Symptoms, diagnosis and treatment of chemical burns

Chemical burns

Injuries from caustic substances usually occur in chemical industry, during transportation and handling of hazardous materials, at home, during job training and at school.

Chemical burns are described as injuries to the skin or mucous membranes caused by chemical substances. Usually, strong acids or bases cause protein denaturation in tissues, resulting in cell damage and apoptosis with subsequent necrosis. In addition some substances may cause toxic as well as thermal damage. The extent of cutaneous damage depends on type, amount, and concentration of the caustic substances, but also on the duration of exposure. Disrupting the pathophysiological mechanism of the chemical reaction at an early stage is therefore the foremost goal of any medical treatment, before treating the actual damage.

specific decontamination: transformation of the acid into its salt, cleavage/hydrolysis of toxic compounds, application of antidotes, etc.

natural decontamination: vaporization of volatile substances

First aid treatment, which has to be initiated immediately after exposure, should ensure in particular the protection of those providing first aid. The effects of hazardous substances must be reduced for the individual involved, for others at risk, and for rescue personnel. In this regard, caustic substances are labeled in the chemical industry with specific hazardous material declarations and accompanied by accident procedure sheets from which instructions can be gathered for administering first aid.

Contamination with caustic substances in solid, liquid or gas form affects several organ systems in different ways depending on the concentration, the way of contact with the body, and the duration of exposure.

Decontamination

As an initial procedure, decontamination of the affected patient is of utmost importance to reduce the contact time between the caustic substance and the tissue. The decontamination process has to be divided into specific procedures:

unspecific decontamination: mechanical removal of toxic agents, when indicated extensive rinsing additionally provides for a desired diluting effect

Marc G. Jeschke et al. (eds.), Handbook of Burns

Affection of different organ systems

Respiratory tract

Odor and irritation of breathing such as coughing following inhalation have a significant warning effect. If vapors are inhaled, symptoms such as burning, dryness of the nose and throat, coughing, dys-

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pnoea, and angina pectoris symptoms may appear [4]. Increased production of secretion, raised capillary permeability, surfactant destruction, bronchoconstriction, and pulmonary hypertension are possible sequelae [12]. Inhalation of higher concentrations can lead to laryngospasm and complete obstruction of the respiratory tract due to a direct caustic toxic effect. All symptoms can occur in two phases. After a transient stimulation phase and a symptom-free interval, toxic pulmonary edema can occur up to 72 hours post exposure [25, 31].

Emergency treatment of inhalation trauma is still a subject of controversy. After first aid such as rescue of the victim, avoiding further exposure and supplying oxygen, has been provided, the question of administering of steroids is still under vehement discussion. In particular, efforts are directed to attain a rapid, unspecific anti-inflammatory effect by inhibiting the biosynthesis of prostaglandins and leukotrienes [12]. In case of doubt, inhalation administration is therefore recommended in various dosages and intervals [4, 26, 31] as well as intravenous administration for prophylactic and anti-ede- matous treatment [4, 19]. On the other hand, the an- ti-inflammatory effect that occurs especially with high-dose intravenous administration is viewed critically, since the immunosuppressive effect of corticoids has to be considered at the same time. This should be avoided at all costs, particularly in the case of more severely injured persons and/ or patients with extensive thermal burns [12, 26]. For bronchial spasm, ß2-mimetics are indicated, such as those approved for the treatment of bronchial asthma [15]. Initially, X-ray images of the thorax typically appear normal. Clear signs of pulmonary edema, such as hilus enlargement or centrally accentuated and patchy shadows, are late radiological signs that often cannot be recognized until the second phase of the injury [25]. For monitoring purposes, an initial chest X-ray should be made, particularly in patients with concomitant cardiopulmonary medical conditions.

Eye

In the eye, the exposure to fumes and vapors leads to painful paresthesias with spasmic eyelid closure, redness, lacrimation, and conjunctivitis. Due to protein denaturation, severe corneal ulcers and necroses

are to be expected, as well as clouding of the cornea and lens through direct contact with acid components. Complete loss of vision and subsequent blindness are possible in severe cases.

