EPIDEMIOLOGY

Compiled data on battery ingestions published by the National Capital Poison Center in 1992 of over 2,300 button battery (BB) ingestions within a 7-year period found no deaths and only a 0.1% prevalence of major occurrence. A major occurrence is described as a complication such as vocal cord paralysis, esophageal stricture or perforation, tracheoesophageal fistula (TEF), and aortoesophageal fistula (AEF). Over the ensuing 18 years, that clinical experience had changed dramatically with a follow-up article from the National Capital Poison Center in 2010. In this cohort of over 8,600 BB ingestions, there was a major effect in 73 (0.8%) with death in 13 patients (0.15%); (Litovitz, Whitaker, Clark, White & Marsolek, 2010a)Figure 1 shows the most current report of moderate, major, or fatal outcomes from the ingestion of lithium batteries (National Capital Poison Center, 2012).

FIGURE 1. Battery ingestion statistics (reprinted with permission from the National Capital Poison Center at

In addition, "a study of battery-related Emergency Room visits during 1990-2010 it was concluded that batteries pose an important hazard to children, especially those less than 5 years of age" (Sharpe, Rochette & Smith, 2012, p. 1). In addition, those patients with underlying pathology such as stricture or eosinophilic esophagitis, developmental delay, and attention-seeking behavior have a higher risk for lodging of foreign bodies. Kremer et al. (2013) discuss the changes in recent years in the types of ingestions encountered, specifically BBs creating an even greater potential for severe morbidity and mortality to children.

LITHIUM BATTERIES/BBs

Lithium batteries (Figures 2 and 3), or better known as BBs, are used as the power source in many household items. They are used in remote controls, baby monitors, key fobs, toys, and numerous other products readily available to the curious child exploring their environment.

FIGURE 2. Anterior view of a lithium (BB; courtesy of Dennis Hiller, BSN, 2014).

FIGURE 3. Posterior view of a lithium (BB; courtesy of Dennis Hiller, BSN, 2014).

"Lithium became the preferred type of cell because of its capacity to have a longer shelf life, better stability at cool temperature, lighter weight, and ability to carry twice the voltage of previous mercuric oxide, manganese dioxide, and zinc-air cells" (Kremer et al., 2013, p. 2). The 20-mm lithium batteries are 3-V cells as compared with 1.5 V for other disk batteries. The higher-voltage battery has an increased potential for injury. It is important to remember that batteries that are considered spent may still hold enough current to cause injury if swallowed (Jatana et al., 2013).

Younger children, usually below 5 years old, have a smaller-diameter esophagus, enabling the largest 20-mm lithium battery to easily become lodged. Smaller-diameter BB (15 mm) may pass without incidence because they migrate through the gastrointestinal (GI) tract more readily. However, depending on the location of battery lodging, it may be necessary to remove even smaller-sized batteries to prevent long-term sequelae, such as impaired gastric emptying and stricture formation (Takagaci, Perito, Jose, & Heyman, 2011).

Symptoms of Lithium (BB) Ingestions

Clinical presentation of foreign body ingestion depends on the type of object ingested, location of lodging, size of object relative to the size of the patient, and duration of the impaction (Jarugula & Dorofaeff, 2011). Symptoms include, but are not limited to, sudden onset of crying or fussiness; drooling or excessive secretions; decrease in eating and drinking; reluctance to swallow; hoarse voice, stridor, or respiratory compromise; chest pain; abdominal pain or vomiting; and fever. Symptoms may mimic those of a viral or respiratory infection as in several reports of missed foreign body diagnosis where children were treated for suspicion of upper respiratory infections for as long as 12 days before the identification of lithium battery ingestion (Kimball, Park, Grimmer & Muntz, 2010).

Many foreign body ingestions are unwitnessed, so caretakers and healthcare providers should always consider foreign body ingestion as a cause of the child's symptoms.

Common Sites of Obstruction

Sixty percent to 70% of ingested foreign bodies lodge within the narrow upper end of the esophagus at the level of the cricopharyngeal muscle (Anderson & Dean, 2011).Other common lodging sites include the aortic arch and the lower esophageal sphincter. Additional anatomic narrowing is present in the pyloris, duodenum (ligament of Trietz), ileocecal valve, and rectum.

