Case Reports

There are many reports in the medical and dental literature of complications arising from a routine delivery of dental care. One complication can include physical injury from swallowing or aspirating foreign objects.¹ However, a review of such literature presents a scarcity of documented instances and no long-term evaluation of the aforementioned events.^2,3

This report presents the case of a patient who aspirated a hex driver tool during a procedure to place a crown on a dental implant. The aspirated object was subsequently removed through flexible fiberoptic bronchoscopy without complications.

Case Report

An 83-year-old man was referred to the Pulmonary and Critical Care Department of the VA Caribbean Healthcare System in San Juan, Puerto Rico, after a hex driver tool was lost during a procedure to place a crown on a dental implant, performed under topical anesthesia. It was first thought that the patient swallowed the hex driver, since he never experienced or complained of coughing or shortness of breath. A chest radiograph revealed a metal object lying within the right main stem bronchus, for which the patient was referred to the Pulmonary and Critical Care Department (Figure 1).

The patient’s past medical history was remarkable for hypertension and hypercholesterolemia. Outpatient medications included hydrochlorothiazide, simvastatin, aspirin, felodipine, and lorazepam. He had no previous history of dysphagia or neurologic disease. A physical examination revealed expiratory and inspiratory wheezing localized to the right lower lobe without associated rhonchi or crackles. No distress, shortness of breath, or coughing was noted.

A flexible fiberoptic bronchoscopy was performed under conscious sedation with 3 mg of IV midazolam and topical anesthesia with nebulized 4% lidocaine. No mucosal edema, hyperemia, or structural damage was noted during direct visualization of both the right and left bronchopulmonary segments. A metallic object was visualized at the entrance of the right lower lobe. The foreign object had irregular borders, providing multiple edges that made it suitable to be embraced (Figure 2).

Using a radial jaw single-use biopsy forceps 1.8 mm, the physician clinched and retrieved the object through the bronchoscope. The object was retrieved on the same day of the dental procedure almost 5 hours after it was aspirated. The patient tolerated the procedure well; no coughing, oxygen desaturation, or bleeding occurred during the procedure.

After a few hours of observation, a postprocedural radiograph confirmed the removal of the foreign body without evidence of pneumothorax. The patient was discharged, and 24 hours after the incident remained asymptomatic without chest pain, cough, hemoptysis, sputum production, or fever.

Discussion

Foreign-body aspiration and inadvertent swallowing remains underrecognized by clinicians. In the U.S., more than 2,700 people, including more than 300 children, die of foreign-body aspiration each year.^4,5 Aspiration or ingestion of a foreign body during a dental procedure is serious and potentially fatal.⁶ Some of the consequences of an aspirated object are complete or partial airway obstruction, respiratory distress and failure, pneumothorax, and hemorrhage.⁷ In addition, inadvertent aspiration of foreign objects in asymptomatic patients may not be evident for months, resulting in late complications as postobstructive pneumonia, bronchiectasis, or lung abscess.⁸ Early recognition and diagnosis of these events are crucial to prevent complications.

Accidental aspiration of foreign objects during dental procedures is not as common as is swallowing. In the normal population, the foreign object enters the gastrointestinal tract in about 92.5% of the time, and the tracheobronchial tree in 7.5% of these instances.

A 10-year review done at the School of Dentistry of the University of North Carolina reported 36 incidents of lost instruments during dental procedures. In only 1 case, an object was aspirated, 25 of the 36 cases were secondary to ingestion, and in the remaining 10 incidents, swallowing or aspiration was ruled out by radiography or after the object’s removal from the patient’s mouth.² Previous reviews about foreign-body aspiration in adults have reported dental appliances as the second most commonly aspirated foreign objects.⁴ Of all aspirated objects, the most common site of impaction is the right lower lobe; however, aspiration has been reported in all pulmonary lobes.⁶

Available literature recognizes that impaction of aspirated objects occurred in 56% of instances within the right lower lobe and 33% in the left lower lobe.^7,9 Identification of risk factors for aspiration is important for any patient who will undergo dental procedures, such as advanced age (ie, elderly patients may have a decreased gag reflex); neurologic conditions, such as stroke; dementia and other degenerative diseases; the use of topical anesthesia; and altered states of consciousness associated with the use of IV sedation.^1,2

The key sign that most dentists recognize when patients aspirate an object during a dental procedure is coughing. It has been reported that coughing resulting from aspiration of foreign objects may range from mild to severe. In this case, the patient was completely asymptomatic during the procedure. The only clue of possible object aspiration was the reported tool loss by the dentist. It is important to always examine, account for, and review all equipment used during dental procedures. Assessment for any lost objects or missing parts of instruments should be done promptly with a high degree of suspicion for possible swallowing or aspiration if an object is missing.

 

It has been recommended to use a gauze throat screen and rubber dam and to avoid a supine position during a procedure, among other techniques, to minimize risk of ingestion or aspiration.² Imaging studies should be used for further evaluation of the patient; however, some instruments, such as dental pieces and impression material, may not be identified by plain films. In those cases, further evaluation with more sophisticated imaging techniques, such as computed tomography (CT), should be considered.^1-10

In a previous case report of a patient who aspirated a third molar during a dental procedure, a chest film failed to identify it. A chest CT was performed, and the object showed in the right main stem bronchus. In another instance, aspiration of impression material in a 45-year-old man was not observed by chest radiography. In this case, the history of coughing and respiratory symptoms days after the procedure pointed toward aspiration of an object as the culprit, with subsequent identification and removal by flexible fiberoptic bronchoscopy.^1-11

Bronchoscopy is the treatment of choice for extraction of aspirated foreign bodies; however, there is still a debate about whether to use flexible or rigid bronchoscopy. The decision is usually made based on the object size, localization, medical facility, and personnel expertise. The rigid bronchoscope has the advantages of offering better control and visualization of the airway and easier use of removal instruments. Its primary disadvantage is that the procedure needs to be done in the operating room under general anesthesia. Flexible fiberoptic bronchoscopy done under conscious sedation and topical anesthesia may be as effective as rigid bronchoscopy and even superior in the case of smaller and more distal impacted objects.^10-14

In this case, flexible fiberoptic bronchoscopy was used successfully for the removal of the foreign object. Biopsy forceps were used to grasp the object and retrieve it from the airway without complication.

Conclusion

Aspiration of foreign objects during a dental procedure is a potential life-threatening complication. A high-level of suspicion is needed for early diagnosis and referral of the patient for extraction of the object and further avoidance of complications. Flexible fiberoptic bronchoscopy is a feasible procedure for removal of objects within the airway. 

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc. , the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

There are many reports in the medical and dental literature of complications arising from a routine delivery of dental care. One complication can include physical injury from swallowing or aspirating foreign objects.¹ However, a review of such literature presents a scarcity of documented instances and no long-term evaluation of the aforementioned events.^2,3

This report presents the case of a patient who aspirated a hex driver tool during a procedure to place a crown on a dental implant. The aspirated object was subsequently removed through flexible fiberoptic bronchoscopy without complications.

Case Report

An 83-year-old man was referred to the Pulmonary and Critical Care Department of the VA Caribbean Healthcare System in San Juan, Puerto Rico, after a hex driver tool was lost during a procedure to place a crown on a dental implant, performed under topical anesthesia. It was first thought that the patient swallowed the hex driver, since he never experienced or complained of coughing or shortness of breath. A chest radiograph revealed a metal object lying within the right main stem bronchus, for which the patient was referred to the Pulmonary and Critical Care Department (Figure 1).

The patient’s past medical history was remarkable for hypertension and hypercholesterolemia. Outpatient medications included hydrochlorothiazide, simvastatin, aspirin, felodipine, and lorazepam. He had no previous history of dysphagia or neurologic disease. A physical examination revealed expiratory and inspiratory wheezing localized to the right lower lobe without associated rhonchi or crackles. No distress, shortness of breath, or coughing was noted.

A flexible fiberoptic bronchoscopy was performed under conscious sedation with 3 mg of IV midazolam and topical anesthesia with nebulized 4% lidocaine. No mucosal edema, hyperemia, or structural damage was noted during direct visualization of both the right and left bronchopulmonary segments. A metallic object was visualized at the entrance of the right lower lobe. The foreign object had irregular borders, providing multiple edges that made it suitable to be embraced (Figure 2).

