Chemical Burns
Chemical burns continue to destroy tissue until the causative agent is inactivated or removed. [9] For example, when hydrotherapy is initiated within 1 minute after skin contact with either an acid or alkali, severity of the skin injury is far less than when treatment is delayed for 3 minutes. Early treatment is followed by a return of skin pH to normal. When contact time exceeds 1 hour, the pH level of a sodium hydroxide (NaOH) burn cannot be reversed. Similarly, brief washing of a hydrochloric acid (HCl) burn more than 15 minutes after exposure does not significantly alter acidity of damaged skin.
Because contact time is a critical determinant of the severity of injury for skin exposed to a toxic liquid chemical, an exposed person or a witness to the injury must initiate hydrotherapy immediately. When workers' clothes are soaked with such agents, valuable time is lost if their clothing is removed before copious washing commences. Gentle irrigation with a large volume of water under low pressure for a long time dilutes the toxic agent and washes it out of the skin. During hydrotherapy, the rescuer should remove the patient's clothes and wear powder-free, latex-free, emergency medical examination gloves to prevent hand contact with the chemical(s).
Hydrotherapy
After exposure to strong alkali, prolonged hydrotherapy is especially important to limit severity of injury. In experimental animals, the pH level of chemically burned skin does not approach normal concentration unless more than 1 hour of continuous irrigation has been maintained, and it often does not return to normal for 12 hours despite hydrotherapy. This differs from HCl skin burns, in which the pH level usually returns to normal within 2 hours after initiating hydrotherapy.
The mechanism by which NaOH maintains an alkaline pH level despite treatment is related to byproducts of its chemical reaction to skin. Alkalis combine with proteins or fats in tissue to form soluble protein complexes or soaps. These complexes permit passage of hydroxyl ions deep into the tissue, limiting their contact with water diluent on the skin surface. Conversely, acids do not form complexes, and their free hydrogen ions are easily neutralized.
Regardless of causative agent, continue hydrotherapy once the patient arrives in the ED. If the chemical is localized in the patient's hand, immerse the injured part in a sink under flowing tap water. For other anatomic sites, place them supine in a hydrotherapy tank in which the temperature of the water can be regulated. Continue hydrotherapy treatment for 2-3 hours for acid burns and for at least 12 hours for strong alkali burns.
When the patient's clothing comes in contact with solid chemical (eg, lye), remove contaminated clothing before instituting hydrotherapy. Remove all visible solid particles from the patient's skin during copious irrigation with water. Deliver water to the wound at the lowest possible pressure, because high-pressure irrigation (shower) may disperse liquid or solid chemical into the patient's or rescuer's eyes.
Water Is the Agent of Choice
Water is the agent of choice for decontaminating acid and alkali skin burns. Deleterious effects of attempting to neutralize acid and alkali burns were first noted in experimental animals in 1927. [10] In every instance, animals with alkali or acid burns that were washed with water survived longer than animals treated with chemical neutralizers. The additional trauma of the heat generated by the neutralization reaction superimposed on the already existing burn accounts for the striking difference between the results of these 2 treatment methods. The same effect may occur when certain chemicals contact water, yet large volumes of water tend to limit this exothermic reaction.
Surgeons are beginning to question the belief that neutralization of an alkaline burn of the skin with acid does, indeed, increase tissue damage due to the exothermic nature of acid-based reactions. [11] In experimental studies in animals, surgeons demonstrated that topical treatment of alkaline burns with a weak acid such as 5% acetic acid (ie, household vinegar) resulted in rapid tissue neutralization and reduction of tissue injury in comparison to water irrigation alone. The observed benefits of treating alkaline burns with 5% acetic acid in the rat model are significant and require clinical testing.
Treating Acid and Alkali Eye Injuries
Acid and alkali injuries involving the eye are among the most disastrous of chemical burns. [12] Regardless of the nature of chemical involved, the primary goal is to immediately institute copious irrigation. At the scene of the injury, the exposed person should submerge his or her eyes in a container of tap water and continuously open and close them. In the absence of a container, hold face and eyes beneath a faucet and continuously irrigate with water. If possible, maintain irrigation during transport to hospital.