In the case that vapors or liquid components come into direct contact with the eyes, they must be flushed immediately with plenty of water or neutral saline solution, if possible while everting the eyelids [19]. The therapeutic aim is the normalization of the conjunctival pH value (7.0). Any possible eyelid spasms can be resolved by applying locally anesthetizing eye drops [8]. Rinsing with chelating agents such as diphoterine is discussed for decontamination purposes. Due to their broad buffering capacity (neutralizing capacity from pH 1 to 13), they can be used for eye-contaminations with acids as well as bases [2, 20].

Gastrointestinal tract

Oral ingestion of diluted concentrations leads to nausea and gastroenteritic symptoms. Retrosternal burning and bloody vomiting have been described [4, 19, 31]. Higher concentrations cause severe damage to the mucous membranes especially of the larynx ant the esophagus. Constrictions and perforations have been described [35].

If caustic substances are ingested orally, inducing emesis is contraindicated. Repeated contact of the esophageal mucosa with the substance raises the risk of perforations. In addition, neutralization and administration of charcoal is not necessary [4, 19, 31]. Administering water by mouth with the aim of rinsing the esophageal tissue and achieving a diluting effect is recommended. The administration of proton pump inhibitors in analogy to gastroesophageal reflux disease (GERD) is recommended, as chemical burns cause dysmotility of the esophagus with gastroesophageal reflux, consequently impairing recovery [1, 19]. In animal experiments it could be shown that omeprazole and vitamin E prevent inflammatory changes of the affected esophagus and can thereby reduce the development of strictures [30].

In case of ingestion or suspected chemical burns, gastroduodenoscopy should be taken into consideration to determine the extent of intra-gastral damage and, if necessary, should be combined with surgical intervention [4, 19, 31].

The primary administration of antibiotics is indicated for deep burns (deep second-degree and thirddegree burns) and perforations and should cover a broad spectrum [17]. Treatment with steroids is a subject of controversy, because an advantage for preventing strictures could not yet be clearly proven [3, 17, 19, 22]. In the case of difficulties of swallowing and when there is no risk of perforation, the use of a nasogastric tube placed under visualization is recommended [19]. Parenteral nutrition is necessary at least in the acute phase (up to 7 days), but in some cases also until healing is completed, to prevent infection and strictures [17].

Hematological signs

Following extensive exposures, methemoglobinemia, hemolysis and methemoglobinuria can develop due to the formation of nitrous gases (NOx) [4, 8, 31]. Depending on the concentration, typical clinical signs consist of gray-blue skin color (15–30% MetHb), headache, fatigue, dizziness, tachycardia, dyspnea (30–50% MetHb), stupor, bradycardia, cardiac arrhythmia, respiratory depression (50–70%), cardiac arrest, unconsciousness, or coma (60–70%). If the MetHb level exceeds 90%, a fatal outcome is to be expected.

Routine laboratory tests should include a complete blood count as well as glucose and electrolyte levels. In symptomatic patients, an arterial blood gas analysis should be carried out with determination of the methemoglobin concentration [7].

It is recommended that toluidine blue, methylene blue or thionine, as well as vitamin C should be given to accelerate the reduction of MetHb to hemoglobin [4, 16]. Therapy with positive end-expiratory pressure (PEEP) and an exchange transfusion should be taken into consideration in life-threatening situations.

Nephrologic symptoms

Acute kidney failure can occur in the form of tubular necrosis due to disturbances of the acid-base balance (metabolic acidosis) and due to hemolytic products [8].

If renal involvement is suspected, all efforts should be directed towards the induction of an in-

creased diuresis. The addition of mannitol to the infusion regimen supports this process with its osmotic diuretic effect. Consequences of acute tubular, necrotic tissue change can be treated symptomatically with the body-weight adapted administration of bicarbonate and fluids [8].

Skin

Tissue damage from contamination is due to protein denaturation. Interaction with acids causes coagulation necroses that in most cases keep the acids from penetrating into deeper-lying tissue. Only those tissue areas are damaged that, depending on duration and concentration, were in direct contact with the acting acid (exception: hydrofluoric acid, see below).