Using a radial jaw single-use biopsy forceps 1.8 mm, the physician clinched and retrieved the object through the bronchoscope. The object was retrieved on the same day of the dental procedure almost 5 hours after it was aspirated. The patient tolerated the procedure well; no coughing, oxygen desaturation, or bleeding occurred during the procedure.

After a few hours of observation, a postprocedural radiograph confirmed the removal of the foreign body without evidence of pneumothorax. The patient was discharged, and 24 hours after the incident remained asymptomatic without chest pain, cough, hemoptysis, sputum production, or fever.

Discussion

Foreign-body aspiration and inadvertent swallowing remains underrecognized by clinicians. In the U.S., more than 2,700 people, including more than 300 children, die of foreign-body aspiration each year.^4,5 Aspiration or ingestion of a foreign body during a dental procedure is serious and potentially fatal.⁶ Some of the consequences of an aspirated object are complete or partial airway obstruction, respiratory distress and failure, pneumothorax, and hemorrhage.⁷ In addition, inadvertent aspiration of foreign objects in asymptomatic patients may not be evident for months, resulting in late complications as postobstructive pneumonia, bronchiectasis, or lung abscess.⁸ Early recognition and diagnosis of these events are crucial to prevent complications.

Accidental aspiration of foreign objects during dental procedures is not as common as is swallowing. In the normal population, the foreign object enters the gastrointestinal tract in about 92.5% of the time, and the tracheobronchial tree in 7.5% of these instances.

A 10-year review done at the School of Dentistry of the University of North Carolina reported 36 incidents of lost instruments during dental procedures. In only 1 case, an object was aspirated, 25 of the 36 cases were secondary to ingestion, and in the remaining 10 incidents, swallowing or aspiration was ruled out by radiography or after the object’s removal from the patient’s mouth.² Previous reviews about foreign-body aspiration in adults have reported dental appliances as the second most commonly aspirated foreign objects.⁴ Of all aspirated objects, the most common site of impaction is the right lower lobe; however, aspiration has been reported in all pulmonary lobes.⁶

Available literature recognizes that impaction of aspirated objects occurred in 56% of instances within the right lower lobe and 33% in the left lower lobe.^7,9 Identification of risk factors for aspiration is important for any patient who will undergo dental procedures, such as advanced age (ie, elderly patients may have a decreased gag reflex); neurologic conditions, such as stroke; dementia and other degenerative diseases; the use of topical anesthesia; and altered states of consciousness associated with the use of IV sedation.^1,2

The key sign that most dentists recognize when patients aspirate an object during a dental procedure is coughing. It has been reported that coughing resulting from aspiration of foreign objects may range from mild to severe. In this case, the patient was completely asymptomatic during the procedure. The only clue of possible object aspiration was the reported tool loss by the dentist. It is important to always examine, account for, and review all equipment used during dental procedures. Assessment for any lost objects or missing parts of instruments should be done promptly with a high degree of suspicion for possible swallowing or aspiration if an object is missing.

 

It has been recommended to use a gauze throat screen and rubber dam and to avoid a supine position during a procedure, among other techniques, to minimize risk of ingestion or aspiration.² Imaging studies should be used for further evaluation of the patient; however, some instruments, such as dental pieces and impression material, may not be identified by plain films. In those cases, further evaluation with more sophisticated imaging techniques, such as computed tomography (CT), should be considered.^1-10

In a previous case report of a patient who aspirated a third molar during a dental procedure, a chest film failed to identify it. A chest CT was performed, and the object showed in the right main stem bronchus. In another instance, aspiration of impression material in a 45-year-old man was not observed by chest radiography. In this case, the history of coughing and respiratory symptoms days after the procedure pointed toward aspiration of an object as the culprit, with subsequent identification and removal by flexible fiberoptic bronchoscopy.^1-11

Bronchoscopy is the treatment of choice for extraction of aspirated foreign bodies; however, there is still a debate about whether to use flexible or rigid bronchoscopy. The decision is usually made based on the object size, localization, medical facility, and personnel expertise. The rigid bronchoscope has the advantages of offering better control and visualization of the airway and easier use of removal instruments. Its primary disadvantage is that the procedure needs to be done in the operating room under general anesthesia. Flexible fiberoptic bronchoscopy done under conscious sedation and topical anesthesia may be as effective as rigid bronchoscopy and even superior in the case of smaller and more distal impacted objects.^10-14

In this case, flexible fiberoptic bronchoscopy was used successfully for the removal of the foreign object. Biopsy forceps were used to grasp the object and retrieve it from the airway without complication.

Conclusion

Aspiration of foreign objects during a dental procedure is a potential life-threatening complication. A high-level of suspicion is needed for early diagnosis and referral of the patient for extraction of the object and further avoidance of complications. Flexible fiberoptic bronchoscopy is a feasible procedure for removal of objects within the airway. 

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc. , the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

There are many reports in the medical and dental literature of complications arising from a routine delivery of dental care. One complication can include physical injury from swallowing or aspirating foreign objects.¹ However, a review of such literature presents a scarcity of documented instances and no long-term evaluation of the aforementioned events.^2,3

This report presents the case of a patient who aspirated a hex driver tool during a procedure to place a crown on a dental implant. The aspirated object was subsequently removed through flexible fiberoptic bronchoscopy without complications.

Case Report

An 83-year-old man was referred to the Pulmonary and Critical Care Department of the VA Caribbean Healthcare System in San Juan, Puerto Rico, after a hex driver tool was lost during a procedure to place a crown on a dental implant, performed under topical anesthesia. It was first thought that the patient swallowed the hex driver, since he never experienced or complained of coughing or shortness of breath. A chest radiograph revealed a metal object lying within the right main stem bronchus, for which the patient was referred to the Pulmonary and Critical Care Department (Figure 1).

The patient’s past medical history was remarkable for hypertension and hypercholesterolemia. Outpatient medications included hydrochlorothiazide, simvastatin, aspirin, felodipine, and lorazepam. He had no previous history of dysphagia or neurologic disease. A physical examination revealed expiratory and inspiratory wheezing localized to the right lower lobe without associated rhonchi or crackles. No distress, shortness of breath, or coughing was noted.

A flexible fiberoptic bronchoscopy was performed under conscious sedation with 3 mg of IV midazolam and topical anesthesia with nebulized 4% lidocaine. No mucosal edema, hyperemia, or structural damage was noted during direct visualization of both the right and left bronchopulmonary segments. A metallic object was visualized at the entrance of the right lower lobe. The foreign object had irregular borders, providing multiple edges that made it suitable to be embraced (Figure 2).

Using a radial jaw single-use biopsy forceps 1.8 mm, the physician clinched and retrieved the object through the bronchoscope. The object was retrieved on the same day of the dental procedure almost 5 hours after it was aspirated. The patient tolerated the procedure well; no coughing, oxygen desaturation, or bleeding occurred during the procedure.

After a few hours of observation, a postprocedural radiograph confirmed the removal of the foreign body without evidence of pneumothorax. The patient was discharged, and 24 hours after the incident remained asymptomatic without chest pain, cough, hemoptysis, sputum production, or fever.

Discussion

Foreign-body aspiration and inadvertent swallowing remains underrecognized by clinicians. In the U.S., more than 2,700 people, including more than 300 children, die of foreign-body aspiration each year.^4,5 Aspiration or ingestion of a foreign body during a dental procedure is serious and potentially fatal.⁶ Some of the consequences of an aspirated object are complete or partial airway obstruction, respiratory distress and failure, pneumothorax, and hemorrhage.⁷ In addition, inadvertent aspiration of foreign objects in asymptomatic patients may not be evident for months, resulting in late complications as postobstructive pneumonia, bronchiectasis, or lung abscess.⁸ Early recognition and diagnosis of these events are crucial to prevent complications.

Accidental aspiration of foreign objects during dental procedures is not as common as is swallowing. In the normal population, the foreign object enters the gastrointestinal tract in about 92.5% of the time, and the tracheobronchial tree in 7.5% of these instances.

