Systemic chemical poisoning is caused by inhalation of carbon monoxide and cyanide. These toxic compounds represent important causes of morbidity and mortality associated with pediatric inhalation injury. They should be suspected in children with inhalation injury or burns by a substantial mechanism.
Carbon monoxide is an invisible, odorless gas and one of the leading causes of immediate mortality associated with fires. Carbon monoxide is produced by incomplete combustion of materials when matter is burned. After inhalation, it binds to all compounds that contain heme. Carbon monoxide affinity for hemoglobin is greater than 200 times that of oxygen, resulting in production of carboxyhemoglobin. Formation of carboxyhemoglobin shifts the oxygen dissociation curve to the left, resulting in more tightly bound oxygen and exponentially decreasing oxygen delivery to tissues. It also binds to myoglobin, reducing oxygen delivery to skeletal muscle and cardiac muscle, which may result in rhabdomyolysis and cardiac dysfunction. Finally, carbon monoxide also causes hypoxia by binding to cytochrome oxidase and decreasing aerobic respiration at the cellular level.
Hydrogen cyanide is a poisonous compound formed when heat from a fire is exposed to nitrogen-containing polymers, such as the glue that holds together laminate. Once inhaled, hydrogen cyanide binds with high affinity to mitochondrial cytochrome oxidase. This association causes immediate arrest of oxidative phosphorylation resulting in conversion of aerobic metabolism to anaerobic metabolism. With impairment of cellular respiration, hypoxia ensues, resulting in lactic acidosis that can progress to cardiovascular and neurologic dysfunction.
Serum carboxyhemoglobin level should be measured in a child potentially exposed to carbon monoxide. Normal carboxyhemoglobin level is 1-3% but may be slightly elevated in children who are regularly exposed to tobacco smoke. A carboxyhemoglobin level greater than 15% directly correlates with severity of symptoms. Minor toxicity often presents as light-headedness, headache, nausea, and vomiting. More than 50% of symptoms progress to neurologic dysfunction, including confusion, ataxia, seizure, coma, and death.
Infants are particularly difficult to diagnose, as they may only be irritable and mildly lethargic until more grave signs appear. The classic cherry red pigmentation of the skin is present in less than 40% of patients with carbon monoxide poisoning and should not be used as a single indicator. Most pulse oximeters and equipment used to measure arterial and venous blood gases cannot discriminate oxyhemoglobin from carboxyhemoglobin, and are inaccurate to assess hypoxemia. To obtain accurate tissue oxygenation, the carboxyhemoglobin must be subtracted from the total oxygenation saturation.
Inhalation of 100% oxygen reduces the half-life of carboxyhemoglobin from 4-5 hours to approximately 1 hour. It is important to remember this as many patients are transported by EMS to the emergency department and have been breathing 100% oxygen prior to arrival. The interval of prehospital treatment may lead to inaccuracy in the initial carboxyhemoglobin level and should be considered on a case-by-case basis.
Similar to carbon monoxide, cyanide poisoning should be suspected in a child who had a potential exposure. Unfortunately, symptoms are often vague and no specific test is readily available in the emergency department to confirm the diagnosis of cyanide toxicity. Patients may show signs and symptoms including headache, confusion, dyspnea, seizures, pulmonary edema, coma, and death. Lactic acidosis not resolved after supplemental oxygen and high venous oxygen saturations may aid in the diagnosis, but both may also occur in many other burn-related pathologies.
Suspicion of significant smoke inhalation injury warrants endotracheal intubation. This includes children with facial or neck burns, carbonaceous sputum, stridor, dyspnea, abnormal lung examination, or significant surface burns. A secure, definitive airway is critical in children with suspected inhalation injury. Compared with adults, airway resistance is more notably increased with relatively less edema due to the smaller diameter of the airway. Even in children with patent airways and moderate injury, endotracheal intubation should be considered. Progressive edema in the subacute phase can lead to difficult intubations and the need for possible surgical airway management.
