical burns: assessment and early management

  https://www.racgp.org.au/afp/2015/march/cutaneous-chemical-burns-assessment-and-early-mana

  Acids: act as proton donors in the biological system. Acid injury causes a coagulative necrosis of the superficial tissue. […] Bases: chemicals are proton acceptors and tend to have greater capability of producing injury. These agents produce heat via reactions with fats, extract water from surrounding tissue and result in liquefactive necrosis. Such necrosis allows penetration deep to the superficial wound and continues to cause injury despite initial removal of the insult. […] Alkali: act as proton acceptors and classically cause progressing injury despite the removal of the harmful agent. As discussed above, alkalis cause liquefactive necrosis, allowing progression to deeper tissues. Initially alkali burns seem superficial, but may progress to full thickness within 48-72 hours.

• #20 Chemical Burns – Clinical Tree

  https://clinicalpub.com/chemical-burns/

  In general, alkaline materials cause more injury than acidic compounds. Whereas acids cause coagulation necrosis with precipitation of protein, the reaction to alkali is liquefaction necrosis, allowing the alkali to penetrate deeper into the injured tissue. […] The presence of hydroxyl ions within these tissues increases their solubility, allowing alkaline proteinases to form when the alkalis dissolve the proteins of the tissues. […] Organic solutions tend to dissolve the lipid membrane of cell walls and cause disruption of cellular architecture as their mechanism of action. Inorganic solutions tend more to remain on the exterior of cells but may act as transporters to carry the above-mentioned agents that denature proteins or form salts with proteins themselves.

• #21 Chemical burns | PPT

  https://www.slideshare.net/UmarBaba/chemical-burns-238918769

  Sulfur mustard rapidly alkylates the purine bases (adenine guanine) of DNA which triggers the activation of endonucleases for depurination (excision) of the alkylated bases, leaving apurinic sites where DNA breaks readily occur. […] Chemical burns represent potentially blinding ocular injuries and constitute a true ocular emergency requiring immediate assessment and initiation of treatment. […] Chemical injuries of the eye produce extensive damage to the ocular surface epithelium, cornea, anterior segment and limbal stem cells resulting in permanent unilateral or bilateral visual impairment. […] The prognosis depends on the type of chemical and extent of the injury. Most small lesions heal well, but larger wounds often do not heal and can develop into scars. […] Chemical burns have the potential to impair short and long-term health and, especially when the eye or esophagus are involved, severely alter the individual’s well-being.

• #22 Severe chemical burns | VicBurns

  https://www.vicburns.org.au/severe-burns/secondary-survey/severe-chemical-burns/

  Chemicals continue to destroy tissue as long as they are in contact with the skin. […] Death from a chemical injury, although rare, can occur due to extensive burns, or the systemic toxicity of absorbed chemicals. […] Mechanism of action of the chemical. […] Treatment is designed to neutralise the fluoride ion and prevent systemic toxicity. […] Cement powder penetrates clothing, combines with sweat, and creates an exothermic reaction. […] White phosphorus ignites in the presence of air and will continue until oxidation of the agent is complete or the oxygen source is removed. […] The use of specific neutralising solutions is not recommended for ocular chemical burns.

• #23 FSI – Chemical Burns|Gossman Forensics

  https://www.gossmanforensics.com/newsletter/vol01_iss06.html

  Acids have a pH below 7 and the lower the pH value, the stronger the acid. […] When an acid comes in contact with tissue, it begins the process of coagulative necrosis. […] This changes the shape of the protein and it essentially stops functioning. […] In the case of acid contact with tissue, the cells die but do not liquefy as with alkaline burns. […] Hydrofluoric acid is a dangerous strong acid that will result in liquefaction necrosis when in contact with tissue. […] This can cause extreme damage to cells and tissue beneath the epidermis, including bones. […] Liquefaction necrosis can occur well below the skin surface and can be some of the most horrific and difficult to manage/treat burns. […] Chemical burn incidents can be highly complicated and may involve a series of chemical interactions and/or reactions.