A 10-year review done at the School of Dentistry of the University of North Carolina reported 36 incidents of lost instruments during dental procedures. In only 1 case, an object was aspirated, 25 of the 36 cases were secondary to ingestion, and in the remaining 10 incidents, swallowing or aspiration was ruled out by radiography or after the object’s removal from the patient’s mouth.² Previous reviews about foreign-body aspiration in adults have reported dental appliances as the second most commonly aspirated foreign objects.⁴ Of all aspirated objects, the most common site of impaction is the right lower lobe; however, aspiration has been reported in all pulmonary lobes.⁶

Available literature recognizes that impaction of aspirated objects occurred in 56% of instances within the right lower lobe and 33% in the left lower lobe.^7,9 Identification of risk factors for aspiration is important for any patient who will undergo dental procedures, such as advanced age (ie, elderly patients may have a decreased gag reflex); neurologic conditions, such as stroke; dementia and other degenerative diseases; the use of topical anesthesia; and altered states of consciousness associated with the use of IV sedation.^1,2

The key sign that most dentists recognize when patients aspirate an object during a dental procedure is coughing. It has been reported that coughing resulting from aspiration of foreign objects may range from mild to severe. In this case, the patient was completely asymptomatic during the procedure. The only clue of possible object aspiration was the reported tool loss by the dentist. It is important to always examine, account for, and review all equipment used during dental procedures. Assessment for any lost objects or missing parts of instruments should be done promptly with a high degree of suspicion for possible swallowing or aspiration if an object is missing.

 

It has been recommended to use a gauze throat screen and rubber dam and to avoid a supine position during a procedure, among other techniques, to minimize risk of ingestion or aspiration.² Imaging studies should be used for further evaluation of the patient; however, some instruments, such as dental pieces and impression material, may not be identified by plain films. In those cases, further evaluation with more sophisticated imaging techniques, such as computed tomography (CT), should be considered.^1-10

In a previous case report of a patient who aspirated a third molar during a dental procedure, a chest film failed to identify it. A chest CT was performed, and the object showed in the right main stem bronchus. In another instance, aspiration of impression material in a 45-year-old man was not observed by chest radiography. In this case, the history of coughing and respiratory symptoms days after the procedure pointed toward aspiration of an object as the culprit, with subsequent identification and removal by flexible fiberoptic bronchoscopy.^1-11

Bronchoscopy is the treatment of choice for extraction of aspirated foreign bodies; however, there is still a debate about whether to use flexible or rigid bronchoscopy. The decision is usually made based on the object size, localization, medical facility, and personnel expertise. The rigid bronchoscope has the advantages of offering better control and visualization of the airway and easier use of removal instruments. Its primary disadvantage is that the procedure needs to be done in the operating room under general anesthesia. Flexible fiberoptic bronchoscopy done under conscious sedation and topical anesthesia may be as effective as rigid bronchoscopy and even superior in the case of smaller and more distal impacted objects.^10-14

In this case, flexible fiberoptic bronchoscopy was used successfully for the removal of the foreign object. Biopsy forceps were used to grasp the object and retrieve it from the airway without complication.

Conclusion

Aspiration of foreign objects during a dental procedure is a potential life-threatening complication. A high-level of suspicion is needed for early diagnosis and referral of the patient for extraction of the object and further avoidance of complications. Flexible fiberoptic bronchoscopy is a feasible procedure for removal of objects within the airway. 

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc. , the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

 

Case

A 50-year-old man ingests two handfuls of small, red berries that he picked from a shrub in front of his apartment building, with the belief that they would have medicinal value. Two hours later, he developed abdominal cramping and vomited multiple times, followed shortly thereafter by profuse diaphoresis, lethargy, and ataxia. His concerned family brought him to the ED where his vital signs on presentation were: blood pressure (BP), 78/43 mm Hg; heart rate (HR), 50 beats/minute; respiratory rate (RR), 12 breaths/minute; temperature (T), 97.8°F. With the exception of bradycardia, the patient’s cardiac, pulmonary, and abdominal examinations were normal. His skin was diaphoretic, and he had no focal motor or sensory deficits or tremor. Initial laboratory values were: hemoglobin, 12.6 g/dL; sodium, 137 mEq/L; potassium, 4.6 mEq/L; bicarbonate, 20 mEq/L; blood urea nitrogen, 17 mg/dL; creatinine, 2.2 mg/dL; glucose, 288 mg/dL. The patient’s troponin I level was slightly elevated at 0.06 ng/mL; electrocardiogram (ECG) results are shown in Figure 1.

 

Why do plant poisonings occur?

There is the general belief that what is natural is not only healthful but also safe. This is clearly not true: cyanide, uranium, and king cobras are all natural but hardly safe. While most plants chosen for their purported medicinal properties are generally harmless in most patients when taken in low doses, there are plants that are sufficiently poisonous to be consequential with even relatively small exposures. Some people, often unknowingly vulnerable due to genetic or other causes, are uniquely susceptible to even minute doses.

Humans probably learned about plant toxicity early on—most likely the hard way. To this day, however, the Internet is replete with traditional and avant-garde natural healing remedies involving the use of naturally-derived plant products. These numerous bioactive compounds are often sold in plant form or as extracts, the latter being more concerning given their more concentrated formulation.

Plant misidentification is a common cause of poisoning, whether the intended use is for food or medicine. For example, some mistake “deadly nightshade” (Atropa belladonna) berries, which are deep blue, for blueberries, or pokeweed roots for horseradish roots due to their similar appearances.¹

Alternatively, even when a plant is correctly identified, patients may experience adverse effects if they exceed the “therapeutic dose” (eg, dysrhythmia from aconite roots used in traditional Chinese medicine) or if the plant is improperly prepared (eg, hypoglycemia from consuming unripe ackee fruit).² In addition, a toxic plant such as Jimson weed (Datura stramonium) or coca leaf extract may be intentionally ingested for its psychoactive hallucinatory effects.² Although rare in the United States, in certain parts of Asia, persons intent on self-harm may consume toxic plants.¹

When ingested, what plants cause bradycardia and hypotension, and why do these effects occur?

The two broad classes of plant-derived toxins that can cause these findings are cardioactive steroids and sodium channel active agents.

Cardioactive Steroids
There are numerous botanical sources of cardioactive steroids (sometimes called cardiac glycosides) such as Digitalis lanata, from which digoxin is derived; and Digitalis purpurea, the source of digitoxin. Poisoning by Digitalis spp, squill, lily of the valley, oleander, yellow oleander, and Cerbera manghas are clinically similar. Cardioactive steroids act pharmacologically to block the sodium-potassium ATPase pump on the myocardial cell membrane. This in turn increases intracellular sodium, which subsequently inhibits the exchange of extracellular sodium for intracellular calcium, leading to inotropy. Clinical manifestations of toxicity include nausea, vomiting, hyperkalemia, bradycardia, cardiac dysrhythmias, and occasionally hypotension—some of which can be life-threatening.

Sodium Channel Active Agents
Several plant toxins affect the flow of sodium by blocking or activating the sodium channel. Both effects alter the rate and strength of cardiac contraction, causing cardiac dysrhythmias.

Aconite is often used in traditional Chinese medicine. In North America, it is mainly derived from Aconitinum napellus, commonly called monkshood, helmet flower, or wolfsbane. It effectively holds open the voltage-dependent sodium channel, increasing cellular excitability. By prolonging the sodium current influx, neuronal and cardiac repolarization eventually slow due to sodium overload, leading to bradycardia and hypotension, as well as neurological effects. Its cardiotoxicity resembles that caused by cardiac glycosides, though a history of paresthesias or muscle weakness may help to differentiate the two toxins.

Veratrum spp include false hellebore, Indian poke, and California hellebore. These plants are occasionally mistaken for leeks (ramps) and can cause vomiting, bradycardia, and hypotension by a mechanism of action similar to aconitine.

Taxine, derived from the English yew (Taxus baccata), a common garden shrub, is another sodium channel effector that closes the sodium and calcium channels. The decreased flow of sodium and calcium leads to a failure of cardiac impulse initiation and propagation, resulting in bradycardia and hypotension. The flesh (aril) around the seed of the berry is the only part of the tree that is not toxic (Figure 2).