Diagnostic Imaging

Radiographic imaging confirms battery location within the esophagus or gastrointestinal tract and is used to differentiate an ingested coin from an ingested lithium battery. Note that a lithium battery (Figure 4) appears similar to a coin (Figure 5) on plain chest radiographs but is distinguishable by a "radiolucent halo and notch on anterior-posterior and lateral neck views" (Parray, Siddiqui, Hughes, & Shah, 2010, p. 471). Additional imaging and lateral views may be required to identify a step-off. If the radiograph is not well defined, presume that the ingested object is a lithium battery to avoid a delay in treatment and object retrieval. An ingested lithium battery can cause significant injury within 2 hours of ingestion (Reilly, 2013). This is an emergency.

FIGURE 4. Anterior/posterior x-ray showing the "halo" or double ring sign (courtesy of Petar Mamula, MD).

FIGURE 5. Anterior/posterior x-ray showing a coin with a homogenous appearance (courtesy of Petar Mamula, MD).

All ingestions should be reported to the National Battery Ingestion Hotline at (202) 625-3333 (Jatana et al., 2013, p. 1395).

Mechanism of Injury

An ingested lithium battery generates an external electrolytic current, released from its negative pole, that hydrolyzes tissue fluids (Figure 6), produces hydroxide, and creates a high-pH (alkaline) environment that can cause liquefaction and necrosis (Jatana et al., 2013).

FIGURE 6. Endoscopic visualization during lithium battery (BB) retrieval. Note the "bubbling" indicative of the battery current hitting the surrounding esophageal tissue and releasing hydroxide (courtesy of Adele Evans, MD).

Alkaline burns cause edematous loosening of the tissue with deep diffusion of the alkali into the surrounding tissues (Figure 7). Unlike acid burns, there is no eschar formation to protect the tissue by limiting deeper penetration. The most severe esophageal burns (and subsequent perforations) occur adjacent to the negative battery pole (anode). Injury can continue after endoscopic battery removal for days to weeks because of residual alkali or weakened tissues (Jatana et al., 2013).

FIGURE 7. Endoscopic visualization after battery removal. Devascularized esophageal tissue is represented by the gray area. Necrosis is present as evidenced by the black-colored area in the esophagus (courtesy of Adele Evans, MD).

Management and Retrieval

Management of the child who has ingested a lithium battery requires the collaborative efforts of a skilled emergency room physician, endoscopist, otolaryngologist, nursing, and possibly, general surgeon for intervention. Positive patient outcomes are associated with immediate identification of the battery on initial imaging and the practitioner's knowledge of injury potential and sequelae. When the practitioner positively identifies the ingested item as a lithium battery, emergent treatment of the child (immediately to the operating room) includes general anesthesia, intubation, and flexible endoscopy to remove the battery (The American Society for Gastrointestinal Endoscopy, 2011). Rigid esophagoscopy is sometimes used to remove ingested lithium batteries lodged at the upper level of the esophageal sphincter or hypopharyngeal region. Laryngoscopy and bronchoscopy can help the practitioner to assess airway injury in the absence of airway symptoms, particularly when the negative pole of the battery is facing anteriorly within the esophagus (Jatana et al., 2013). Treatment may consist of intravenous (IV) fluids, steroids, and antibiotics to reduce inflammation and prevent infection, and do not give the child anything by mouth. Admit the child for close assessment and observation. Evaluate for complications, and provide immediate intervention to minimize long-term complications. "Progression of injury is a hallmark of button battery injury, and sometimes, it takes days to weeks for tissue to declare itself as viable or nonviable" (Jatana et al., 2013, pp. 1395-1396). Follow-up testing includes esophagram, magnetic resonance imaging, computed tomography (CT), esophagoscopy, and bronchoscopy. At discharge, teach parents and caregivers the importance of follow-up care. Despite removal of the battery, the child can develop a TEF within 9 days, an AEF within 28 days, or esophageal strictures or spondylodiscitis within weeks to months (Jatana et al., 2013; refer to the National Capital Poison Control Center triage http://www.poison.org/battery/guideline.asp).

Complications

BB ingestion can cause many complications such as "vocal cord paralysis (from laryngeal nerve damage), tracheal stenosis, tracheal malacia, tracheal-esophageal fistula, esophageal stricture, aorticesophageal fistulization (AEF), empyema, abscess, and spondylodiscitis" (Litovitz et al., 2010b, p. 1173).

Vocal Cord Paralysis

Bernstein, Burrows and Saunders (2007) describe a case study of an 11-month-old infant who presented with respiratory distress. Anteroposterior and lateral radiographs showed a round, opaque object lodged at the sixth cervical level. This was presumed to be a coin.