In the ED, subject the eye to immediate hydrotherapy. This is most easily accomplished using a low-flow stream of 0.9% NaCl from intravenous (IV) tubing. The patient's response to chemical spillage into the eye can frustrate emergency treatment: responses include severe blepharospasm, tearing, and forceful rubbing of the eye. Topical anesthetic agents help limit pain and improve patient cooperation. Lid retractors may be necessary to evert eyelids and ensure adequate evaluation and irrigation of conjunctival sac. First, remove any foreign material or solid chemical. Continue irrigation until the pH level of the conjunctival sac returns to its physiologic level (pH 7.4). Monitor the pH level of the conjunctival sac with a Ninhydrin reagent strip. Compare the pH levels of the affected and unaffected eye.
After irrigation, stain eyes with fluorescein to detect corneal injury. Then perform slit-lamp examination of the eye with corneal injury to determine the extent of damage to the anterior segment of the eye and anterior third of the vitreous chamber. Initial slit-lamp examination of alkali burn often reveals corneal erosion, swelling of the corneal epithelium, and clouding of the anterior chamber. Treat all eyes that demonstrate corneal abrasion with a broad-spectrum antibiotic emollient instilled in the conjunctival sac (eg, chloramphenicol, gentamicin).
Ophthalmologic consultation and close follow-up care are warranted in all significant exposures, and hospitalization for continuous irrigation occasionally may be required. (For more information, see Medscape Reference article Ophthalmologic Approach to Chemical Burns.) Measure intraocular pressure serially to detect pressure increases. Occasionally treat the injured eye with long-acting cycloplegic, mydriatic, and carbonic anhydrase inhibitor for 2 weeks or until pain disappears. This treatment decreases the potential for pupillary constriction, increased intraocular pressure, and early glaucoma. Encourage mobility of the globe to avoid development of conjunctival adhesions (symblepharon).
Ocular chemical injury remains one of the most difficult ocular emergencies. The prognosis for a burned eye depends not only on the severity of the injury, but also on the rapidity and mode of treatment.
Recently, amniotic membrane patching (AMP) has been demonstrated to be useful toward achieving a desirable outcome for acute ocular chemical burns. The human placenta was obtained shortly after elective caesarean delivery from a donor mother. Human immunodeficiency virus, hepatitis virus type B, hepatitis virus type C, and syphilis were serologically excluded. Temporary AMP with modifications in suture placement was performed in patients inflicted with acute chemical injury. Clinical results suggest that immediate AMP is quite useful for managing moderately severe acute ocular chemical injury by facilitating rapid epithelialization and pain relief and by securing ocular surface integrity.
Effects of Alkali Burns
Alkali substances are the most toxic chemicals, and anhydrous ammonia appears to be the worst offender. Even alkali burns that seem mild can result in devastating injury, because alkalis tend to react with the lipid in corneal epithelial cells to form soluble soap that penetrates corneal stroma. Alkali moves rapidly through the stroma and endothelial cells to enter the anterior chamber. Anhydrous ammonia can penetrate the anterior chamber in less than 1 minute.
Alkali usually kills each tissue layer of the anterior segment of the eye that it contacts. This results in occlusive vasculitis around the corneoscleral limbus, which makes repair of these tissues difficult. As the tissues of the anterior segment of the eye degenerate, perforation follows with the development of endophthalmitis and loss of the eye. If perforation can be prevented, recovery of sight may be possible through eventual corneal transplantation. Recent experimental studies conclude that destruction of corneal stroma can be minimized by drug therapy (eg, N-acetylcysteine, steroids). However, drug therapy has limited therapeutic usefulness because of the need for frequent applications, significant number of clinical failures, and potential adverse effects.