 

Grayanotoxins, a group of diterpenoid toxins found in death camas, azalea, Rhododendron spp, and mountain laurel, can become concentrated in honey made from these plants. Depending on the specific toxin, they variably open or close the sodium channel. In addition to causing bradycardia and hypotension, patients may exhibit mental status changes (“mad honey” poisoning) and seizures.²

 

Case Continuation

After rapid infusion of 1-liter of normal saline, the patient’s BP was 80/63 mm Hg and HR was 52 beats/minute. His wife arrived to the ED 30-minutes later with a plastic bag containing the red berries the patient had ingested. The emergency physician identified them as Taxus baccata, or more commonly, yew berries. The patient stated that he ingested both the red fleshy aril and chewed the hard central seed. 

 

How is cardiotoxicity from yew berries treated?

Within hours of ingestion, toxicity progresses from nausea, abdominal pain, paresthesias, and ataxia, to bradycardia, cardiac conduction delays, wide-complex ventricular dysrhythmias and mental status changes.³ Although toxicity of Taxus has been known since antiquity, no antidote exists. Ventricular dysrhythmias causing hemodynamic instability should be electrically cardioverted, although there is no evidence to support the safety or efficacy of such therapy. Since the serum, and therefore cardiac concentration of taxine will be identical after cardioversion to its value prior, recurrent dysrhythmias are common.¹ Sodium bicarbonate has been inconsistently effective in the treatment of wide-complex tachydysrhythmias,⁴ but its use seems counterintuitive for most cases. There may be merit to raising the sodium gradient on an already sodium overloaded myocyte, but short-term gain may lead to unintended consequences. Success with antidysrhythmics has been limited: although amiodarone is often used to treat wide-complex tachydysrhythmias, its efficacy in Taxus toxicity has been conflicting.^4-6

There have been a few reported cases of yew alkaloid crossreactivity with digoxin assays, suggesting that digoxin-specific antibody fragments may bind taxine.⁷ There is no evidence, however, that cardioactive steroids are present in yew, and empiric use of antidigoxin Fab-fragments cannot be recommended. A single case report demonstrated that hemodialysis was ineffective in the removal of taxines, likely due to the toxin’s large volume of distribution.⁸ As a last resort, extracorporeal life support with membrane oxygenation is described favorably in two cases of yew berry poisoning refractory to conventional therapy.^9,10

 

Case Conclusion

The patient’s ECGs showed a morphologically abnormal rhythm, possibly with a Brugada pattern, which are representative of the dysrhythmias caused by taxine’s inhibitory effects on the sodium and calcium channels. Despite an attempt at electrical cardioversion, the dysrhythmia persisted. He was given intravenous boluses of fluids and started on an amiodarone infusion. The patient’s BP gradually improved over the following 2 hours, and the dysrhythmia resolved with hemodynamic improvement. The amiodarone infusion was then discontinued, and he was admitted to the hospital for further testing. Echocardiography, electrophysiology studies, and cardiac catheterization were all normal. The absence of structural, dysrhythmogenic, and ischemic abnormalities supported the toxic etiology of his hemodynamic aberrations. He was discharged from the hospital 3 days later without report of sequelae.

Dr Nguyen is a medical toxicology fellow in the department of emergency medicine at New York University Langone Medical Center. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board.

 

Case

A 50-year-old man ingests two handfuls of small, red berries that he picked from a shrub in front of his apartment building, with the belief that they would have medicinal value. Two hours later, he developed abdominal cramping and vomited multiple times, followed shortly thereafter by profuse diaphoresis, lethargy, and ataxia. His concerned family brought him to the ED where his vital signs on presentation were: blood pressure (BP), 78/43 mm Hg; heart rate (HR), 50 beats/minute; respiratory rate (RR), 12 breaths/minute; temperature (T), 97.8°F. With the exception of bradycardia, the patient’s cardiac, pulmonary, and abdominal examinations were normal. His skin was diaphoretic, and he had no focal motor or sensory deficits or tremor. Initial laboratory values were: hemoglobin, 12.6 g/dL; sodium, 137 mEq/L; potassium, 4.6 mEq/L; bicarbonate, 20 mEq/L; blood urea nitrogen, 17 mg/dL; creatinine, 2.2 mg/dL; glucose, 288 mg/dL. The patient’s troponin I level was slightly elevated at 0.06 ng/mL; electrocardiogram (ECG) results are shown in Figure 1.

 

Why do plant poisonings occur?

There is the general belief that what is natural is not only healthful but also safe. This is clearly not true: cyanide, uranium, and king cobras are all natural but hardly safe. While most plants chosen for their purported medicinal properties are generally harmless in most patients when taken in low doses, there are plants that are sufficiently poisonous to be consequential with even relatively small exposures. Some people, often unknowingly vulnerable due to genetic or other causes, are uniquely susceptible to even minute doses.

Humans probably learned about plant toxicity early on—most likely the hard way. To this day, however, the Internet is replete with traditional and avant-garde natural healing remedies involving the use of naturally-derived plant products. These numerous bioactive compounds are often sold in plant form or as extracts, the latter being more concerning given their more concentrated formulation.

Plant misidentification is a common cause of poisoning, whether the intended use is for food or medicine. For example, some mistake “deadly nightshade” (Atropa belladonna) berries, which are deep blue, for blueberries, or pokeweed roots for horseradish roots due to their similar appearances.¹

Alternatively, even when a plant is correctly identified, patients may experience adverse effects if they exceed the “therapeutic dose” (eg, dysrhythmia from aconite roots used in traditional Chinese medicine) or if the plant is improperly prepared (eg, hypoglycemia from consuming unripe ackee fruit).² In addition, a toxic plant such as Jimson weed (Datura stramonium) or coca leaf extract may be intentionally ingested for its psychoactive hallucinatory effects.² Although rare in the United States, in certain parts of Asia, persons intent on self-harm may consume toxic plants.¹

When ingested, what plants cause bradycardia and hypotension, and why do these effects occur?

The two broad classes of plant-derived toxins that can cause these findings are cardioactive steroids and sodium channel active agents.

Cardioactive Steroids
There are numerous botanical sources of cardioactive steroids (sometimes called cardiac glycosides) such as Digitalis lanata, from which digoxin is derived; and Digitalis purpurea, the source of digitoxin. Poisoning by Digitalis spp, squill, lily of the valley, oleander, yellow oleander, and Cerbera manghas are clinically similar. Cardioactive steroids act pharmacologically to block the sodium-potassium ATPase pump on the myocardial cell membrane. This in turn increases intracellular sodium, which subsequently inhibits the exchange of extracellular sodium for intracellular calcium, leading to inotropy. Clinical manifestations of toxicity include nausea, vomiting, hyperkalemia, bradycardia, cardiac dysrhythmias, and occasionally hypotension—some of which can be life-threatening.

Sodium Channel Active Agents
Several plant toxins affect the flow of sodium by blocking or activating the sodium channel. Both effects alter the rate and strength of cardiac contraction, causing cardiac dysrhythmias.

Aconite is often used in traditional Chinese medicine. In North America, it is mainly derived from Aconitinum napellus, commonly called monkshood, helmet flower, or wolfsbane. It effectively holds open the voltage-dependent sodium channel, increasing cellular excitability. By prolonging the sodium current influx, neuronal and cardiac repolarization eventually slow due to sodium overload, leading to bradycardia and hypotension, as well as neurological effects. Its cardiotoxicity resembles that caused by cardiac glycosides, though a history of paresthesias or muscle weakness may help to differentiate the two toxins.

Veratrum spp include false hellebore, Indian poke, and California hellebore. These plants are occasionally mistaken for leeks (ramps) and can cause vomiting, bradycardia, and hypotension by a mechanism of action similar to aconitine.

Taxine, derived from the English yew (Taxus baccata), a common garden shrub, is another sodium channel effector that closes the sodium and calcium channels. The decreased flow of sodium and calcium leads to a failure of cardiac impulse initiation and propagation, resulting in bradycardia and hypotension. The flesh (aril) around the seed of the berry is the only part of the tree that is not toxic (Figure 2).

