Upper airway involvement should be suspected in the event of smoke inhalation in closed spaces, burns to the face, neck, lips and oropharyngeal mucosa, singed nasal hairs and the presence of progressive hoarseness or a cough productive of carbonaceous sputum.

The clinical picture may progress to obstructive symptoms. Stridor, dyspnea, increased respiratory effort and cyanosis appear only once critical narrowing of the airway occurs. Stridor often precedes obstruction. Airway edema and swelling of burnt skin tissues follow a similar course, with internal and external anatomical distortion.

All burn patients should undergo inspection of the oropharynx for the presence of soot, or evidence of chemical or thermal damage. Direct laryngoscopy is a useful, quick and simple procedure. Immediate injury to the airway mucosa manifests itself by the presence of edema, erythema and ulceration. Due to the fact that edema may progress over 24h, multiple examinations are required if airway injury is confirmed and no intubation was performed. Fibroscopy may also be useful if airway damage is suspected and to assess known lung damage.

It is important to decide whether to protect the airway by endotracheal intubation or if it can safely be managed without this procedure. One should not wait for signs of obstruction to proceed with intubation. When in doubt of whether progressive edema is likely, it is safest to intubate. There are three categories of patients at risk for airway compromise.22

• (a)

  Heat and smoke injury plus extensive facial and neck burns: this group invariably requires intubation.

• (b)

  Significant oral burns but no smoke injury: these patients have difficulty controlling secretions as edema evolves. Early intubation is the safest approach, as anatomical distortion of the mouth may hinder the process at later stages.

• (c)

  Heat and smoke injury, no facial burns: if there are no signs of severe upper airway edema, close monitoring may suffice.

Severity is diagnosed based on the clinical course rather than initial findings.

Soot remains present in lung secretions for several days after injury. Roncus and wheezing appear at the onset of inflammation. Continuous cough, bronchospasm and bronchorrhoea can lead to fatigue and hypoventilation. The most serious clinical consequences are airway obstruction and bronchospasm, which usually start within the first 24h, and intrapulmonary shunting and pulmonary infection, which usually develop in the next few days.

The diagnosis of inhalation injury is clinical and accompanied by a set of indirect observations. While the presence of carbonaceous secretions is an indicator of exposure to smoke, it does not establish the diagnosis or the severity of inhalation injury. Chest X-rays lack the necessary sensitivity to detect lung damage in the early stages, but its use is helpful as a baseline for determining future changes. Chest CT can be used to complement bronchoscopy in detecting clinically significant inhalation injury.23

Patients with smoke inhalation and burn injury require greater resuscitation volumes than patients with skin burns alone.

Adequate oxygenation must be maintained and bronchial hygiene facilitated. Some patients may receive non-invasive ventilation in the absence of usual contraindications.24 Endotracheal intubation may be necessary if the patient has increased work of breathing or if gas exchange is compromised. The consensus recommendations for mechanical ventilation also apply in this context, as do strategies for the prevention of ventilator-associated pneumonia (keep the head of the bed elevated, optimize endotracheal tube cuff pressure, adjust the patient's posture and perform mouth care). Prone positioning may be helpful in hypoxic patients. Bronchodilators may be administered to help optimize ventilation in the event of bronchospasm.22,24 Bronchoscopy can help improve pulmonary hygiene and patient prognosis by clearing secretions and sloughed epithelial cells.24

The effectiveness of aerosolised heparin is unclear. Inhaled nitric oxide (INO) causes selective vasodilation in well-ventilated lung segments, and may improve oxygenation and pulmonary hemodynamics. Antioxidants aerosols, cytokine inhibitors and neutrophil adherence inhibitors were tested in experimental studies, showing a reduction of mucosal and alveolar edema and atelectasis.

Extracorporeal membrane oxygenation (ECMO) is used as a rescue treatment in refractory situations and is not a standard therapeutic option at this time.

The clinical manifestations of CO poisoning appear when levels of carboxyhemoglobin (COHb) rise above 15%. The symptoms are typical of tissue hypoxia, most notably neurological impairment and myocardial dysfunction (the organ systems most vulnerable to hypoxia). There is no set combination of symptoms that confirms or rules out a diagnosis of CO poisoning. The intensity of clinical manifestations varies and does not correlate closely with COHb levels. Early signs tend to be neurological. CNS injury can lead to progressive and permanent damage. Severe myocardial dysfunction may occur, especially in patients with pre-existing coronary disease. The clinical diagnosis of CO poisoning should be confirmed by demonstrating elevated COHb levels. COHb can be measured by laboratory spectrophotometry of blood obtained at the scene and transported with the patient to the hospital, or obtained at the time of patient evaluation in the emergency department. Pulse CO-oximetry, where a probe is positioned on the fingertip is a technology which has been available since 2005. Although its accuracy and reliability have been reviewed, the results are somewhat controversial. As such, if pulse CO-oximetry supports the diagnosis, spectrophotometry measurements are recommended for confirmation. The determination of elevated COHb levels also indicates significant exposure to smoke, which points to the likelihood of chemical airway injury. Low COHb levels do not always mean minimal exposure, as oxygen management in the early stages can reduce levels during transport to the emergency department.