Management of Ingested Alkali
Corrosive esophagitis has been a long-lasting problem, especially in olive-producing areas. In recent years, household lye products have come into routine use and have unfortunately been associated with increased frequency of caustic esophagitis induced by accidental ingestion. Frequently, the concentration of the ingested agent is unknown because of the absence of manufacturers' labels on the containers. The victims are usually children in families of low socioeconomic status. The ingestion of lye can cause serious injury to the esophagus, frequently causing corrosive esophagitis and the even more serious complication of esophageal strictures. Esophageal burns vary in burn location, burn length, burn severity, admission time after ingestion, and complications. Consequently, the management of these injuries has been a challenge to pediatric surgeons and the gastroenterologist.
Atabeck et al outlined a strategy for treating caustic burns. [13] If strictures formed, they were treated at 2-3 week intervals by antegrade dilatation via a rigid esophagoscope with the patient under general anesthesia. A nasogastric tube was placed into the stomach to allow feeding and to prevent complete luminal obstruction. (Click here to view Medscape Reference’s illustrated guide to nasogastric tube placement.)
In cases of severe burns and when difficulty was encountered with antegrade dilatation, a gastrostomy was performed with a trans-stricture string, followed by antegrade string-guided dilation of the stricture. Initial dilation was performed with a dilator 1-2 sizes smaller than the estimated diameter of the stricture. In general, the patients were only dilatated 2-3 French (F) sizes larger than the first dilator that met resistance per dilation session. Patients with recalcitrant esophageal strictures were entered into their esophageal stenting treatment program.
In cases that did not respond to 3 consecutive dilations, gastrostomy and esophageal stenting were performed. Polytetrafluoroethylene (PTFE) intraluminal stenting was used to treat serious cases. The esophageal stent was inserted 12 weeks after caustic ingestion. The length and caliber of the esophageal stricture was determined by esophagoscopy. PTFE esophageal stent was custom-made for each patient. The length of the strictured segment of the esophagus was measured; the stent was made 2 cm longer so that the stent would overlap 1 cm beyond the stricture on each end when correctly positioned. Both ends of the stent were secured to a 4F ureteral catheter with zero polypropylene. The proximal part of the ureteral catheter was fixed to the nose, while the distal part was fixed to the gastrostomy tube.
If gastroesophageal reflux was diagnosed with 24-hour pH monitoring before or during the stenting period, a Collis gastroplasty was performed. During the stenting period, the patients underwent barium esophagogram every 2 months. No esophagoscopy was performed in this period. The esophageal stenting program was terminated after 9-14 months of stenting. All patients were swallowing fluids and semisolid foods easily. The most severe complication was esophageal perforation.
Ingestion of caustic agents often causes severe corrosive gastritis, in which ulceration is most extensive in the antrum. Early perforation with peritonitis and late cicatricial stenosis with thickening of the gastric wall are the most important complications of corrosive gastritis. Kamijo et al reported the case of a patient in whom high-resolution images of the gastric wall were obtained by endoscopic ultrasonography (EUS). [14] This visualization documented severe corrosive gastritis and helped to predict the development of antral stenosis, which ultimately required surgical intervention. The patient was subsequently treated with a laparoscopic gastrectomy.
A retrospective study by Boskovic and Stankovic indicated that in children who have ingested a caustic substance, endoscopic evaluation is necessary because the sensitivity and specificity of clinical signs for predicting the severity of injury are too low. The study included 176 children who had ingested either alkali (96 patients), acid (41 patients), or another caustic agent (39 patients). The investigators found that clinical findings could predict the severity of esophageal injury with a sensitivity and specificity of 74% and 73%, respectively, and the severity of gastric injury with a sensitivity and specificity of 75% and 68%, respectively. [15]
Effects of Acid Burns
Eyes tolerate acid burns better because like other living tissue, they have significant acid-buffering capacity. Tear film, the proteins present in tears, and conjunctival epithelial cells rapidly neutralize acid. Consequently, acid typically causes epithelial and basem*nt membrane damage, yet rarely damages deep endothelial cells. Acid burns that injure the periphery of the cornea and conjunctiva often heal uneventfully, leaving a clear corneal epithelium. In contrast, acid burns of the central part of the cornea may lead to corneal ulcer formation with neovascularization and scarring, requiring later reconstruction.