 

Grayanotoxins, a group of diterpenoid toxins found in death camas, azalea, Rhododendron spp, and mountain laurel, can become concentrated in honey made from these plants. Depending on the specific toxin, they variably open or close the sodium channel. In addition to causing bradycardia and hypotension, patients may exhibit mental status changes (“mad honey” poisoning) and seizures.²

 

Case Continuation

After rapid infusion of 1-liter of normal saline, the patient’s BP was 80/63 mm Hg and HR was 52 beats/minute. His wife arrived to the ED 30-minutes later with a plastic bag containing the red berries the patient had ingested. The emergency physician identified them as Taxus baccata, or more commonly, yew berries. The patient stated that he ingested both the red fleshy aril and chewed the hard central seed. 

 

How is cardiotoxicity from yew berries treated?

Within hours of ingestion, toxicity progresses from nausea, abdominal pain, paresthesias, and ataxia, to bradycardia, cardiac conduction delays, wide-complex ventricular dysrhythmias and mental status changes.³ Although toxicity of Taxus has been known since antiquity, no antidote exists. Ventricular dysrhythmias causing hemodynamic instability should be electrically cardioverted, although there is no evidence to support the safety or efficacy of such therapy. Since the serum, and therefore cardiac concentration of taxine will be identical after cardioversion to its value prior, recurrent dysrhythmias are common.¹ Sodium bicarbonate has been inconsistently effective in the treatment of wide-complex tachydysrhythmias,⁴ but its use seems counterintuitive for most cases. There may be merit to raising the sodium gradient on an already sodium overloaded myocyte, but short-term gain may lead to unintended consequences. Success with antidysrhythmics has been limited: although amiodarone is often used to treat wide-complex tachydysrhythmias, its efficacy in Taxus toxicity has been conflicting.^4-6

There have been a few reported cases of yew alkaloid crossreactivity with digoxin assays, suggesting that digoxin-specific antibody fragments may bind taxine.⁷ There is no evidence, however, that cardioactive steroids are present in yew, and empiric use of antidigoxin Fab-fragments cannot be recommended. A single case report demonstrated that hemodialysis was ineffective in the removal of taxines, likely due to the toxin’s large volume of distribution.⁸ As a last resort, extracorporeal life support with membrane oxygenation is described favorably in two cases of yew berry poisoning refractory to conventional therapy.^9,10

 

Case Conclusion

The patient’s ECGs showed a morphologically abnormal rhythm, possibly with a Brugada pattern, which are representative of the dysrhythmias caused by taxine’s inhibitory effects on the sodium and calcium channels. Despite an attempt at electrical cardioversion, the dysrhythmia persisted. He was given intravenous boluses of fluids and started on an amiodarone infusion. The patient’s BP gradually improved over the following 2 hours, and the dysrhythmia resolved with hemodynamic improvement. The amiodarone infusion was then discontinued, and he was admitted to the hospital for further testing. Echocardiography, electrophysiology studies, and cardiac catheterization were all normal. The absence of structural, dysrhythmogenic, and ischemic abnormalities supported the toxic etiology of his hemodynamic aberrations. He was discharged from the hospital 3 days later without report of sequelae.

Dr Nguyen is a medical toxicology fellow in the department of emergency medicine at New York University Langone Medical Center. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board.

 

Case

A 50-year-old man ingests two handfuls of small, red berries that he picked from a shrub in front of his apartment building, with the belief that they would have medicinal value. Two hours later, he developed abdominal cramping and vomited multiple times, followed shortly thereafter by profuse diaphoresis, lethargy, and ataxia. His concerned family brought him to the ED where his vital signs on presentation were: blood pressure (BP), 78/43 mm Hg; heart rate (HR), 50 beats/minute; respiratory rate (RR), 12 breaths/minute; temperature (T), 97.8°F. With the exception of bradycardia, the patient’s cardiac, pulmonary, and abdominal examinations were normal. His skin was diaphoretic, and he had no focal motor or sensory deficits or tremor. Initial laboratory values were: hemoglobin, 12.6 g/dL; sodium, 137 mEq/L; potassium, 4.6 mEq/L; bicarbonate, 20 mEq/L; blood urea nitrogen, 17 mg/dL; creatinine, 2.2 mg/dL; glucose, 288 mg/dL. The patient’s troponin I level was slightly elevated at 0.06 ng/mL; electrocardiogram (ECG) results are shown in Figure 1.

 

Why do plant poisonings occur?

There is the general belief that what is natural is not only healthful but also safe. This is clearly not true: cyanide, uranium, and king cobras are all natural but hardly safe. While most plants chosen for their purported medicinal properties are generally harmless in most patients when taken in low doses, there are plants that are sufficiently poisonous to be consequential with even relatively small exposures. Some people, often unknowingly vulnerable due to genetic or other causes, are uniquely susceptible to even minute doses.

Humans probably learned about plant toxicity early on—most likely the hard way. To this day, however, the Internet is replete with traditional and avant-garde natural healing remedies involving the use of naturally-derived plant products. These numerous bioactive compounds are often sold in plant form or as extracts, the latter being more concerning given their more concentrated formulation.

Plant misidentification is a common cause of poisoning, whether the intended use is for food or medicine. For example, some mistake “deadly nightshade” (Atropa belladonna) berries, which are deep blue, for blueberries, or pokeweed roots for horseradish roots due to their similar appearances.¹

Alternatively, even when a plant is correctly identified, patients may experience adverse effects if they exceed the “therapeutic dose” (eg, dysrhythmia from aconite roots used in traditional Chinese medicine) or if the plant is improperly prepared (eg, hypoglycemia from consuming unripe ackee fruit).² In addition, a toxic plant such as Jimson weed (Datura stramonium) or coca leaf extract may be intentionally ingested for its psychoactive hallucinatory effects.² Although rare in the United States, in certain parts of Asia, persons intent on self-harm may consume toxic plants.¹

When ingested, what plants cause bradycardia and hypotension, and why do these effects occur?

The two broad classes of plant-derived toxins that can cause these findings are cardioactive steroids and sodium channel active agents.

Cardioactive Steroids
There are numerous botanical sources of cardioactive steroids (sometimes called cardiac glycosides) such as Digitalis lanata, from which digoxin is derived; and Digitalis purpurea, the source of digitoxin. Poisoning by Digitalis spp, squill, lily of the valley, oleander, yellow oleander, and Cerbera manghas are clinically similar. Cardioactive steroids act pharmacologically to block the sodium-potassium ATPase pump on the myocardial cell membrane. This in turn increases intracellular sodium, which subsequently inhibits the exchange of extracellular sodium for intracellular calcium, leading to inotropy. Clinical manifestations of toxicity include nausea, vomiting, hyperkalemia, bradycardia, cardiac dysrhythmias, and occasionally hypotension—some of which can be life-threatening.

Sodium Channel Active Agents
Several plant toxins affect the flow of sodium by blocking or activating the sodium channel. Both effects alter the rate and strength of cardiac contraction, causing cardiac dysrhythmias.

Aconite is often used in traditional Chinese medicine. In North America, it is mainly derived from Aconitinum napellus, commonly called monkshood, helmet flower, or wolfsbane. It effectively holds open the voltage-dependent sodium channel, increasing cellular excitability. By prolonging the sodium current influx, neuronal and cardiac repolarization eventually slow due to sodium overload, leading to bradycardia and hypotension, as well as neurological effects. Its cardiotoxicity resembles that caused by cardiac glycosides, though a history of paresthesias or muscle weakness may help to differentiate the two toxins.

Veratrum spp include false hellebore, Indian poke, and California hellebore. These plants are occasionally mistaken for leeks (ramps) and can cause vomiting, bradycardia, and hypotension by a mechanism of action similar to aconitine.

Taxine, derived from the English yew (Taxus baccata), a common garden shrub, is another sodium channel effector that closes the sodium and calcium channels. The decreased flow of sodium and calcium leads to a failure of cardiac impulse initiation and propagation, resulting in bradycardia and hypotension. The flesh (aril) around the seed of the berry is the only part of the tree that is not toxic (Figure 2).

