With the exception of hydrofluoric acid, strong acids produce coagulation necrosis from the desiccating action of the acid on proteins in the superficial tissue. Injury severity is related to the physical characteristics of the acid. Most substances with a pH less than 2 are strong corrosives. Other important tissue-damaging properties of acids include concentration, molarity, and complexing affinity for hydroxy ions. The higher each of these factors is, the greater is the tissue damage. Contact time with the skin is the most important chemical burn feature that health care professionals may alter. Instantaneous skin decontamination of 18 M sulfuric acid will cause no burn; however, a 1-min exposure can cause full-thickness skin damage. Examination of a patient with a significant chemical burn from these acids should not be limited to observation of the skin, because several of these acids are respiratory and mucous membrane irritants as well. Furthermore, skin absorption of some compounds may occur and result in systemic signs and symptoms. The most commonly used chemicals that cause burns are listed in Table 19,5-1.

ACETIC ACID The dilute (<40%) acetic acid solution found in hair-wave neutralizer solutions is perhaps the most common cause of chemical burns to the scalp in women. Prolonged contact, especially with an already damaged scalp, may cause a partial-thickness burn that heals slowly because of the constant bacterial flora on the hair. Initial treatment is copious water irrigation. As trimming the hair is not a viable option in these patients, oral antibiotics are often given if the entire scalp is involved.

PHENOL Phenol (carbolic acid), a corrosive organic acid used widely in industry and medicine, denatures proteins and causes chemical burns characterized by a white or brown coagulum that is relatively painless. Systemic absorption may result in life-threatening complications. Its unpleasant, acrid odor, detectable in air at 0.047 parts per million, and its low volatility help prevent airborne exposure. Though commercially available in concentrations of 1 to 90%, even dilute solutions of 1 to 2% phenol may cause a burn if contact is prolonged. Hexylresorcinol is a bactericidal phenol derivative. Chemically related phenolic compounds that induce skin damage include cresol, creosote, and cresylic acid.

Coagulation necrosis of the involved area is common. Necrotic tissue may delay absorption temporarily, but phenol may become entrapped under the eschar. Contaminated clothing should be removed and water lavage begun immediately. Water lavage alone may be ineffective, presumably because the necrotic coagulum inhibits water penetration to the deeper layers. Paradoxically, dilute phenol penetrates tissue more readily than when concentrated.

More effective decontamination has been demonstrated with a 5- to 10-min swab with a combination of polyethylene glycol 300 (PEG 300) and industrial methylated spirits (IMS) in a 2:1 mixture. This should not only reduce the extent of cutaneous corrosion but also decrease systemic toxicity. The PEG 300 is mixed with the IMS for a more liquid (and therefore easier to use) formulation. However, the viscous PEG 300 or PEG 400 may be used alone, and, indeed, glycerol is an acceptable substitute if the PEG-IMS mixture is not available. The use of an isopropyl alcohol rinse appears to be equal to PEG-IMS in removing phenol. 4 The advantage of isopropyl alcohol is its easy availability.

CHROMIC ACID The toxicity of chromium compounds is related to the powerful oxidizing action of the hexavalent compounds (Cr6+). The chromate ion in chromic acid will produce a chronic penetrating ulcerating lesion of the skin. Associated signs and symptoms are conjunctivitis, lacrimation, ulceration of the nasal septum, and systemic chromium toxicity. A 10-percent total body surface area cutaneous burn caused by chromic acid can be fatal due to systemic toxicity. Any acute skin exposure to chromic acid should be treated with copious water irrigation and observation for systemic effects.

FORMIC ACID Formic acid in 60% solution is used by acrylate-glue makers, cellulose formate workers, and tanning workers. Formic acid produces coagulation necrosis of the skin. Systemic effects including decreased respirations and an anion-gap metabolic acidosis have been reported. 5 Treatment includes immediate decontamination and irrigation with water. Open lesions should be treated like any damaged skin: with debridement of devitalized tissue, prevention of further damage and infection, and skin grafting if the defect is full thickness and of a size requiring closure.