Hydrofluoric Acid
During 1985 and 1986, the American Association of Poison Control Centers Data Collection System received 2367 reports of human exposures to hydrofluoric acid (HF). [16, 17] Four fatalities occurred, three from ingestion and one as a result of dermal exposure. Significant local and systemic toxicity can result from exposure of eye, skin, or lung to HF.
HF is one of the strongest inorganic acids. Its use is mainly industrial, involving glass etching, metal cleaning, electronic industries, and biochemical laboratories. However, it can also be found in households as a component of rust removers and aluminum-cleaning products. Because of these numerous applications, there is a large risk for accidental human exposure to HF. In the United States, more than 1000 incidents of accidental exposures to HF are reported annually. The risk and potential toxicity associated with such exposure are often underestimated by persons handling this liquid in households, laboratories, and industrial plants. Significant local and systemic toxicity can result from exposures of the eyes, skin, or lungs to HF.
Inhalation of HF vapor is rare and usually involves explosions that produce fumes or high concentrations of liquid HF (>50%) that soak the clothing of the upper body. Patient outcomes vary considerably depending on concentration and duration of exposure to HF. Inhalation and skin exposure to 70% HF has caused pulmonary edema and death within 2 hours.
Pulmonary injuries that are not evident until several days after exposure also can occur. The patient has no respiratory symptoms and a normal chest radiograph initially, yet massive purulent tracheobronchitis that is refractory to treatment may develop. Respiratory symptoms may persist for months after inhalation of HF fumes. Sustained irritation of the larynx and pharynx with fibrinous, granulating deposits on thickened vocal cords may cause persistent cough and hoarseness.
Management of exposure to HF
Management of inhalation exposure involves removing the patient from the source, then decontaminating clothes and skin. [18, 19] If respiratory symptoms are present, monitor the patient with pulse oximetry, administer humidified oxygen using a nonrebreathing reservoir bag mask system, and evaluate him or her for laryngeal edema, pneumonitis, pulmonary edema, pulmonary hemorrhage, and systemic toxicity.
Treatment of HF inhalation injury is primarily symptomatic. Administration of 2.5-3% calcium gluconate solution by nebulizer as therapy for inhalation of HF has been suggested but not tested. Admit asymptomatic patients with possible HF inhalation for observation.
Eye exposure to HF vapors produces more extensive damage than that of other acids at similar concentration. The extent of damage by HF depends on its concentration. Exposure of rabbits to 0.5% HF causes mild initial conjunctival ischemia that resolves in 10 days; 8% HF causes severe initial ischemia that is still noted after 65 days. Corneal opacification and necrosis occur after exposure to 20% HF.
Irrigation therapy for HF
Initiate immediate and copious irrigation of the exposed eyes at the scene of exposure and continue for at least 30 minutes during transport to the ED, where an ophthalmologic examination can be performed promptly. Local ophthalmic anesthetic drops enhance patient comfort and cooperation during irrigation and evaluation.
In experimental animals, single irrigations with 1 L of water, isotonic saline, or magnesium chloride are the only treatments that are therapeutically beneficial without causing toxicity. Benefits include decreased epithelial loss and reduced corneal inflammation. Repeated irrigations over time have no therapeutic merit and are associated with an increased occurrence of corneal ulceration. Patients with significant ocular exposure to HF should be seen emergently by an ophthalmologist.
HF skin exposures
A large number of personnel in industry and research handle concentrated solutions of HF. Relatively dilute solutions of HF (0.6-12%) are available to the public in the form of rust removal and aluminum cleaning products. During handling of containers holding HF, inadvertent contamination of unprotected fingers and hands often occurs, resulting in chemical burn injury. HF skin burns have certain distinct characteristics.