In contrast, bases cause colliquative necroses that permit progression of the corrosive effect into deeper layers of the skin and thus more extensive damage. The results are diffusion and penetration into underlying tissues with a subsequent more extensive corrosive effect [31].

Skin contact with less concentrated fumes or vapors of caustic substances can lead to burning pain, redness, and inflammation. Firstto third-degree burns with their respective subsequent scarring result from direct contact with the concentrated substance [31]. The classification of chemical burn injuries and their signs and symptoms follows that of thermal burn injuries.

As initial treatment, decontamination and extensive flushing of the affected skin areas are certainly of critical importance to reduce the duration of contact between the substance and the skin as much as possible. In addition, unspecific anti-in- flammatory, analgesic and skin care ointments for first-degree injuries are well established. Dermal chemical burns, however, require more specific therapy. Particularly during the exudative and proliferative phase, treatment regimens must allow protection against dehydration and microbial colonization [27]. Both goals can be accomplished using the commonly used therapy with silver sulfadiazine [23], which is effective against a broad spectrum of germs including gram-negative ones and Candida albicans. Silver sulfadiazine, however, carries the risk of leukopenias and disturbances of the acid-base balance when applied to large areas [32]. Likewise, top-

ically effective antiseptics such as polyhexanide combined with polyethylene glycol in Ringer’s solution or octenidine with phenoxyethanol in gel form can be used. In their main indication as surface antiseptics, such substances permit a better clinical assessment of the injury compared to sulfadiazines [32].

Depending on the state of the wound, enzymatic conditioning with plant and bacterial proteases may also be applied. If the wounds are in the process of normal healing but are still secreting fluid, absorbent foam bandages can be used that can be left in place for up to 3 days but which still permit assessment of the wound at all times. The silver sulfadiazine dressings used at the beginning should be changed to the procedure described above to ensure a reliable clinical assessment of the wounds. Later in the healing process, they can be changed to simple cremes with a high fatty component. Until healing and possible scarring are complete, sunblocker should be applied before the wound is exposed to UV and sunlight.

The role of modern methods of semi-permanent wound dressings (for example Acticoat , Biobrane , Suprathel and Matriderm ) widely used in he treatment of superficial and partial thickness thermal burns is not yet defined in the treatment of acid burns at the present time. Since clinical experience with such injuries is much lower than that with thermal burns, it is our opinion that procedures using permanent wound dressings should not be recommended for chemical burns. Clinical monitoring of such wounds should be possible at all times.

Specific agents

Nitric acid

Nitric acid, also called hydrogen nitrate and having the chemical formula HNO3, is an inorganic oxoacid of nitrogen. At room temperature, concentrated nitric acid (65% HNO3) is a colorless to yellow or brown liquid with a pungent odor. Its corrosiveness is due to both its acidic effect and an oxidation reaction [31]. Contact with metal has an explosive effect. It is used in the production of fertilizers, explosives and dyes, and in metal processing [4].

The maximum allowable concentration (MAC value) of nitric acid at which no health risks can be expected is 2.6 mg/m3 or 1 ml/m3 [11]. According to the German Ordinance on Hazardous Materials (GefStoffV), it is classified depending on its concentration as Xi (irritant) to C/O (corrosive, oxidizing agent) and carries the risk phrase R 35 [6]. There is no known antidote.

Due to the so-called xanthoproteic reaction, in which nitration takes place on the benzene ring of aromatic amino acids, contact between the skin and nitric acid results in coagulative tissue damage with specific, partially persisting neon-like yellowing of the wound areas (Figs. 1, 2) [8, 31]. Overall, the typically yellow nitric acid burns demarcate more slowly than thermally damaged areas (Fig. 2) [18]. Plastic surgical procedures and follow-up treatment of nitric acid burns follow the same principles as in thermal burn injuries.

Attention must be paid to possible involvement of the eyes, ingestion trauma, kidney function, and the development of MetHb.