• #24 The chemical burns – Ouvry – CBRN Protective System

  https://ouvry.com/en/the-chemical-burns/

  The main mechanisms of action of acid burns are dehydration, protein coagulation, and exothermic reaction. Lesions are most often well defined and not very deep with dry necrosis resulting in less exudation, reduced risk of infection and slow detersive action. In 76% of cases, chemical burns are caused by sulphuric or nitric acid. […] Sulfuric acid is the most dehydrating. It gives black or brownish, dry, hard and painless necroses. The exothermic reaction is strong. There is a risk of systemic passage with glottis edema and shock. […] Nitric acid is a liquid at ordinary temperature but it produces toxic nitrogen oxide fumes that can cause corneal and lung burns, sometimes delayed by 5 to 48 hours. Necrosis is yellow in appearance. […] Hydrofluoric acid has a double action: corrosive, bound to the H+ ion which attacks tissues on the surface, then toxic, bound to the fluorine ion which penetrates cells and binds to calcium and magnesium (chelation) causing cell death. This results in a significant release of potassium. Lesions are liquefaction necroses close to those of the bases. There is then a lethal risk of hypocalcemia, hypomagnesemia, and hyperkalemia.

• #25 Chemical burns – pathophysiology and treatment – handout | PDF

  https://www.slideshare.net/slideshow/chemical-burns-pathophysiology-and-treatment-handout-25126187/25126187

  Acids with a pH 2 can produce coagulation necrosis on contact with the skin. A better predictor than pH alone is the amount of alkali needed to raise the pH of an acid to neutrality. This may reflect the strength of the acid involved. […] Alkalis with a pH 11.5 produce severe tissue injury through liquefaction necrosis, which loosens tissue planes and allows deeper penetration of the agent. For this reason, alkali burns tend to be more severe than acid burns. […] Hydrofluoric acid easily available and present in the community. Used in frosting, etching and polishing glass and ceramics, removal of metal castings, cleaning stone and marble, and in the treatment of textiles. […] Hydrofluoric acid causes severe burns and systemic effects, despite minimally apparent cutaneous damage. H+ ions cause superficial burns.

• #26 Chemical burns – pathophysiology and treatment – handout | PDF

  https://www.slideshare.net/slideshow/chemical-burns-pathophysiology-and-treatment-handout-25126187/25126187

  Fl- penetrates down to the deeper soft tissue interferes with cellular metabolism causing cell death and liquefactive necrosis binds Ca++ and Mg++ causing systemic hypocalcemia and hypomagnesemia inhibits Na+ -K+ ATPase causing efflux of K+ and E+ shifts at nerve endings causing extreme pain. […] Treatment includes four phases: o Hydrotherapy immediate and prolonged o Topical treatment Controversial. Try to inactive Fl- and create insoluble fluoride salt. […] Infiltration Ca++ gluconate 10% 0.5ml SC/cm2 of burned tissue until painless. […] Strong Alkali Lime(CaO + Ca(OH)2), NaOH, and KOH present in many household cleaners Mechanisms 1. Saponification of fat is an exothermic reaction severe tissue damage through heat. […] Alkalis dissolve proteins of the tissues to form alkaline proteinates, which are soluble and contain OH- ions that cause further chemical reaction initiating deeper tissue injury (liquefaction necrosis). […] All clothes should be removed and the dry residues of alkali (e.g. lime) should be brushed away.

• #27 Ophthalmologic Approach to Chemical Burns: Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/1215950-overview

  Hydrofluoric acid is an exception; it behaves like an alkaline substance because the fluoride ion has better penetrance through the stroma than most acids, leading to more extensive anterior segment disruption. […] Alkaline substances are lipophilic and can penetrate cell membranes. They dissociate into a hydroxyl ion and a cation in the ocular surface. The hydroxyl ion saponifies cell membrane fatty acids, whereas the cation interacts with stromal collagen and glycosaminoglycans. This interaction facilitates deeper penetration into and through the cornea and into the anterior segment. […] Higher-grade injuries are more susceptible to secondary complications. Grading of the severity can offer the patient a better idea of the prognosis. Therefore it is important to note the amount of limbal, corneal and conjunctival involvement at the time of the initial injury and to document changes over time.