Cyanide poisoning has a similar clinical presentation, with metabolic acidosis and blurred vision in severe cases.28 The level of toxicity depends on the concentration of cyanide in the smoke. Persistent metabolic acidosis in a burn patient with adequate fluid resuscitation and cardiac output suggests carbon monoxide or cyanide poisoning. Acid–base balance and plasma lactate measurements are useful to determine intoxication. However, diagnosis is more difficult, as it is not possible to determine levels of cyanide (values below 0.1mg/L are considered normal).

“In situ” treatment is the same in both cases: remove the victim from the enclosure as soon as possible, and immediately administer high-flow oxygen.

The goal of oxygen therapy in patients with carbon monoxide poisoning is to displace CO from Hb. Levels of COHb decrease about 50% every 20min under administration of 100% oxygen. To successfully treat CO poisoning, it is important to know the concentration of COHb as soon as possible and administer oxygen therapy until levels of COHb fall below 10%.

Hyperbaric oxygen therapy (HBOT) (2–3atm) achieves faster CO displacement and is more useful in cases of prolonged exposure, when it is harder to displace CO from the cytochrome system. The drawback of HBOT is the need to transfer the burn patient to a treatment facility equipped with a hyperbaric chamber during the critical period of hemodynamic and pulmonary instability. It may be considered in patients with severe neurological involvement and levels of COHb greater than 50%, without extensive burns or severe lung damage, and whose symptoms fail to improve despite high-flow oxygen.22

Endotracheal intubation with 100% oxygen and mechanical ventilation is indicated in patients with severe neurological impairment and elevated COHb.

The management of cyanide poisoning focuses on cardiopulmonary optimization. This measure is usually sufficient, as the liver clears cyanide from the bloodstream.

Hydroxocobalamin should be given as early as possible in patients with possible smoke injury (traces of soot in the mouth, pharynx or sputum) who exhibit neurological impairment (confusion, coma, agitation, seizures) or one of the following: bradypnoea or respiratory/cardiac arrest; shock or hypotension; lactate ≥7.5mmol/L or metabolic acidosis. Dosage: 5g (2 vials) hydroxocobalamin administered as an intravenous (IV) infusion over 15min in adults; repeat dose (5g) if no improvement.22,29 The action of hydroxocobalamin in the treatment of cyanide poisoning is based on its ability to tightly bind to cyanide ions. Each hydroxocobalamin molecule can bind one cyanide ion by substituting it for the hydroxo ligand linked to the trivalent cobalt ion, to form cyanocobalamin. Cyanocobalamin is a stable, non-toxic compound which is excreted in the urine. Patients may show reversible red coloration of the skin and mucous membranes. Fairly marked, dark red chromaturia is normal in the 3 days following administration of the drug.

Amyl nitrite, sodium nitrite and sodium thiosulfate are helpful in cyanide poisoning when used individually, but a synergistic effect may occur with concomitant use. Nitrites induce methaemoglobinaemia which, together with carboxihemoglobinaemia may interfere with oxygen transport, thus contributing to hypoxia. Nitrites should therefore be used with caution in patients with smoke inhalation syndrome, and one should be reasonably sure of the diagnosis before administering these compounds.22,30,31 Sodium nitrite 3% is administered at doses of 300mg IV over 5–10min. High (or even recommended) sodium nitrite infusion rates may cause hypotension, so that vasopressor support may be required. Sodium thiosulfate acts as sulfhydryl group donor and promotes the conversion of cyanide to thiocyanate (which is less toxic). Dosage: 12.5g (50ml of 25% solution) over 10–15min, IV. Amyl nitrite is administered by inhalation at doses of 0.2–0.4ml. In the event of inadequate patient response, further doses of sodium nitrite and thiosulfate may be administered 30min later at half the initial dose.31

Chemical injuries have some important biochemical differences when compared to thermal burns. In thermal injuries, there is a rapid coagulation of protein due to irreversible cross-linking reactions, whereas in chemical burns the protein destruction is continued by hydrolysis mechanisms. These mechanisms may continue so long as traces of the offending agent are present especially in deeper skin layers. In addition, chemical agents may produce a systemic toxicity.

The severity of a chemical burn injury is determined by: concentration of agent, quantity of burning agent, duration of skin contact, penetration power and mechanism of action.

Chemical injury is classified either by the mechanism of action or by chemical class of the agent.

There are six mechanisms of action for chemical agents in biological systems: Oxidation (sodium hypochlorite, potassium permanganate, chromic acid) reduction (hydrochloric acid, nitric acid) corrosion (phenols, sodium hypochlorite, white phosphorous), protoplasmic poisons (formic and acetic acids), vesicants (mustard gas) and desiccants (sulfuric and muriatic acids).

• Acids: They release hydrogen ions and reduce pH from 7 to values as low as 0. Acids with a pH less than 2 can produce coagulation necrosis on contact with the skin.