First, exposure causes progressive tissue destruction associated with intense pain that can be delayed in onset for hours and can persist for days if untreated. Skin at the site of contact develops a tough, coagulated appearance. Untreated sites progress to indurated, whitish, and blistered vesicles that contain caseous, necrotic tissue. In exposure of the digits, HF has a predilection for subungual tissue. Severe untreated burns may progress to full-thickness burns and may even result in loss of digits.
Treatment of HF skin exposure
Initial treatment of HF skin exposure is immediate irrigation with copious amounts of water or a saturated solution of sodium bicarbonate for at least 15-30 minutes. Most exposures to dilute solutions of HF respond favorably to immediate irrigation. Severe pain or any pain that persists after irrigation denotes a more severe burn that requires detoxification of fluoride ion by promoting the formation of an insoluble calcium salt.
Remove all blisters first because necrotic tissue may harbor fluoride ions. Then detoxify fluoride ion through topical treatment, local infiltrative therapy, or intra-arterial infusion of calcium. Calcium gluconate (2.5%) gel is the preferred topical agent. Because skin is impermeable to calcium, topical treatment is effective only for mild, superficial burns. Because this gel is not stocked in most hospital pharmacies, it must be formulated by mixing 3.5 g of calcium gluconate powder in 150 mL of water-soluble lubricant (eg, K-Y Jelly). An occlusive cover (eg, latex glove) should secure the gel.
Infiltrative therapy for HF burns
Infiltrative therapy is necessary to adequately treat deep and painful HF burns. Calcium gluconate is the agent of choice and can be administered either by direct infiltration or intra-arterial injection.
Direct infiltration
A commonly used technique involves injecting 10% calcium gluconate subcutaneously through a 30-gauge needle at a maximum dose of 0.5 mL/cm2 of skin. Using 5% calcium gluconate made by diluting the aforementioned solution with an equal amount of isotonic saline recently has been shown to reduce irritation of tissues and decrease subsequent scarring. Hospitalize patients receiving this treatment for observation and toxicologic consultation.
Despite its wide acceptance, the infiltration technique has notable disadvantages, especially when treating digits. A regional nerve block is recommended because injections may be very painful. Removal of the nail to expose the nail bed is required if subungual tissue is involved. Vascular compromise can occur if excessive fluid is injected into skin exposure sites, and unbound calcium ions have a direct toxic effect on tissue.
Intra-arterial injection
Place an intraarterial catheter in the appropriate vascular supply close to the site of HF exposure (eg, radial, ulnar, brachial, carotid artery). A variety of dilute solutions of calcium salts have been infused over 4 hours, including the following: (1) 10-mL solution of 10% calcium gluconate or calcium chloride mixed in 40-50 mL of D5W, repeated if pain returns within 4 hours; (2) 10-mL solution of 20% calcium gluconate in 40 mL of normal saline for radial or ulnar artery infusion; and (3) 20 mL of 20% calcium gluconate in 80 mL of normal saline for brachial artery infusion, repeated at 12-hour intervals if needed. If more than 6 hours have elapsed since the time of HF exposure, tissue necrosis cannot be prevented, even though pain relief can occur up to 24 hours after exposure.
A study by Yuanhai et al indicated that intra-arterial infusion of calcium gluconate relieves pain from HF burns to the distal limbs. The study, which involved 118 patients with such burns, reported a quick reduction in pain scores on the visual analog scale (VAS) for 107 patients following the first infusion of calcium gluconate. The remaining patients scored higher than 4.0 on the VAS 4 hours after the first infusion, necessitating a second one. [20]
As with direct infiltration, the intra-arterial infusion technique has potential disadvantages. The procedure may induce arterial spasm or thrombosis, resulting in significant skin loss. It is also more costly because it requires hospitalization for use of the infusion pump and monitoring of serum calcium if repeated infusions are used.