• #28 Researchers identify mechanism of retina damage following chemical eye burns | Harvard Medical School Department of Ophthalmology

  https://eye.hms.harvard.edu/news/researchers-identify-mechanism-retina-damage-following-chemical-eye-burns

  Chemical eye burns caused by alkali agents not only injure the front of the eye the cornea, where the contact takes place but also cause widespread damage to the light-sensitive tissue at the back of the eye (the retina) as well, often leading to optic nerve damage and glaucoma. […] In a report published online today in the American Journal of Pathology, a research team from Schepens Eye Research Institute of Massachusetts Eye and Ear has identified an inflammatory factor, tumor necrosis factor alpha (TNF-alpha), as the mechanism responsible for causing retinal damage from alkali eye burns. […] The teams findings are the first to show that the pH or pressure is not the mediator of retinal damage and that TNF-alpha mediated inflammation is a key driver of neurodegeneration. […] Our finding suggests that if we can neutralize the TNF-alpha inflammatory response shortly after the injury, perhaps we can stop the whole process and rescue the retina. […] With this new knowledge regarding the TNF-alpha pathway, we can potentially target the major inflammatory pathway responsible for retinal damage in alkali burns and stop the process before irreparable damage occurs.

• #29 FSI – Chemical Burns|Gossman Forensics

  https://www.gossmanforensics.com/newsletter/vol01_iss06.html

  This can allow damage to areas deep within the tissue, including bone and internal organs. […] Inhalation, ingestion and chronic exposure can also cause serious effects to the respiratory and gastrointestinal tract, including death in some cases. […] Both of these hypochlorites can cause chemical burns to the skin and also respiratory damage if inhaled. […] Ingestion may cause burns to the mouth and throat, gastrointestinal irritation, vomiting and in some cases death. […] Organic acids can be corrosive to skin and mucous membranes and can cause deep-seated burns on contact with the skin. […] Mineral acids are corrosive and can cause severe irritation and burns to skin, eyes, mucous membrane, and the respiratory tracts. […] They tend to injure tissues by dehydration and heat production which can result in cellular death.

• #30

  https://insight.jci.org/articles/view/147564

  Cutaneous burns by lewisite and PAO caused ALI by PAD4-mediated NETosis. […] PAD4 inhibitors may have potential as countermeasures to suppress detrimental lung injury after chemical burns. […] In this study, we characterize and define the underlying mechanisms of nonthermal burn-induced ALI in a nonthermal skin injury model. This study demonstrates that the development of ALI is secondary to the activation of PAD4 and the release of citrullinated histones containing NETs in the systemic circulation and lungs. […] Lewisite skin burns resulted in acute inflammation in the lungs at 6 hours as demonstrated by the infiltration of inflammatory cells in the parenchyma. […] The lung injury scoring system as per American Thoracic Society guidelines demonstrated a high lung injury score in lewisite-exposed mice.

• #31

  https://insight.jci.org/articles/view/147564

  Lewisite skin burn instigates ALI. […] The aforementioned data confirmed that PAO skin burns instigate ALI in mice. […] To detect the role of neutrophils in our extrapulmonary ALI model, we evaluated the presence of NETosis by detecting dsDNA and citrullinated histone 3 (Cit-H3) in the lungs of lewisite and PAO-exposed mice. […] Overall, lewisite and its analog, PAO-induced skin burns, caused NETosis in the lungs. […] Our mouse model for chemical burn-induced ARDS demonstrated high amounts of dsDNA and NETs in their lungs. […] Our data demonstrated that the lack of PAD4 has no effect on neutrophil influx but inhibits NETosis that results in attenuated PAO-induced ALI. […] Overall, these data suggested that PAD4 is essential for the NETosis-mediated injury in the cutaneous exposure model of PAO-induced ALI, and the PAD4 activity product Cit-H3 acts as a spearhead to cause lung injury. […] Our results demonstrate that inhibition of PAD4 activity by GSK484 attenuates PAO skin burn-induced ALI.