Bernstein, Burrows and Saunders (2007)) describe a case study of an 11-month-old infant who presented with respiratory distress. Anteroposterior and lateral radiographs showed a round, opaque object lodged at the sixth cervical level. This was presumed to be a coin. A microlaryngoscopy 5 hours after ingestion revealed a corroded 2-cm wide BB lodged in the hypopharynx; corrosion injury was noted, affecting the mucosa of the anterior and lateral walls of the hypopharynx. The patient was intubated and received antibiotics, antifungals, and steroids. A nasogastric tube was placed.

Microlaryngoscopy at 6 days after ingestion confirmed significant corrosive injury of the anterior and lateral hypopharynx and bilateral vocal cord palsy. The patient was extubated with no signs of respiratory distress but some residual stridor. However, there was no return of her voice. The authors expressed the need for prolonged nasogastric feeds, follow-up laryngoscopy, and most likely, dilations for esophageal stricture. This case study supports the recent literature (Reilly, 2013) for the need of early identification of a BB versus a coin and immediate retrieval to limit exposure time and injury.

Esophageal Stricture/Perforation

Esophageal stricture or narrowing of the esophagus can occur after removal of a lithium battery from the esophagus. Edema and necrosis occur at the lodging site (Figures 8 and 9) in the esophageal wall. During healing, fibrosis and scarring with potential residual narrowing of the esophagus can occur. Treatment requires frequent esophageal dilatations (balloon) to increase the diameter of the esophagus. Despite battery retrieval, the destructive properties of alkali leaking into the surrounding tissues can cause an esophageal perforation. Treatment requires surgical intervention to repair the esophagus with diversional gastrointestinal tube feedings to allow for healing. On occasion, there can be no obvious signs of perforation, but significant injury can result from the alkali leak affecting surrounding structures such as the mediastinum.

FIGURE 8. Endoscopic view of a BB lodged in the esophagus (courtesy of Petar Mamula, MD).

FIGURE 9. Post-BB removal (courtesy of Petar Mamula, MD).

Tracheal Stenosis and Tracheal Malacia

The normal trachea begins immediately caudal to the cricoid cartilage at the level of the sixth cervical vertebra and extends to the carina, where it bifurcates between thoracic vertebrae 4 and 5 (Zur, 2014). The normal trachea (Figure 10) contains about 20 rings of cartilage. Muscle and connective tissue make up the back part of each ring, and moist, smooth tissue (mucosa) lines the inside of the trachea. Normally, the trachea widens and lengthens slightly with inhalation and returns to its resting size with exhalation.

FIGURE 10. Normal trachea showing intact cartilage and airway support (courtesy of David Low, MD).

Tracheal stenosis is a narrowing of the airway. Alkaline burn injury after ingestion of a lithium battery causes inflammation and devascularization of the tracheal wall. The tracheal cartilage becomes inflamed (chondritis) and scarred, causing stenosis. Treatment of severe tracheal stenosis with respiratory compromise is a tracheostomy (Zur, 2014).

Tracheal malacia is airway compression caused by laxity in the tracheal cartilage rings. Tracheal cartilage damage can occur after battery ingestion because of the sustained alkaline injury. Clinical indications of tracheal malacia include coughing, grunting, oxygen desaturation, bradycardia, and periods of apnea. The gold standard for the diagnosis of tracheal malacia is bronchoscopy. The findings of tracheomalacia (Figure 11) will include flattening of the tracheal rings with a fish mouth appearance of the airway (Zur, 2014, p. 145). Treatment of severe tracheal malacia includes tracheostomy and possible tracheal reconstruction surgery.

FIGURE 11. Trachea stenosis/tracheal malacia. There is flattening of the tracheal rings with a fish mouth appearance of the airway (courtesy of David Low, MD).

TEF

Fistulas are an atypical connection between any two epithelialized surfaces. A TEF results from an abnormal connection between the trachea and the esophagus (Figure 12). This abnormal connection can be the result of injury acquired during impaction of the BB in the esophagus; destruction of the surrounding tissue from the alkaline environment can lead to a fistula formation. A TEF secondary to BB ingestion can be diagnosed at the time of BB retrieval or a delayed occurrence.

FIGURE 12. Tracheoesophageal fistula. The arrow indicates the communication between the esophagus and the trachea (courtesy of Petar Mamula, MD).

A 15-month-old infant had an unwitnessed ingestion of a 20-mm BB. The estimated duration of impaction was approximately 4-6 hours. Chest x-ray showed the BB at the level of the carina. He was taken emergently to the operating room for rigid esophagoscopy with removal of the BB (Russell, Cohen & Billmire, 2013, p. 441).