HF action
HF binds calcium and magnesium with strong affinity. Systemic fluoride toxicity, including dysrhythmias and hypocalcemia, can occur from ingestion, inhalation, or dermal exposure to HF. Consequently, all patients with significant HF exposure should be hospitalized and monitored for cardiac dysrhythmias and electrolyte status for 24-48 hours.
Hypocalcemia can occur after significant exposures to HF and should be corrected with 10% calcium gluconate administered intravenously. If left untreated, a burn caused by 7 mL of 99% HF can theoretically bind all available calcium in a 70-kg man. Prolonged QT interval on electrocardiogram is a reliable indicator of hypocalcemia.
Formic Acid
Formic acid is a caustic organic acid used in industry and agriculture. [21, 22, 23] It causes cutaneous injury by coagulation necrosis. Systemic toxicity occurs after absorption and manifests as acidosis, hemolysis, and hemoglobinuria. Hemolysis is the result of the direct effect of formic acid on red blood cells. Institute copious wound lavage immediately. Treat acidosis with sodium bicarbonate. Mannitol may be used to expand plasma volume and promote osmotic diuresis in patients with hemolysis. Exchange transfusions and hemodialysis may be needed in patients with severe formic acid poisoning.
Anhydrous Ammonia
Ammonia is used in the manufacture of explosives, petroleum, cyanide, plastic, and synthetic fibers. [24] In addition, it is widely used as a cleaning agent and as a coolant in refrigerator units. As an agricultural fertilizer, ammonia is ideal because of its high nitrogen content (82%).
Sudden release of liquid ammonia can cause injury through two different mechanisms. It has an extremely low temperature (-33°C) and freezes any tissue it contacts. Ammonia vapors readily dissolve in the moisture of skin, eyes, oropharynx, and lungs to form hydroxyl ions, which cause chemical burns through liquefaction necrosis. The severity of injury directly relates to the concentration and duration of exposure to ammonia.
Irrigation for anhydrous ammonia injury
Treatment consists of prompt irrigation of eyes and skin with water and management of inhalation injury. If necessary, secure the airway by nasal or oral intubation. Use a large diameter tube to prevent distal airway obstruction from sloughing of mucosa. After intubation, manage lower airway injury with positive end expiratory pressure (PEEP) ventilation.
Cement
Cement burns are alkali burns. [25] When dry cement is combined with water, hydrolysis occurs. Resulting mixture is essentially a solution of slated lime saturated in water with an initial pH of 10-12. As hydrolysis continues, the pH level may continue to rise to 12 or 14, which is comparable to that of sodium, potassium hydroxide, or lye. In addition, contact dermatitis from chromate (a trace element) has been reported.
Treatment of cement burns
The best treatment of cement burns is immediate copious irrigation until the substance is completely gone, a practice performed by experienced workers who habitually wash off cement throughout the day. Prominent warning labels on packages containing cement products direct the user to wear protective gloves when using the product in either its wet or dry state.
Cement burns of the lower extremities respond well to immediate copious irrigation followed by coverage with a medicated bandage (eg, Gelocast Unna boot) that allows patient to ambulate.
Phenol and its Derivatives
Phenols are used industrially as starting materials for many organic polymers and plastics. They are used widely in agricultural, cosmetic, and medical fields. Because of their antiseptic properties (first appreciated by Lister), they are used commonly in many commercially available germicidal solutions. A number of phenol derivatives (eg, hexylresorcinol, resorcinol) are more bactericidal than phenol itself.
Chemical peels
Plastic surgeons use dilute solutions of phenol for chemical facial peels. [26] Phenol (which is usually mixed with water, soap, and croton oil for this application) can produce a partial-thickness burn of predictable depth in a controlled manner. It has been the standard for many years for new technologies in skin resurfacing to remove both coarse and fine wrinkles, irregular facial pigmentation, and actinic keratoses.