• #32 Chemical Burns: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/769336-overview

  The severity of the burn is related to a number of factors, including the pH of the agent, the concentration of the agent, the length of the contact time, the volume of the offending agent, and the physical form of the agent. The ingestion of solid pellets of alkaline substances results in prolonged contact time in the stomach, thus, more severe burns. In addition, concentrated forms of some acids and bases generate significant heat when diluted or neutralized, resulting in thermal and caustic injury. […] The long-term effect of caustic dermal burns is scarring, and, depending on the site of the burn, scarring can be significant. Ocular burns can result in opacification of the cornea and complete loss of vision. Esophageal and gastric burns can result in stricture formation. An oral burn is shown in the images below.

• #33 Chemical Burns | Burn and Reconstructive Centers of America

  https://burncenters.com/burns/burn-services/chemical-burns/

  A chemical burn occurs when an external agent (chemical) causes tissue irritation or damage as a result of direct contact. Most chemical burns are caused by either strong acids or bases, with prolonged exposure leading to severe injuries, scarring, disability or worse. […] The amount of tissue damage from an agent depends on a number of factors, including: The strength or concentration of agent, Where the chemical had direct contact (skin, eyes, mouth, etc.), Whether the agent was ingested, swallowed or inhaled, The amount of agent you came into contact with, Length of exposure to the agent. […] Not all chemicals can be removed with water. Some may need to be removed in alternative ways by a doctor. All chemical burns should be assessed by a healthcare professional as soon as possible, no matter how minor they are.

• #34 Hydrofluoric Acid Injuries and Illness for First Responders | Tactical and Law Enforcement Medicine

  https://www.acep.org/talem/newsroom/mar2021/hydrofluoric-acid-injuries-and-illness-for-first-responders

  At lower HF concentrations, which represent a majority of HF burns, immediate visible tissue destruction does not occur and there may be no initial evidence of chemical burn. […] Systemic HF toxicity can be difficult to manage. The effects are primarily related to massive electrolyte disturbances, mainly hypocalcemia, hypomagnesemia, acidosis, fluorosis, and hyper- or hypokalemia. […] In systemic HF toxicity it is beneficial to maintain normal acid base status. […] Local calcium gluconate injections have been widely adopted for use on moderate to severe HF burns as it has been shown to reliably reduce pain. […] For patients with severe HF burns with unrelenting pain despite aggressive calcium gel topical therapy, typically of the digits or other poorly distensible areas that will not tolerate intradermal injection, intra-arterial calcium infusion has been used.

• #35 Decreasing incidence of cutaneous chemical burns in a resource limited burn centre: is this a positive effect of modernization? | Burns & Trauma | Full Text

  https://burnstrauma.biomedcentral.com/articles/10.1186/s41038-017-0072-1

  Burns caused by chemical agents, present a worse scenario. […] In Nigeria, the common sources of these chemicals, following interaction with persons accused of using such, suggests that wet lead-acid battery vendors provide readily available source for acids while traditional soap makers are the major outlet for caustic alkalis. […] The increasing preference and availability of dry cell batteries might also have played a role. […] Our study revealed a marked decline in the sale of corrosive chemicals. Sulphuric acid and caustic soda are the commonest corrosive agents in common use, and most chemical burns in our environment are caused by these two agents. […] We therefore believe that improved lifestyles and improved technology has a positive bearing on the reduced accessibility to corrosive chemicals. […] This may be attributed to the improving technological and economic developments in the country with the subsequent change in lifestyle.