HYDROCHLORIC AND SULFURIC ACIDS The dermal toxicity of hydrochloric acid and sulfuric acid is so well recognized that early decontamination and water irrigation usually prevent severe burns to the skin. These acids can burn the skin dark brown or black. Toilet bowl cleaners may contain 80% solutions of sulfuric acid. Some drain cleaners may be 95 to 99% sulfuric acid solutions. Munitions, chemical, and fertilizer manufacturers commonly use 95 to 98% sulfuric acid solutions in their industrial processes. Automobile battery fluid is 25% sulfuric acid. Most household bleaches are only 3 to 6% hypochlorite solutions, which, though acidic, cause little damage unless they are in contact with skin for a prolonged time. Treatment is the same as for formic acid burns.

HYDROFLUORIC ACID Hydrofluoric acid (HF) is unique among the corrosives in its mechanism of action and degree of toxicity. HF acts like alkalis and will cause progressive tissue loss, including bony destruction. HF, considered a protoplasmic poison, penetrates the skin, dissociates, and releases fluoride ions. Fluoride ions immobilize intracellular calcium and magnesium and poison cellular enzymatic reactions. Potassium permeability is increased and results in spontaneous depolarization of nerve tissue and pain.

Industrial applications include use in production of high-octane fuel, etching and frosting glass, semiconductors, microelectronics/microinstruments, germicides, dyes, plastics, tanning, and fireproofing material and use in cleaning stone and brick buildings. It is also a very effective rust remover.

HF rapidly penetrates the skin and causes both local and systemic toxicity. Its systemic effects include hypocalcemia, hypomagnesemia, and hyperkalemia. The dermal effects may not be immediately noted and appear to be more related to the concentration of HF than to the duration of exposure. Solutions greater than 50% produce immediate pain and tissue destruction; solutions less than 20% may not produce signs and symptoms until 12 to 24 h after exposure. The skin may develop a blue-gray appearance with a surrounding region of erythema.

Unlike the treatment of dermal injury caused by other acids, the treatment of HF burns consists of two phases. The first, which should be immediate, is copious water irrigation of the affected skin for 15 to 30 min. This may be the only treatment that is needed if the HF solution is less than 20% concentrated, the duration of exposure was very brief, and decontamination is begun immediately. Unfortunately, this is rarely the case. Severe, persistent pain denotes a more serious injury requiring the second phase of treatment.

The second phase of treatment is aimed at detoxifying the enzyme-poisoning fluoride ion. Two ions—calcium (Ca2+) and magnesium (Mg2+)—have been shown to be beneficial in binding the fluoride and curtailing its toxic effects. However, the overwhelming clinical experience to date has been with the use of calcium gluconate, and it should be considered the agent of choice at present. Several therapeutic modalities are available for using calcium gluconate: topical, subcutaneous/intradermal injection, or intraarterial infusion. An intravenous regional perfusion technique based on Bier's method has been described and reported effective.6 High-dose intravenous magnesium sulfate appears to be effective in animal models, but human data are lacking.7

A calcium gluconate gel made of either Surgilube (E. Fougera & Co.) or dimethyl sulfoxide (DMSO) in a 2.5 to 10% concentration may be applied directly to the affected area.8 The main limitation of topical therapy is the impermeability of the skin to calcium. Penetration into the dermis and subcutaneous tissues may be enhanced if the formulation with DMSO is used. The topical therapy can be used in the outpatient setting, and industries utilizing HF should keep this topical formulation on hand for emergency use.

Subcutaneous and intradermal injection of a 5 to 10% calcium gluconate solution through a 30-gauge needle into the HF-burned skin is the most widely used treatment. A maximum dose of 0.5 mL of 10% calcium gluconate per square centimeter of burned skin is recommended. Pain relief is nearly immediate, and indeed, the elimination of pain may be used as a guide for further therapy. Recurrence of pain indicates the need for further therapy. Unfortunately, injection therapy has several disadvantages: (1) only limited amounts of calcium are delivered to the tissue; (2) hyperosmolarity and inherent toxicity of free calcium ions cause more pain initially, and more tissue damage is possible if calcium is not bound to fluoride; (3) vascular compromise can result if too much fluid is injected, especially into digits; and (4) rapid penetration of HF beneath the nail requires nail removal to administer the calcium gluconate into the nailbed adequately.

