Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression.The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital.There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation. [2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents.Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression.The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital.There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation.[2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents.Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression. The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital.There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation.[2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents.Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression.The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital.There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation.[2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents.Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression.The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital. There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation.[2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents. Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression.The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital.There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation. [2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents.Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression.The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital.There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation.[2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents.Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression. The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital.There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation.[2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents.Rationale: Digoxin is a frequently prescribed medication for the management of both acute and chronic cardiac insufficiency. The overdose ingestion of digoxin can result in a range of arrhythmias, with severe cases potentially leading to malignant arrhythmias and fatal outcomes. To date, there is a lack of documented cases related to acute digoxin intoxication resulting from the administration of massive digoxin overdose in the short term.A 37-year-old female patient was admitted to the emergency department following a suicide attempt involving the administration of 330 tablets of digoxin (each tablet containing 0.25 mg). The patient exhibited symptoms of confusion, nausea, and vomiting for around 30 minutes. The patient had a history of depression.The patient was diagnosed with digoxin intoxication.The patient underwent many medical interventions including stomach lavage, administration of laxatives, correction of cardiac arrhythmias, provision of myocardial nutrition, diuresis, correction of acid-base balance, and management of electrolyte disturbances, among others.Following a treatment of 9 days, the patient exhibited no signs of discomfort, maintained consciousness, and the serum concentration of digoxin was indeterminable. Upon reevaluation of the electrocardiogram, it was determined that no arrhythmia was present. Consequently, the patient was authorized to be discharged from the hospital.There is currently no documented evidence of cases involving a significant overdose of digoxin resulting in intoxication. The patient had a comprehensive treatment regimen consisting of stomach lavage, administration of a laxative, correction of cardiac arrhythmias, provision of myocardial nutrition, fluid replacement, diuresis, and supportive therapy, resulting in successful outcomes.There have been no known cases of intoxication resulting from a significant overdose of digoxin, specifically with the consumption of 330 tablets (0.25 mg/tablet). However, in the event of ingesting excessive amounts of digoxin, it is imperative to promptly administer stomach lavage, administration of a laxative, and arrhythmia correction. The administration of temporary pacemaker therapy is recommended for patients presenting with high atrioventricular block, whereas hemoperfusion is advised for patients with renal insufficiency as a means to eliminate digoxin from the body.Digoxin, a well-established pharmacological drug with cardiotonic properties, has a historical origin in the 18th century when it was initially employed by William Withering for the management of patients presenting with edema. Currently, digoxin is widely employed as a drug in the clinical management of chronic heart failure. Digoxin primarily acts as an inhibitor of the Na+-K+-ATPase enzyme located on the myocardial cell membrane. This mechanism of action leads to an augmentation of myocardial contractility, resulting in an elevation of the left ventricular ejection fraction in patients suffering from heart failure. Additionally, it contributes to a reduction in pulmonary capillary wedge pressure.[1] Digoxin, on the one hand, has the ability to enhance vagal tone through the inhibition of Na+-K+-ATPase in the afferent nerve fibers of the vagus nerve. This action leads to a reduction in the automaticity of the sinoatrial node, a decrease in the conduction velocity of the atrioventricular node, and an extension of the effective refractory period. Consequently, the ventricular rate is slowed down in cases of atrial flutter and atrial fibrillation.[2,3] On the other hand, it has the potential to reduce the duration of the atrial refractory period, accelerate the atrial rate, and enhance occult conduction, hence resulting in a deceleration of the ventricular rate.[4] Therefore, digoxin is used in the treatment of heart failure through its positive inotropic effect and reducing the activity of the neuroendocrine system. However, it is worth noting that the therapeutic range of digoxin is characterized by a limited margin, as the therapeutic dosage closely approaches the toxic dosage. Furthermore, numerous factors exert an influence on this range, hence contributing to the occurrence of digoxin intoxication in clinics on an intermittent basis.Digoxin intoxication frequently occurs during the treatment of chronic heart failure. The toxic threshold for digoxin concentration is commonly observed to range between 1.5 and 2.0 ng/mL. Although acute digoxin intoxication cases have been reported, acute digoxin intoxication resulting from an extremely high dose of digoxin (e.g., 330 tablets, each containing 0.25 mg) have not been reported in the literature. In this study, we report the diagnosis and treatment of a massive digoxin overdose intoxication case (330 tablets, each containing 0.25 mg), which will provide valuable guidance to doctors in effectively managing patients presenting with similar intoxication incidents.