• #36

  https://journals.lww.com/ijob/fulltext/2020/28010/epidemiological_analysis_of_chemical_burns__does.4.aspx

  Chemical burns constitute small proportion of cases among the total admissions due to burn injuries. The spectrum of severity of illness can vary from mild injuries to life-threatening trauma. In the Indian scenario, the incidence of chemical burns has been reported to be 2.25%2.4% of total burn admissions. […] It was observed that acid burns have decreased in comparison to the initial 3 years. […] Downward trend in the incidence of overall chemical burns was noted. Acid burns decreased with simultaneous increase in alkali burns. The study period coincided with the Supreme Court’s verdict with the formulation of guidelines on sale of acids in 2013 and this could be the major factor in declining trends of acid burns. […] The yearly data show decreasing trend in acid-related burns with increase in alkali burns. The number of acid injuries has reduced from 31 patients in 2013 to 5 patients in 2018. […] On year-to-year basis analysis of chemical burns at our institute, we found a downward trend in the chemical burns with more so specific to acid burns. […] The Supreme Court-induced stricter norms for sale of acids did have impact on reducing numbers.

• #37 Emergency Management of Chemical Burns

  https://www.heraldopenaccess.us/openaccess/emergency-management-of-chemical-burns

  Clinical assessment of the depth and extent of a chemical burn is required. […] Although chemical burns constitute a small percentage of the overall burn affecting the human body, their morbidity and mortality rates are high. Proper history taking, clinical examination and early management of such cases can greatly reduce the morbidity and mortality rates of these patients.

• #38 Management Strategies of Ocular Chemical Burns: Current Perspectives | OPTH

  https://www.dovepress.com/management-strategies-of-ocular-chemical-burns-current-perspectives-peer-reviewed-fulltext-article-OPTH

  Ocular chemical burns are absolute ophthalmic emergencies and require immediate management to minimize devastating sequelae. Management of alkali and acid burns is started at the scene of the accident by copious irrigation. Treatment is directed at improving epithelial integrity and stromal stability, reduction of undue inflammation, and prevention or timely management of complications. […] Any liquid or solid material with alkaline or acidic ingredients may cause an ocular burn. An alkali is especially notorious for severe damage to ocular tissues. The difference in the ocular effects between acids and alkali resides in their mechanism of action. Acids and alkali cause coagulative and liquefactive necroses respectively. […] It is noteworthy, however, that acids are equally as devastating as alkalis in severe burns. The chemical structure of the material is not the only determinant of the severity of the damage.

• #39 Topical chemical burns: Initial evaluation and management – UpToDate

  https://www.uptodate.com/contents/topical-chemical-burns-initial-evaluation-and-management

  Chemical burns are unique injuries that require individualized evaluation and management depending upon the causative agent. […] The evaluation and management of common topical chemical burns will be reviewed here, with a focus on the basic principles of management. […] Chemical burns differ from thermal burns in that they continue to cause damage as long as some active component of the chemical remains in the wound. […] The principles of management of chemical burns are similar to those for thermal injuries (with the addition of clinician protection, immediate decontamination, and extensive irrigation). […] Skin decontamination — Complete removal of the toxic chemical is essential. Tissue damage continues for as long as the chemical remains in contact with skin. […] The most important component of active therapy is thorough irrigation of all wounds and areas of exposure with copious amounts of water.

• #40 Topical chemical burns: Initial evaluation and management – UpToDateChemical_burns.htm

  https://www.uptodate.com/contents/topical-chemical-burns-initial-evaluation-and-management/print

  Chemical burns are unique injuries that require individualized evaluation and management depending upon the causative agent. […] The evaluation and management of common topical chemical burns will be reviewed here, with a focus on the basic principles of management. […] Chemical burns differ from thermal burns in that they continue to cause damage as long as some active component of the chemical remains in the wound. […] The principles of management of chemical burns are similar to those for thermal injuries (with the addition of clinician protection, immediate decontamination, and extensive irrigation). […] Skin decontamination is essential. Tissue damage continues for as long as the chemical remains in contact with skin. […] Complete removal of the toxic chemical is essential. […] The most important component of active therapy is thorough irrigation of all wounds and areas of exposure with copious amounts of water.