Succinylcholine is a safe paralytic to use for rapid sequence intubation within 24 hours of initial injury without concern for hyperkalemia. It should not be utilized after 24 hours. The use of cuffed endotracheal tubes is now recommended, a change from prior recommendations. This is a result of an attempt to decrease the number of uncuffed endotracheal tubes that need to be exchanged for cuffed tubes in order to adequately ventilate children. There is significant risk of distortion of the airway associated with exchanging the tube after edema is present. There are documented cases of cardiac arrest in uncomplicated tube exchange lasting less than 30 seconds, secondary to the patient’s critically ill status and fragile cardiopulmonary balance.
Once a definitive airway has been secured or deemed unnecessary, high-flow oxygen should be initiated. Arterial blood gas evaluation and carboxyhemoglobin levels should be obtained. Venous blood gas and lactate levels may also be helpful. Patients with thermal or localized chemical inhalation injury should receive inhaled bronchodilators such as albuterol. An aggressive pulmonary toilet should also be instituted. In the emergency department, suction secretions aggressively, and avoid oversedation to allow for coughing. These measures will be continued and augmented by chest physiotherapy and bronchoscopy once in the intensive care unit.
Carbon Monoxide–Specific Therapy
Elevated carboxyhemoglobin levels or suspected carbon monoxide poisoning should be treated with high-flow 100% oxygen by an appropriate route. Oxygen alone reduces the half-life of carboxyhemoglobin to less than one-third of the corresponding half-life while breathing room air as noted previously.
Hyperbaric oxygen therapy further reduces the half-life and may be considered as a treatment if readily available or possible with transport. It should be considered in patients who are hemodynamically stable with ongoing neurologic dysfunction or unresolved metabolic acidosis. Benefit from hyperbaric treatment for carbon monoxide poisoning is not completely clear, and the decision to institute this therapy should be made on a case-by-case basis. Take into account the small amount of space within the chamber for medical equipment and stability of the patient.
Cyanide toxicity has been treated in the past with many different compounds, most notably sodium thiosulfate and hydroxycobalamin. Sodium thiosulfate is no longer routinely recommended in children secondary to the production of the byproduct methemoglobin. Children are especially susceptible to methemoglobinemia due to lower levels of methemoglobin reductase and the ease at which fetal hemoglobin converts to methemoglobin. Hydroxycobalamin combines with cyanide to form the nontoxic compound cyanocobalamin and is treatment of choice in children with suspected cyanide poisoning. Prophylactic treatment of cyanide toxicity is not recommended and hydroxycobalamin should be administered in suspected poisoning only.
Children with suspected inhalation injury should be observed in the hospital for at least 24 hours to monitor for delayed onset of signs and symptoms. Patients who are intubated or for whom there is concern for likely intubation should be monitored in an intensive care unit. Patients with carboxyhemoglobin level of 20% or higher should be admitted for observation.
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Caustic ingestion is the most frequent mechanism for chemical burns in children, compared with occupational exposures in adults. Children younger than 6 years often go through a physical exploratory phase that includes touching and sometimes tasting items within their reach. Many household items are toxic when they contact skin or mucosa. A number of substances have been implicated in pediatric chemical burns, and generally fall into two types: acids and alkalis. Factors that contribute to the mortality and morbidity associated with such ingestions include pH and preparation of the chemical, tissue contact time, and exposed location (especially if location impairs irrigation).
Burns caused by acidic substances cause coagulative necrosis, limiting the depth of the burn. Commonly ingested household acids include toilet bowl cleaners, battery acids, and drain cleaners. In contrast, alkali burns produce liquefactive necrosis that leads to a deeper burn and increased mortality and morbidity. Alkaline substances also induce thrombosis in surrounding vasculature, which causes additional tissue ischemia. Common household alkalis are drain cleaner, lye-containing soaps, and oven cleaners. Each type of chemical burns can cause gastrointestinal injury including perforation and esophageal and pyloric strictures.