 

Grayanotoxins, a group of diterpenoid toxins found in death camas, azalea, Rhododendron spp, and mountain laurel, can become concentrated in honey made from these plants. Depending on the specific toxin, they variably open or close the sodium channel. In addition to causing bradycardia and hypotension, patients may exhibit mental status changes (“mad honey” poisoning) and seizures.²

 

Case Continuation

After rapid infusion of 1-liter of normal saline, the patient’s BP was 80/63 mm Hg and HR was 52 beats/minute. His wife arrived to the ED 30-minutes later with a plastic bag containing the red berries the patient had ingested. The emergency physician identified them as Taxus baccata, or more commonly, yew berries. The patient stated that he ingested both the red fleshy aril and chewed the hard central seed. 

 

How is cardiotoxicity from yew berries treated?

Within hours of ingestion, toxicity progresses from nausea, abdominal pain, paresthesias, and ataxia, to bradycardia, cardiac conduction delays, wide-complex ventricular dysrhythmias and mental status changes.³ Although toxicity of Taxus has been known since antiquity, no antidote exists. Ventricular dysrhythmias causing hemodynamic instability should be electrically cardioverted, although there is no evidence to support the safety or efficacy of such therapy. Since the serum, and therefore cardiac concentration of taxine will be identical after cardioversion to its value prior, recurrent dysrhythmias are common.¹ Sodium bicarbonate has been inconsistently effective in the treatment of wide-complex tachydysrhythmias,⁴ but its use seems counterintuitive for most cases. There may be merit to raising the sodium gradient on an already sodium overloaded myocyte, but short-term gain may lead to unintended consequences. Success with antidysrhythmics has been limited: although amiodarone is often used to treat wide-complex tachydysrhythmias, its efficacy in Taxus toxicity has been conflicting.^4-6

There have been a few reported cases of yew alkaloid crossreactivity with digoxin assays, suggesting that digoxin-specific antibody fragments may bind taxine.⁷ There is no evidence, however, that cardioactive steroids are present in yew, and empiric use of antidigoxin Fab-fragments cannot be recommended. A single case report demonstrated that hemodialysis was ineffective in the removal of taxines, likely due to the toxin’s large volume of distribution.⁸ As a last resort, extracorporeal life support with membrane oxygenation is described favorably in two cases of yew berry poisoning refractory to conventional therapy.^9,10

 

Case Conclusion

The patient’s ECGs showed a morphologically abnormal rhythm, possibly with a Brugada pattern, which are representative of the dysrhythmias caused by taxine’s inhibitory effects on the sodium and calcium channels. Despite an attempt at electrical cardioversion, the dysrhythmia persisted. He was given intravenous boluses of fluids and started on an amiodarone infusion. The patient’s BP gradually improved over the following 2 hours, and the dysrhythmia resolved with hemodynamic improvement. The amiodarone infusion was then discontinued, and he was admitted to the hospital for further testing. Echocardiography, electrophysiology studies, and cardiac catheterization were all normal. The absence of structural, dysrhythmogenic, and ischemic abnormalities supported the toxic etiology of his hemodynamic aberrations. He was discharged from the hospital 3 days later without report of sequelae.

Dr Nguyen is a medical toxicology fellow in the department of emergency medicine at New York University Langone Medical Center. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board.

Case

A 3-year-old girl presented to the ED with a 1-week history of cough and new-onset abdominal pain. She was accompanied by her grandfather, who stated that the child had been dropped-off at his house around 5:00 pm the previous day. He noted that after putting his granddaughter to bed, she awoke around 4:30 am complaining of a stomachache. After rocking her, he said she went back to sleep but did not wake up again until 1:00 pm that afternoon. Over the first few hours of awakening, she became less active and had three episodes of posttussive emesis. The grandfather denied the child had any recent nasal congestion, fever, nausea, vomiting, or diarrhea. When questioned about possible toxic ingestion, he said there were no medications in the house and that he did not witness any substance ingestion or trauma.

Regarding history, the patient was born full-term without any complications. She did not have any significant medical or surgical history. There were no documented allergies, and she was not on any medications. All of her immunizations were up-to-date. The family history was not significant for chronic diseases except for asthma in distant relatives. Her grandfather denied any recent exposures or travel.

At presentation, the patient’s vital signs were: blood pressure (BP) 86/49 mm Hg; heart rate (HR), 178 beats/minute and regular; respiratory rate (RR), 26 breaths/minute; temporal artery temperature, 104.7°F. Oxygen saturation was 99% on room air. On physical examination, she was normocephalic; there was no scleral icterus; and the throat and bilateral tympanic membranes were normal. Her extremities were warm and well perfused, with normal capillary refill. Patient’s lungs were clear, and heart sounds were normal with no detection of a murmur. The abdomen was soft and nontender; there was no evidence of organomegaly.

Laboratory evaluation included assessment of sodium, chloride, carbon dioxide, calcium, magnesium, amylase, lipase, and creatine levels; liver function test; complete blood count; and red-cell indices. All of the laboratory values were within normal limits, and urinalysis was negative for infection. Blood and urine cultures were also taken. A chest X-ray showed no acute intrathoracic process (Figure 1).

Secondary to the patient’s fever and tachycardia, the presumed diagnosis was systemic inflammatory response syndrome, and an intravenous (IV) bolus of normal saline 20 mL/kg along with ibuprofen and ondansetron were administered to treat fever and nausea, respectively. In addition, a dose of ceftriaxone was also given. The patient’s repeat set of vitals were: BP, 86/64 mm Hg; HR, 195 beats/minute; RR, 20 breaths/minute; and temporal artery temperature, 97.9°F; oxygen saturation was 98% on room air.

During treatment, the patient became increasingly fussy with new-onset abdominal distension. Repeat physical examination revealed hepatomegaly. A bedside echocardiogram showed hyperdynamic heart with fractional shortening* (FS) of 20% and ejection fraction (EF) of 43%, but no structural abnormalities. An electrocardiogram (ECG) was then ordered, which revealed narrow complex tachycardia with inverted P-waves in inferior leads.

The patient was transferred to the intensive care unit where she was started on IV milrinone for development of secondary hypotension and reduced cardiac function. Based on inverted P waves on ECG leads II, III, and aVF, three doses of adenosine (0.1 mg/kg, 0.2 mg/kg, and 0.2 mg/kg) were given, which interrupted the tachycafrdia for only a few beats. After consultation with a cardiac electrophysiologist, a diagnosis of persistent junctional reentrant tachycardia (PJRT) was reached based on the patient’s ECG features and nonresponse to adenosine. She was started on IV amiodarone (loading dose of 5 mg/kg followed by infusion of 5 mcg/kg/min), which relieved the tachycardia (Figure 3). Her vital signs stabilized and her clinical status gradually improved. After 3 days, she was discharged on oral amiodarone and close follow-up with cardiology. A repeat echocardiogram just prior to discharge showed improvement in FS to 23% and EF to 48%.

Discussion

Normal cardiac conduction involves an originating impulse from a sinus node followed by atrial muscle activation reaching the atrioventricular (AV) node. There is a necessary delay at the AV node, which is required for ventricular filling and activation of ventricles through the His-Purkinje fiber system and the bundle branches. An abnormality or interruption of this pathway results in an arrhythmia such as supraventricular tachycardia (SVT).

Supraventricular Tachycardia

Supraventricular tachycardia is the most common symptomatic abnormality in the pediatric population.¹ Among the various forms of SVT, AV reentrant tachycardia (AVRT) and AV node reentrant tachycardia (AVNRT) account for most case presentations.² Supraventricular tachycardia may be classified by duration of RP interval compared to PR interval on ECG. Short RP interval SVT includes AVNRT and AVRT through a rapidly conducting accessory path. Long RP interval SVT includes atypical AVNRT, atrial tachycardia, and PJRT.