A 15-month-old infant had an unwitnessed ingestion of a 20-mm BB. The estimated duration of impaction was approximately 4-6 hours. Chest x-ray showed the BB at the level of the carina. He was taken emergently to the operating room for rigid esophagoscopy with removal of the BB (Russell, Cohen & Billmire, 2013, p. 441).

There was significant necrosis of the esophagus but no perforation noted at this time. He was admitted, placed on IV fluids, IV antibiotics, and nothing by mouth. An esophagram was performed the next day, which was normal; he tolerated fluids and was discharged. The patient returned 1 week later with symptoms of fever, tachypnea, oral refusal, diarrhea, and marked abdominal distention. Practitioners were concerned for an acquired TEF and obtained a chest CT with contrast. Imaging was conclusive for a 7-mm fistula between the esophagus and the right mainstem bronchus (Russell et al., 2013). Additional imaging identified concerning findings of significant edema and inflammation of the mediastinum. His course of treatment was nasogastric tube placement with suction decompression, parenteral nutrition, and broad-spectrum antibiotics. When bowel function returned, nasogastric feedings were initiated and tolerated. A repeat chest CT and esophagram at 1 month after intervention showed resolution of the acquired TEF and some narrowing of the right mainstem bronchus from apparent granulation tissue. At this time, oral intake was initiated to progress to a soft diet. The patient was discharged 2 months from admission and remained asymptomatic with a follow-up esophagram showing no stricture or residual TEF.

Several authors have advocated the use of esophageal rest as a conservative management of acquired TEF to permit closure by secondary intention and delay the primary surgical repair because of the presence of an acute inflammatory response. However, late recurrence of a TEF after this chosen treatment modality "illustrates the importance of long term follow-up of at least 6 months before assuming complete fistula resolution" (Grisel, Richter, Casper & Thompson, 2008, p. 699).

Definitive surgical repair varies on the location of the TEF. Repair can involve a partial median sternotomy to provide surgical exposure of the tracheal and esophageal injury. "Tracheal end-to-end reanastomosis, primary repair of esophageal perforation, and a local strap muscle interposition between the 2 structures can be utilized" (Kimball et al., 2010, para. 14). An alternative surgical approach described by Grisel et al. (2008) involves an imbricated suture technique via a transtracheal approach. A running-purse string suture is utilized to approximate the opposing edges, thereby enhancing complete epithelialization. "Immediate surgical intervention can be complicated by high mortality rates, but delayed surgical interventions is also fraught with significant complication risk such as nerve injury, recurrence, and need for multiple procedures" (Russell et al., 2013, p. 443).

AEF

The National Capital Poison Control Center (2013) reported 34 cases of fatal hemorrhage from 1977 to 2013 (http://www.poison.org/battery/fatalcases.asp). Most of these hemorrhages were the result of an AEF with other documented cases of erosion into the thyroid artery, subclavian artery, and mediastinal vessels. AEF is collectively fatal with only one documented case of survival.

A 10-month-old infant who ingested a 20-mm BB had removal 14 hours after ingestion. Radiography then showed pneumomediastinum, but a contrast study showed no esophageal leakage. After 5 days of antibiotics, he was discharged. Twenty-one days later, he woke with dyspnea and hematemesis and was flown to a pediatric hospital. The patient required intubation and resuscitation for continued hematemesis. Endoscopy revealed severe ulceration at the gastroesophageal junction and a very slow but persistent bleed.

The ulcer was oversewn and covered with omentum by a general surgeon. The patient was stabilized. Because of concern for aortic involvement, the patient was sent for a CT, which showed an AEF. Shortly afterward, brisk arterial bleeding ensued, and cardiothoracic surgeons performed an emergency thoracotomy and repaired the fistulous section of the aorta. Antibiotics were given because of a complication of sepsis from which the patient recovered completely (Spiers et al., 2012, p. 187). Obviously, the identification of the AEF through imaging and the patient present in the hospital setting during these events allowed for emergent intervention with surgical repair. Research indicates no other survivors of AEF secondary to BB ingestions.