Children presenting to the emergency department following chemical ingestion or skin exposure can have a wide range of presentations, from asymptomatic to sepsis secondary to a perforated viscus. Studies have attempted to define signs and symptoms that put a patient at increased risk for significant gastrointestinal injury after ingestion, but no clear guidelines exist. History and physical examination should be directed to complaints of nausea, vomiting, dysphagia, difficulty handling secretions, stridor, visible mucosal injury or ulcerations, and abdominal pain. Absence of visible injury in the oropharynx does not exclude possible esophageal or gastrointestinal pathology. Substantial ingestions can lead to disseminated intravascular coagulation, acute renal failure, and acute liver failure.
The mainstay of treatment for a cutaneous chemical-related burn is irrigation with large amounts of water. Ingested caustic agents require a more complicated treatment plan. Irrigating the esophagus and stomach with large quantities can lead to emesis of the offending toxic substance, which should be avoided to limit reexposure of the esophageal and oral tissues. A considerable amount of liquid within the stomach also obstructs the view of gastric mucosa during endoscopy, which is currently the gold standard for diagnosis of esophageal and gastric damage.
Antiemetics should be used to prevent or limit emesis. Poison Control should be contacted (in the United States, call (800) 222-1222) for more information about specific chemical exposures and to report the ingestion to the national databank. The airway should be assessed upon initial examination and secured if necessary.
A child presenting with what appears to be a surgical abdomen secondary to perforated esophagus or viscus warrants emergent evaluation by a surgeon. Endoscopy may be needed to determine extent of injury. Significant symptoms or worsening clinical condition indicates the need for further emergency department observation or admission.
Contact burns are the second most common cause of pediatric burns that present to emergency departments nationwide. Contact burns occur when skin touches a hot surface, including irons, ovens, stovetops, curling irons, motorcycle exhaust pipes, and related heat sources. An additional mechanism for contact burns is prolonged exposure to an object with a lesser temperature, such as a heating pad.
Contact burns occur predominately on the upper extremities secondary to the mechanism of injury. Burns are usually limited to a small percent of body surface area but can extend quite deep. As with all pediatric injuries, close examination for patterns should be conducted to help rule out non-accidental trauma as a cause (see Chapter 5).
Treatment of contact burns varies upon the degree of dermal involvement and correlates with the treatment regiments for pediatric thermal burns. Local wound care and analgesia are the primary emergent treatments. Most contact burns are accidental in nature. Caregiver and patient education should also be provided in an effort to prevent future contact burns.
Minor contact burns can be managed similarly to thermal burns with local wound care, oral analgesia, and outpatient follow-up. More extensive contact burns should be managed as major thermal burns with admission and possible transfer to a burn center.
Sunburns are caused by an inflammatory response within the skin in reaction to ultraviolet (UV) ray exposure. They are more prominent in fair-skinned individuals but can occur with any skin type. Sunburns are usually limited to first-degree and minor second-degree burns but can be more extensive with prolonged exposure to UV rays and underlying predisposition. Tanning beds are now a significant cause of sunburn and have been implicated in the sunburns of even young children but are more common in adolescents.
Sunburns are very common and easy to recognize clinically by a basic history and physical examination. Skin inflammation peaks in approximately 12-24 hours and declines in clinical significance thereafter. Sunburns are staged with the same criteria as all other thermal burns based on physical examination findings.
The primary treatment for most sunburns is supportive care with analgesia by oral nonsteroidal agents. Although uncommon, more serious sunburns may be treated like thermal burns with fluid resuscitation and parenteral analgesia. Patient and caregiver education should be provided while in the emergency department as an endeavor to prevent future sunburns and the long-term sequelae of skin cancers.
Most patients with sunburns evaluated and treated within the emergency department can be discharged home to follow-up with their primary care physician as needed. More extensive burns and requiring fluid resuscitation or parenteral analgesia should be admitted for additional observation and treatment.
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