 

Persistent Junctional Reentrant Tachycardia

Persistent junctional reentrant tachycardia is a rare form of long RP tachycardia, accounting for approximately 1% of SVT in a study review of 21 patients.³ As with the patient in this case, PJRT usually presents in early childhood.³   In a recent review of 194 patients with PJRT, 57% were infants.⁴ The condition involves an accessory pathway most commonly located in the posterior-superior septal region; conduction involves a retrograde impulse through the decremental accessory pathway.⁵ On ECG, findings include a negative P wave in inferior leads, a long RP interval, and a 1:1 AV conduction.⁶

A long-term multicenter follow-up study of 32 patients showed that rates of tachycardia vary among patients, from 100 to 250 beats/minute.⁷ Tachycardia-induced cardiomyopathy (TIC), which is secondary to the incessant nature of tachycardia, may be present in up to 30% to 50% of patients.^3,8 In a recent multicenter study, PJRT was responsible for 23% of cases of TIC.⁹ Although the exact mechanism of this property is unknown, decremental conduction and unidirectional block of the accessory pathway appear to be contributing factors.⁶

Treatment

Adenosine is the initial drug of choice for narrow complex tachycardia with stable hemodynamic status and an available intravascular access.¹⁰ In a study evaluating the effectiveness of adenosine for managing SVT in the pediatric ED setting, it was more than 70% effective in cardioverting patients presumed to have SVT.¹¹ However, in PJRT, owing to the incessant pattern, adenosine may either terminate the tachycardia (causing asystole) or, as seen in this patient, convert tachycardia to sinus rhythm for only a few seconds.¹² Reinitiation of tachycardia in sinus beat without the need for a premature complex contributes to its incessant nature.¹³

In a multicenter study looking at clinical profile and outcome for PJRT, Vaksmann et al⁸ found a greater than 80% success rate in controlling the dysrhythmia with amiodarone and verapamil. For long-term management of tachyarrhythmia, medical therapy has been recommended in early childhood compared to older children in whom catheter ablation is an effective approach.⁷ Spontaneous resolution of PJRT has been documented but is rare.¹⁴

Conclusion

Pediatric cardiac emergencies require very specific treatment. As such, it is important that the emergency physician distinguish the different the types of tachyarrhythmias—especially in cases that do not respond to treatment with adenosine. In the pediatric patient, PJRT is a potentially life-threatening arrhythmia that requires a high index of suspicion. Clues to diagnosis include negative P waves in inferior leads, long RP interval, and 1:1 atrioventricular conduction.

Dr Fichadia is a fellow, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan. Dr Perez is a clinical instructor, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan.

Case

A 3-year-old girl presented to the ED with a 1-week history of cough and new-onset abdominal pain. She was accompanied by her grandfather, who stated that the child had been dropped-off at his house around 5:00 pm the previous day. He noted that after putting his granddaughter to bed, she awoke around 4:30 am complaining of a stomachache. After rocking her, he said she went back to sleep but did not wake up again until 1:00 pm that afternoon. Over the first few hours of awakening, she became less active and had three episodes of posttussive emesis. The grandfather denied the child had any recent nasal congestion, fever, nausea, vomiting, or diarrhea. When questioned about possible toxic ingestion, he said there were no medications in the house and that he did not witness any substance ingestion or trauma.

Regarding history, the patient was born full-term without any complications. She did not have any significant medical or surgical history. There were no documented allergies, and she was not on any medications. All of her immunizations were up-to-date. The family history was not significant for chronic diseases except for asthma in distant relatives. Her grandfather denied any recent exposures or travel.

At presentation, the patient’s vital signs were: blood pressure (BP) 86/49 mm Hg; heart rate (HR), 178 beats/minute and regular; respiratory rate (RR), 26 breaths/minute; temporal artery temperature, 104.7°F. Oxygen saturation was 99% on room air. On physical examination, she was normocephalic; there was no scleral icterus; and the throat and bilateral tympanic membranes were normal. Her extremities were warm and well perfused, with normal capillary refill. Patient’s lungs were clear, and heart sounds were normal with no detection of a murmur. The abdomen was soft and nontender; there was no evidence of organomegaly.

Laboratory evaluation included assessment of sodium, chloride, carbon dioxide, calcium, magnesium, amylase, lipase, and creatine levels; liver function test; complete blood count; and red-cell indices. All of the laboratory values were within normal limits, and urinalysis was negative for infection. Blood and urine cultures were also taken. A chest X-ray showed no acute intrathoracic process (Figure 1).

Secondary to the patient’s fever and tachycardia, the presumed diagnosis was systemic inflammatory response syndrome, and an intravenous (IV) bolus of normal saline 20 mL/kg along with ibuprofen and ondansetron were administered to treat fever and nausea, respectively. In addition, a dose of ceftriaxone was also given. The patient’s repeat set of vitals were: BP, 86/64 mm Hg; HR, 195 beats/minute; RR, 20 breaths/minute; and temporal artery temperature, 97.9°F; oxygen saturation was 98% on room air.

During treatment, the patient became increasingly fussy with new-onset abdominal distension. Repeat physical examination revealed hepatomegaly. A bedside echocardiogram showed hyperdynamic heart with fractional shortening* (FS) of 20% and ejection fraction (EF) of 43%, but no structural abnormalities. An electrocardiogram (ECG) was then ordered, which revealed narrow complex tachycardia with inverted P-waves in inferior leads.

The patient was transferred to the intensive care unit where she was started on IV milrinone for development of secondary hypotension and reduced cardiac function. Based on inverted P waves on ECG leads II, III, and aVF, three doses of adenosine (0.1 mg/kg, 0.2 mg/kg, and 0.2 mg/kg) were given, which interrupted the tachycafrdia for only a few beats. After consultation with a cardiac electrophysiologist, a diagnosis of persistent junctional reentrant tachycardia (PJRT) was reached based on the patient’s ECG features and nonresponse to adenosine. She was started on IV amiodarone (loading dose of 5 mg/kg followed by infusion of 5 mcg/kg/min), which relieved the tachycardia (Figure 3). Her vital signs stabilized and her clinical status gradually improved. After 3 days, she was discharged on oral amiodarone and close follow-up with cardiology. A repeat echocardiogram just prior to discharge showed improvement in FS to 23% and EF to 48%.

Discussion

Normal cardiac conduction involves an originating impulse from a sinus node followed by atrial muscle activation reaching the atrioventricular (AV) node. There is a necessary delay at the AV node, which is required for ventricular filling and activation of ventricles through the His-Purkinje fiber system and the bundle branches. An abnormality or interruption of this pathway results in an arrhythmia such as supraventricular tachycardia (SVT).

Supraventricular Tachycardia

Supraventricular tachycardia is the most common symptomatic abnormality in the pediatric population.¹ Among the various forms of SVT, AV reentrant tachycardia (AVRT) and AV node reentrant tachycardia (AVNRT) account for most case presentations.² Supraventricular tachycardia may be classified by duration of RP interval compared to PR interval on ECG. Short RP interval SVT includes AVNRT and AVRT through a rapidly conducting accessory path. Long RP interval SVT includes atypical AVNRT, atrial tachycardia, and PJRT.

 

Persistent Junctional Reentrant Tachycardia

Persistent junctional reentrant tachycardia is a rare form of long RP tachycardia, accounting for approximately 1% of SVT in a study review of 21 patients.³ As with the patient in this case, PJRT usually presents in early childhood.³   In a recent review of 194 patients with PJRT, 57% were infants.⁴ The condition involves an accessory pathway most commonly located in the posterior-superior septal region; conduction involves a retrograde impulse through the decremental accessory pathway.⁵ On ECG, findings include a negative P wave in inferior leads, a long RP interval, and a 1:1 AV conduction.⁶

A long-term multicenter follow-up study of 32 patients showed that rates of tachycardia vary among patients, from 100 to 250 beats/minute.⁷ Tachycardia-induced cardiomyopathy (TIC), which is secondary to the incessant nature of tachycardia, may be present in up to 30% to 50% of patients.^3,8 In a recent multicenter study, PJRT was responsible for 23% of cases of TIC.⁹ Although the exact mechanism of this property is unknown, decremental conduction and unidirectional block of the accessory pathway appear to be contributing factors.⁶

Treatment

Adenosine is the initial drug of choice for narrow complex tachycardia with stable hemodynamic status and an available intravascular access.¹⁰ In a study evaluating the effectiveness of adenosine for managing SVT in the pediatric ED setting, it was more than 70% effective in cardioverting patients presumed to have SVT.¹¹ However, in PJRT, owing to the incessant pattern, adenosine may either terminate the tachycardia (causing asystole) or, as seen in this patient, convert tachycardia to sinus rhythm for only a few seconds.¹² Reinitiation of tachycardia in sinus beat without the need for a premature complex contributes to its incessant nature.¹³

In a multicenter study looking at clinical profile and outcome for PJRT, Vaksmann et al⁸ found a greater than 80% success rate in controlling the dysrhythmia with amiodarone and verapamil. For long-term management of tachyarrhythmia, medical therapy has been recommended in early childhood compared to older children in whom catheter ablation is an effective approach.⁷ Spontaneous resolution of PJRT has been documented but is rare.¹⁴

Conclusion

Pediatric cardiac emergencies require very specific treatment. As such, it is important that the emergency physician distinguish the different the types of tachyarrhythmias—especially in cases that do not respond to treatment with adenosine. In the pediatric patient, PJRT is a potentially life-threatening arrhythmia that requires a high index of suspicion. Clues to diagnosis include negative P waves in inferior leads, long RP interval, and 1:1 atrioventricular conduction.