In the review of fatal cases of hemorrhage caused by BBs, two critical themes emerged. First, most deaths took place after battery removal, which suggests that the process of tissue injury, healing, and remodeling can lead to fistula development even several weeks after the battery is removed. Continued active surveillance through endoscopy and radiologic approaches may allow for earlier diagnosis of battery-induced complications. The second major theme to emerge is that 70% of fatal cases of hemorrhage presented with a history of mild bleeding preceding their exsanguination. If these "sentinel bleeds" are recognized in the stable patient, a time window exists in which surgical intervention can be accomplished (Brumbaugh et al., 2011, p. 588).

In the review of fatal cases of hemorrhage caused by BBs, two critical themes emerged. First, most deaths took place after battery removal, which suggests that the process of tissue injury, healing, and remodeling can lead to fistula development even several weeks after the battery is removed. Continued active surveillance through endoscopy and radiologic approaches may allow for earlier diagnosis of battery-induced complications. The second major theme to emerge is that 70% of fatal cases of hemorrhage presented with a history of mild bleeding preceding their exsanguination. If these "sentinel bleeds" are recognized in the stable patient, a time window exists in which surgical intervention can be accomplished (Brumbaugh et al., 2011, p. 588).

A 4-year-old presented to the emergency room (ER) with cardiopulmonary arrest after an acute episode of vomiting large amounts of bloody emesis. There was no medical history and no witnessed foreign body ingestion. Once stabilized, she was admitted to the pediatric care unit. A chest x-ray revealed a 23-mm BB located at the central mediastinum within the distal esophagus posterior to the heart (Pae, Habte, McCloskey & Schwartz, 2012). The operating room was set up in anticipation of the patient's emergent arrival. A team of anesthesiologists, surgeons, nurses, and intensivists was summoned, and a massive hemorrhage protocol was instituted. The patient arrived in grave condition, and during transfer to the operating room table, the patient experienced cardiopulmonary arrest. The surgeon performed a thoracotomy, cross-clamped the aorta, and initiated open-chest cardiopulmonary resuscitation and open-paddle defibrillation. The patient never regained a sustainable cardiac rhythm and died.

The postmortem examination confirmed the presence of the BB and an AEF (Figure 13).

FIGURE 13. BB lodging in the esophagus: postmortem illustration (reproduced with permission from Brian Dunhum, MD [retained copyrights]).

Education of Healthcare Providers

Decreased pediatric morbidity and mortality from lithium battery ingestion requires early recognition and treatment. Healthcare providers in emergency departments and pediatrician offices should recognize the signs and symptoms of battery ingestion and initiate emergency treatment. Effective practitioner education includes publications, lectures, and in-services. Each facility should develop a clinical pathway for the early recognition and treatment of lithium battery ingestion (view an example of a clinical pathway at http://www.chop.edu/pathways/shared-pathways/foreign-body-ingestion/button-batte).

Anticipatory Guidance and Education on Prevention

Prevent lithium battery ingestion among children by teaching parents, caregivers, teachers, and daycare providers about the hazards of this common household item (Litovitz et al., 2010). Registered nurses can help decrease injury and promote pediatric health and safety by increasing public awareness and providing family education about the dangers of lithium battery ingestion.

Keep these batteries out of the reach of children, and secure all battery compartments.

Utilize available educational materials at http://www.chop.edu/export/download/pdfs/articles/pfe/lithium-batteries-dangers., http://www.safekids.org/sites/default/files/documents/battery_safety_tips.pdf, http://www.aap.org/en-us/about-the-aap/Committees-Councils-Sections/Section-on-O, and http://www.cpsc.gov/en/Safety-Education/Neighborhood-Safety-Network/Posters/Butt.

Teach families about proper disposal of used lithium batteries, and advise them to seek immediate medical attention if they suspect their child has swallowed a lithium battery. Suggest that the family post the number to the National Battery Ingestion Hotline (202-625-3333) or the poison control center (800-222-1222) in an easily accessible area close to the telephone or that family members program these numbers into their cellular phones.

For more information about lithium battery safety, visit the American Academy of Pediatrics Button Battery Task Force page at http://www.aap.org/en-us/advocacy-and-policy/aap-health-initiatives/pages/Button.

Acknowledgments

A sincere thanks to Dr. David Low and Dr. Brian Dunham for dedicating their time and gifted artistic talent in creating the illustrations specifically for this article. I would also like to thank Adele Evans, MD, for the use of her endoscopic images and Denise Farone-Diaz, MSN, BA, RN, CPAN, for her independent review of article content. Finally, I would like to express my very great appreciation to Dr. Petar Mamula for his valuable and constructive suggestions during the planning and development of this article and the use of the images he provided. His willingness to give his time so generously has been very much appreciated.

References