Intraarterial infusion of calcium gluconate may be used to prevent tissue necrosis and stop the pain associated with HF burns. This should be performed as soon as possible after the initial burn, preferably within 6 h of insult. An intraarterial catheter should be placed in the appropriate vascular supply (the brachial artery if the entire hand is affected) and connected to a three-way stopcock to which is attached an arterial pressure-monitoring device and the infusion syringe of calcium gluconate. A 50-mL syringe may be filled with 10 mL of a 10% calcium gluconate solution and 40 mL of 5% dextrose. This should be infused over 2 to 4 h. The arterial pressure-monitoring device ensures that the catheter has not dislodged from the lumen of the cannulated artery. Infusion of the calcium solution into the deep tissues may cause further tissue damage. Repeat infusion may be needed if pain recurs within 4 h. This intraarterial infusion avoids the disadvantages of local infiltration therapy; however, it has its own disadvantages: an invasive vascular procedure (1) may result in arterial spasm or thrombosis and (2) requires more time and resources, including hospital admission.

Nebulized calcium gluconate is a recognized treatment for inhalational exposures to HF. Ocular exposure to HF requires water irrigation for at least 30 min. Treatment with calcium chloride or magnesium chloride by subconjunctival injection or irrigation may increase corneal damage. There is a reported case, however, of complete and quick recovery by utilizing 1% calcium carbonate eyedrops in a patient who had sustained a large corneal erosion due to a 49% HF burn.

Systemic toxicity related to dermal HF exposure has resulted in death. This appears to be related to myocardial irritability and subsequent ventricular fibrillation as a result of systemic acidosis, hyperkalemia, hypomagnesemia, and hypocalcemia. Cardiac monitoring, intravenous access, and electrolyte monitoring should be performed in cases of all significant HF dermal burns.

NITRIC ACID Nitric acid is used in industry for casting iron and steel, electroplating, engraving, and fertilizer manufacturing. Upon contact with skin, nitric acid can produce tissue damage by oxidation and may turn the skin yellowish as it is burned.

OXALIC ACID Oxalic acid is used for leather tanning and blueprint paper. Like hydrofluoric acid, it poisons enzymatic processes. Oxalic acid binds calcium and prevents muscle contraction. The burn wounds should be irrigated with water, intravenous calcium may be required. Serum electrolytes and renal function should be checked, and cardiac monitoring should be performed after serious dermal exposure.

METHACRYLIC ACID Methacrylic acid found in many artificial nail cosmetic products can produce severe dermal burns, usually in preschoolers. 9 Alkalis

Alkalis penetrate skin much more deeply and longer than acids, causing liquefaction necrosis of tissue, with danger of toxicity from systemic absorption. Wounds may look superficial and in 2 to 3 days become full-thickness burns. Alkalis combine with protein and lipids in tissue to form soluble protein complexes and soaps that permit passage of hydroxyl ions deep into tissue. Soft, gelatinous, friable, brownish eschars are often produced. Strong alkalis have a pH 312.

LYES Strong, corrosive alkalis ("lyes") include ammonium, barium, calcium, lithium, potassium (caustic potash), and sodium (caustic soda) hydroxides. Lyes are widely used in industry and found in home products (drain and toilet cleaners, washing powders, and paint removers). The urine sugar reagent tablet Clinitest (Bayer) contains anhydrous sodium hydroxide. As a mode of assault, lyes have a lower mortality rate than gunshot wounds or stabbings, but victims often suffer long-term pain, scarring, and blindness.10 Lyes are extremely corrosive and penetrating, and burns require copious irrigation for long periods. Suicidal ingestion of lye requires aggressive airway management. Early death results from upper airway occlusion. Late morbidity related to esophageal and gastric necrosis may be minimized by early surgical intervention with esophagogastrectomy.

LIME Lime (calcium oxide) is found in agriculture products and cements. It is converted by water to the alkali calcium hydroxide. Contact with lime draws water out of the skin. All dry particles should be brushed away prior to irrigation. Paradoxically, a small amount of water may generate an exothermic reaction with tissue injury secondary to calcium hydroxide formation. A large amount and strong stream of water (taking care to avoid splashing in eyes) should be used and will permit dissipation of heat. There is considerable variability of lime content in different grades of cement, with fine to textured masonry cement having more than concrete.

PORTLAND CEMENT Portland cement, which accounts for a major proportion of the cement used in the United States, is a mixture of sand, lime, and other metal oxides. In the presence of water, calcium hydroxide, sodium hydroxide, and potassium hydroxide may all be formed. Workers who kneel in wet cement or get cement in their boots may discover burns hours after initial contact. In addition, skin may become irritated from gritty material, and a contact dermatitis may develop in individuals sensitive to the chromate contained in the material.

Peripheral Neuropathy Natural Treatment Options

Peripheral Neuropathy Natural Treatment Options

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