Dr Fichadia is a fellow, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan. Dr Perez is a clinical instructor, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan.

Case

A 3-year-old girl presented to the ED with a 1-week history of cough and new-onset abdominal pain. She was accompanied by her grandfather, who stated that the child had been dropped-off at his house around 5:00 pm the previous day. He noted that after putting his granddaughter to bed, she awoke around 4:30 am complaining of a stomachache. After rocking her, he said she went back to sleep but did not wake up again until 1:00 pm that afternoon. Over the first few hours of awakening, she became less active and had three episodes of posttussive emesis. The grandfather denied the child had any recent nasal congestion, fever, nausea, vomiting, or diarrhea. When questioned about possible toxic ingestion, he said there were no medications in the house and that he did not witness any substance ingestion or trauma.

Regarding history, the patient was born full-term without any complications. She did not have any significant medical or surgical history. There were no documented allergies, and she was not on any medications. All of her immunizations were up-to-date. The family history was not significant for chronic diseases except for asthma in distant relatives. Her grandfather denied any recent exposures or travel.

At presentation, the patient’s vital signs were: blood pressure (BP) 86/49 mm Hg; heart rate (HR), 178 beats/minute and regular; respiratory rate (RR), 26 breaths/minute; temporal artery temperature, 104.7°F. Oxygen saturation was 99% on room air. On physical examination, she was normocephalic; there was no scleral icterus; and the throat and bilateral tympanic membranes were normal. Her extremities were warm and well perfused, with normal capillary refill. Patient’s lungs were clear, and heart sounds were normal with no detection of a murmur. The abdomen was soft and nontender; there was no evidence of organomegaly.

Laboratory evaluation included assessment of sodium, chloride, carbon dioxide, calcium, magnesium, amylase, lipase, and creatine levels; liver function test; complete blood count; and red-cell indices. All of the laboratory values were within normal limits, and urinalysis was negative for infection. Blood and urine cultures were also taken. A chest X-ray showed no acute intrathoracic process (Figure 1).

Secondary to the patient’s fever and tachycardia, the presumed diagnosis was systemic inflammatory response syndrome, and an intravenous (IV) bolus of normal saline 20 mL/kg along with ibuprofen and ondansetron were administered to treat fever and nausea, respectively. In addition, a dose of ceftriaxone was also given. The patient’s repeat set of vitals were: BP, 86/64 mm Hg; HR, 195 beats/minute; RR, 20 breaths/minute; and temporal artery temperature, 97.9°F; oxygen saturation was 98% on room air.

During treatment, the patient became increasingly fussy with new-onset abdominal distension. Repeat physical examination revealed hepatomegaly. A bedside echocardiogram showed hyperdynamic heart with fractional shortening* (FS) of 20% and ejection fraction (EF) of 43%, but no structural abnormalities. An electrocardiogram (ECG) was then ordered, which revealed narrow complex tachycardia with inverted P-waves in inferior leads.

The patient was transferred to the intensive care unit where she was started on IV milrinone for development of secondary hypotension and reduced cardiac function. Based on inverted P waves on ECG leads II, III, and aVF, three doses of adenosine (0.1 mg/kg, 0.2 mg/kg, and 0.2 mg/kg) were given, which interrupted the tachycafrdia for only a few beats. After consultation with a cardiac electrophysiologist, a diagnosis of persistent junctional reentrant tachycardia (PJRT) was reached based on the patient’s ECG features and nonresponse to adenosine. She was started on IV amiodarone (loading dose of 5 mg/kg followed by infusion of 5 mcg/kg/min), which relieved the tachycardia (Figure 3). Her vital signs stabilized and her clinical status gradually improved. After 3 days, she was discharged on oral amiodarone and close follow-up with cardiology. A repeat echocardiogram just prior to discharge showed improvement in FS to 23% and EF to 48%.

Discussion

Normal cardiac conduction involves an originating impulse from a sinus node followed by atrial muscle activation reaching the atrioventricular (AV) node. There is a necessary delay at the AV node, which is required for ventricular filling and activation of ventricles through the His-Purkinje fiber system and the bundle branches. An abnormality or interruption of this pathway results in an arrhythmia such as supraventricular tachycardia (SVT).

Supraventricular Tachycardia

Supraventricular tachycardia is the most common symptomatic abnormality in the pediatric population.¹ Among the various forms of SVT, AV reentrant tachycardia (AVRT) and AV node reentrant tachycardia (AVNRT) account for most case presentations.² Supraventricular tachycardia may be classified by duration of RP interval compared to PR interval on ECG. Short RP interval SVT includes AVNRT and AVRT through a rapidly conducting accessory path. Long RP interval SVT includes atypical AVNRT, atrial tachycardia, and PJRT.

 

Persistent Junctional Reentrant Tachycardia

Persistent junctional reentrant tachycardia is a rare form of long RP tachycardia, accounting for approximately 1% of SVT in a study review of 21 patients.³ As with the patient in this case, PJRT usually presents in early childhood.³   In a recent review of 194 patients with PJRT, 57% were infants.⁴ The condition involves an accessory pathway most commonly located in the posterior-superior septal region; conduction involves a retrograde impulse through the decremental accessory pathway.⁵ On ECG, findings include a negative P wave in inferior leads, a long RP interval, and a 1:1 AV conduction.⁶

A long-term multicenter follow-up study of 32 patients showed that rates of tachycardia vary among patients, from 100 to 250 beats/minute.⁷ Tachycardia-induced cardiomyopathy (TIC), which is secondary to the incessant nature of tachycardia, may be present in up to 30% to 50% of patients.^3,8 In a recent multicenter study, PJRT was responsible for 23% of cases of TIC.⁹ Although the exact mechanism of this property is unknown, decremental conduction and unidirectional block of the accessory pathway appear to be contributing factors.⁶

Treatment

Adenosine is the initial drug of choice for narrow complex tachycardia with stable hemodynamic status and an available intravascular access.¹⁰ In a study evaluating the effectiveness of adenosine for managing SVT in the pediatric ED setting, it was more than 70% effective in cardioverting patients presumed to have SVT.¹¹ However, in PJRT, owing to the incessant pattern, adenosine may either terminate the tachycardia (causing asystole) or, as seen in this patient, convert tachycardia to sinus rhythm for only a few seconds.¹² Reinitiation of tachycardia in sinus beat without the need for a premature complex contributes to its incessant nature.¹³

In a multicenter study looking at clinical profile and outcome for PJRT, Vaksmann et al⁸ found a greater than 80% success rate in controlling the dysrhythmia with amiodarone and verapamil. For long-term management of tachyarrhythmia, medical therapy has been recommended in early childhood compared to older children in whom catheter ablation is an effective approach.⁷ Spontaneous resolution of PJRT has been documented but is rare.¹⁴

Conclusion

Pediatric cardiac emergencies require very specific treatment. As such, it is important that the emergency physician distinguish the different the types of tachyarrhythmias—especially in cases that do not respond to treatment with adenosine. In the pediatric patient, PJRT is a potentially life-threatening arrhythmia that requires a high index of suspicion. Clues to diagnosis include negative P waves in inferior leads, long RP interval, and 1:1 atrioventricular conduction.

Dr Fichadia is a fellow, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan. Dr Perez is a clinical instructor, pediatric emergency medicine, Wayne State University, Children’s Hospital of Michigan.