The concentration of phenol is kept sufficiently low to reduce the occurrence of systemic complications. Interestingly, higher concentrations of phenol result in a shallower burn depth. A higher concentration of phenol results in increased coagulation of the keratin in the skin, thus forming a barrier to further penetration. Histologic studies have demonstrated that 100% concentrations of phenol produce 35-50% less penetration than a 50% phenol solution.
The physician performing phenol chemical peels should be concerned about the possibility of rapid phenol absorption. When phenol is applied to more than 50% of the facial surface in less than 30 minutes, a high incidence of cardiac arrhythmias is reported. When the application time over the same area was increased to 60 minutes, arrhythmias were avoided. Because of the complication of cardiac arrhythmias, all patients undergoing phenol peeling should be monitored electrocardiographically and have an intravenous line in place.
Following application of the phenol solution, the skin is covered with an occlusive dressing that consists either of multiple layers of waterproof tape or petroleum jelly to prevent evaporation of the phenol, allowing for increased penetration and burn depth. The peeled skin is maintained by daily cleansing and consequent reapplication of ointment, which keeps the surface moist and prevents desiccation. If this protocol is followed, healing is completed within 5-7 days.
Phenol is an aromatic acidic alcohol. [27] This compound and its derivatives are highly reactive, corrosive, contact poisons that damage cells by denaturing and precipitating cellular proteins. Their characteristic odor usually signals their presence. After phenol penetrates dermis, it produces necrosis of papillary dermis. This necrotic tissue may temporarily delay its absorption.
When skin comes in contact with phenol, institute treatment immediately. Irrigate exposed area with large volumes of water delivered under low pressure. Dilute solutions of phenol are more rapidly absorbed through skin than concentrated ones, thus avoid gentle swabbing of surface of skin with sponges soaked in water. Because phenol may become trapped in the victim's hair or beard, remove any hair that has come into contact with the chemical agent as soon as possible.
Symptoms of exposure
In animal studies, exposure to as little as 0.625 mg/kg of phenol causes death. In humans, absorbed phenol causes profound CNS depression, resulting in coma and death from respiratory failure. Marked hypotension may occur as a result of central vasomotor depression in addition to a direct effect on the myocardium and small blood vessels. Phenol also is a powerful antipyretic that produces a fall in body temperature. Metabolic acidosis may result from shock as well as from the direct effect of acidic phenol.
A number of substituted phenols (eg, resorcinol, picric acid) have systemic actions distinct from that of phenol. Stimulation of CNS is commonly encountered after absorption of resorcinol. Picric acid hemolyzes RBCs and causes acute hemorrhagic glomerulonephritis and acute liver injury.
Treatment of phenol exposure
Experimental studies indicate that water alone is effective in reducing the severity of burns and preventing death in animals with skin exposed to phenol and its derivatives. The most effective treatment is undiluted 200-400 molecular weight polyethylene glycol (PEG) or isopropanol. This material should be stocked in hospitals located near areas of phenol use. Often, it can be located in the chemical section of hospital pharmacies.
A quick wipe of the skin with PEG solution reduces mortality and burn severity in experimental animals. These solutions can be used in phenol burns of the face because they are not irritating to eyes. Decontaminate with water until the PEG solution is obtained. Use large amounts of water because small amounts are detrimental, enhancing dermal absorption of phenol. Remove phenol in a well-ventilated room to avoid exposing hospital personnel to high concentrations of phenol fumes.
Treatment of systemic symptoms is purely symptomatic. Respiratory depression may require ventilatory support. Treat hypotension with isotonic crystalloid fluid and pressor agents as needed. Metabolic acidosis may require treatment with sodium bicarbonate. Alkalinization also prevents the precipitation of hemoglobin in urine that occurs with hemolysis. Administering mannitol intravenously, which causes osmotic diuresis, can enhance hemochromogen excretion in urine. Anticonvulsants may be required to treat seizures resulting from CNS stimulation.