• #41 Chemical burns

  https://dermnetnz.org/topics/chemical-burn

  Chemical burns involving elemental metals (lithium, potassium, sodium and magnesium) should not be irrigated with water as this can result in a chemical reaction that causes burns to worsen. […] For example, hydrofluoric acid burns should be promptly treated with calcium gluconate gel applied every 15 minutes, so the gel should be kept at relevant work sites.

• #42 Glaucoma Associated With Chemical Burns – Glaucoma Today

  https://glaucomatoday.com/articles/2012-may-june/glaucoma-associated-with-chemical-burns

  The severity of damage from a chemical burn varies with the type and concentration of the causative agent and with exposure time. […] The standard of care for a chemical injury demands the long-term use of topical steroids. Multiple surgeries can also necessitate months of topical and/or oral steroids and possibly a peribulbar and/or intravitreal steroid. Steroid treatment can cause glaucoma.

• #43 Chemical Burns: Symptoms, Causes & Treatment

  https://my.clevelandclinic.org/health/diseases/22350-chemical-burns

  Chemical burns require immediate treatment. […] Once you arrive at the hospital, your healthcare team will evaluate the severity of your burn. […] Most mild chemical burns heal without leaving permanent scars. However, long-term effects of severe chemical burns may include: Cancers of your skin, stomach or esophagus. Esophageal strictures (narrowed esophagus, sometimes due to scarring). Perforations (holes) in your stomach, esophagus or cornea. Scars. Skin discoloration. Vision loss. […] Chemical burns can happen if you work with chemicals or other harsh substances for your job. People, especially children, can also get chemical burns if they accidentally touch or swallow certain household chemicals. You should seek medical attention from your healthcare provider for any chemical burn, even if it seems mild. Unlike heat burns, chemical burns can continue causing tissue damage even after you come into contact with them. Immediate treatment is essential to prevent scarring or complications.

• #44 Chemical Burns: Causes, Symptoms, and Diagnosis

  https://www.healthline.com/health/chemical-burn-or-reaction

  In general, the common symptoms associated with chemical burns include: blackened or dead skin, which is mainly seen in chemical burns from acid. […] Your doctor will classify the burn according to the extent of the injury and the depth of the burn itself. […] First aid should be given to chemical burns immediately if possible. This includes removing the chemical that caused the burn and rinsing the skin under running water for 10 to 20 minutes. […] Depending on the severity of your condition, your healthcare provider may use the following methods to treat your burn: antibiotics, anti-itch medications, debridement, skin grafting, intravenous (IV) fluids. […] The outlook depends on the severity of the burn. Minor chemical burns tend to heal fairly quickly with the appropriate treatment. More severe burns, however, may require long-term treatment. […] Some people who have experienced severe chemical burns may have complications, including: disfigurement, limb loss, infection, scarring, muscle and tissue damage.

• #45 EyeRounds.org: Chemical Eye Injury: A Case Report and Tutorial

  http://eyerounds.org/cases/307-chemical-eye-injury.htm

  On the other hand, acidic agents are associated with milder ocular injury. This is because the anion in acidic agents causes protein precipitation and denaturation in the corneal epithelium and superficial stroma, which then acts as a barrier to prevent deeper penetration of the H+ cation into the eye. The important exceptions to this are hydrofluoric acid and, to a lesser extent, sulfurous acid (H2SO3), both of which can penetrate rapidly into the eye due to their small size and low molecular weight. Sulfuric acid (H2SO4), the most common acidic agent implicated in chemical ocular injury, does react exothermically with water and can lead to thermal injury of the eye as well. […] Other than pH, other factors to consider are temperature, volume, propensity to form precipitates, velocity of impact, and concentration of the agent, as these also affect the degree of injury and therefore the patients long term visual prognosis. […] Chronic complications of chemical ocular injuries include limbal stem cell deficiency, vision-limiting corneal scarring, secondary glaucoma, entropion, and cicatrization of the conjunctiva with symblepharon formation.

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