• Bases: Alkalis with a pH greater than 11.5 produce severe tissue damage through liquefaction necrosis. This tissue liquefaction allows deeper penetration of the agent. For this reason, alkali burns tend to be more severe than acid burns.

The ABC of Trauma, Primary and Secondary Assessment and all general principles of Trauma and Burn Care apply to chemical burns. However, there are also some measures of first aid that must be applied in chemical burns:

• -

  Removal of the chemical agent and irrigation of burn area: the duration of the chemical's contact with skin is the major determinant of injury severity. This removal involved clothing and a thorough irrigation with water at the scene of accident. It should be repeated when patient arrives at Burn Center. Periods of 30min to 2h of lavage may be necessary to keep pH between 5 and 11. There are a few notable exceptions, because same chemicals produce significant exothermy when combined with water and also other chemicals are insoluble in water. These are the cases of dry lime, muriatic acid and concentrated sulfuric acid.

• -

  Neutralizing agents: this is a controversial point. In most instances, antidotes should be avoided. Dilution, not neutralization, is the key to therapy. There are two notable exceptions: hydrofluoric acid (subeschar injection of 10% calcium gluconate until pain is relieved) and white phosphorous (lavage with 1% or 2% copper sulfate immerse in water).33,34

• -

  General support and local care: conventional thermal burn formula for resuscitation is used with urine output monitoring to assessment of adequacy of end-organ perfusion. Disturbances of pH are the major systemic complications. Blood gas and electrolyte analysis should be performed until metabolic disorder has been treated.

On the other hand, clinical assessment of the deep and extent of a chemical burn is difficult because of the unusual skin tanning and anesthetic properties of same chemical agents. After lavage and debridement of blisters, chemical burns can be treated with similar local chemotherapeutic agents and dressings. Early excision and grafting should be planning as soon as possible.

Eyes are often involved in chemical burns. In these cases, immediate treatment with copious irrigation, prior to ophthalmic evaluation.35 Topical anesthetic drops may be applied to reduce the pain and to facilitate irrigation. According to the American National Standards Institute (Standard Z358.1-1990) severe eye burns have to be rinsed for 15min. At least 500–1000ml of irrigation is thus necessary. This intensive irrigation has a decisive influence on the clinical course and prognosis of such eyes.36

An anmphoteric solution for irrigation is Diphoterine (Previn®, Fa. Prevor). This synthesized fluid is able to bind both alkalis and acids, with a rapid reduction of pH in the conjunctival sac and in the corneal stroma.

Systemic toxicity: Burn team must be aware of any possible toxicity derived of systemic absorption of the chemical agent. Hydrofluoric acid toxicity includes hypocalcemia and ventricular fibrillation. Formic acid absorption can produce intravascular hemolysis, renal failure and pancreatitis. Liver dysfunction may appear also in hydrocarbures. Inhalation injury may occur in chemical burns when aerosolized chemical or smoke is inhaled. They are managed like smoke inhalation injuries.

In conclusion, patients must be treated by specialized burn team and referred to a Burn Center as soon as possible. The gold standard for treatment is still copious irrigation immediately after accident and prolonged in Burn Unit for maximal effect. Systemic toxicity and inhalation injury are rare but often severe and increase mortality.37

Special focus in chemical eye burn is necessary. First aid with intensive sterile irrigation with normal saline after injury has the greatest influence on prognosis and outcome. Irrigation should not be interrupted during transport to a Burn Unit.

Electrical current exists in two forms, the alternating current (AC) and the direct current (DC). AC current is the most commonly used in households and offices, and it is standardized to a frequency of 60Hz. When the current is direct, the electrons flow only in one direction. This type of current is produced by various batteries and is used in certain medical equipment such as defibrillators, pacemakers, and electric scalpels. Although AC is considered to be a far more efficient energy, it is also more dangerous than DC (approx. three times) because it causes titanic muscle contractions that prolong the contact of the victim with the source. Lighting is a form of DC.

Burn electrical injury is caused by passage of current through the body (solid conductor) resulting in conversion of electrical energy to heat. In general, the type and extent of an electrical injury depends on the intensity of the electric current. Exposure of different parts of the body to the same voltage will generate a different current because resistance varies significantly between various tissues. The least resistance is found in nerves, blood, mucous membranes and muscles; the highest resistance is found in bones, fat and tendons. Skin has intermediate resistance.

The duration of the contact with electrical current is an important determinant of injury. In the same way, the pathway of the current through the body, from the entry to the exit point, determines the number of organs that are affected and, as a result, the type and severity of the injury. A vertical pathway parallel to the axis of the body is the most dangerous because it involves virtually all the vital organs (central nervous system, heart, respiratory muscles and in pregnant women, the uterus and the fetus). A horizontal pathway through the lower part of body may cause severe local damage but will probably not be lethal.39,40

Electric shock from a low-voltage line is delivered on contact of the victim with the source, and in high-voltage injury, the current is carried from the source to the person though an arc before any actual physical contact is made. Arcs can generate extremely high temperatures (up to 5000°C) that are usually responsible for the severe thermal injuries from high voltage (Table 3).