Overview
Definition:
Beta-blocker overdose in adolescents refers to the ingestion of a toxic amount of beta-adrenergic blocking agents, leading to significant cardiovascular compromise
Glucagon therapy is a crucial antidote in managing severe manifestations like profound bradycardia and hypotension unresponsive to standard measures.
Epidemiology:
Beta-blocker toxicity is a common cause of drug-related emergency department visits in children and adolescents, often resulting from intentional ingestion or accidental exposure
Specific incidence in teens is difficult to pinpoint but remains a significant concern in pediatric toxicology
Risk factors include availability of medications and underlying psychological conditions.
Clinical Significance:
Beta-blocker overdose can lead to life-threatening arrhythmias, cardiogenic shock, and central nervous system depression
Prompt and effective management, including the judicious use of glucagon, is critical to improving outcomes and preventing mortality, making this topic essential for pediatricians and residents preparing for DNB and NEET SS exams.
Clinical Presentation
Symptoms:
Drowsiness
Dizziness
Nausea and vomiting
Shortness of breath
Syncope
Blurred vision
Cold and clammy skin.
Signs:
Bradycardia (heart rate < 60 bpm in infants, < 80 bpm in older children)
Hypotension (systolic BP < 50 mmHg in infants, < 70 mmHg in older children)
Altered mental status (lethargy, coma)
Wheezing or bronchospasm
Conduction abnormalities on ECG (e.g., AV block, QT prolongation)
Hypoglycemia.
Diagnostic Criteria:
Diagnosis is primarily clinical, based on a history of beta-blocker ingestion (known or suspected) and characteristic signs of cardiotoxicity
Electrocardiogram (ECG) findings consistent with beta-blocker effects, such as sinus bradycardia, AV block, or QRS widening, support the diagnosis
Exclusion of other causes of bradycardia and hypotension is also important.
Diagnostic Approach
History Taking:
Detailed history of the ingested substance (name, dose, time of ingestion)
Previous medical history, especially cardiac conditions or psychiatric disorders
Accompanying symptoms and onset
Availability of medications at home
Any co-ingestions.
Physical Examination:
Assess airway, breathing, and circulation (ABC)
Vital signs (heart rate, blood pressure, respiratory rate, oxygen saturation)
Neurological examination (GCS score, pupillary response)
Skin examination (color, temperature)
Auscultation of heart and lungs
Assess for signs of shock.
Investigations:
Electrocardiogram (ECG): essential for assessing heart rate, rhythm, and conduction system
Serial ECGs are crucial
Blood glucose level: to rule out or manage hypoglycemia
Complete blood count (CBC), electrolytes, renal and liver function tests: to assess overall metabolic status
Toxicology screen: may be helpful for co-ingestions but is often not immediately available for beta-blockers
Serum beta-blocker levels: rarely useful in acute management due to slow turnaround time and variability.
Differential Diagnosis:
Other drug overdoses (e.g., calcium channel blockers, digoxin, opioids, anticholinergics)
Vasovagal syncope
Cardiac arrhythmias of other etiologies
Electrolyte imbalances
Hypoglycemia from other causes
Sepsis.
Management
Initial Management:
Airway management, oxygenation, and circulatory support (A-B-C)
Activated charcoal (if recent ingestion and no contraindications)
Gastric lavage (rarely indicated, risk of aspiration)
Continuous cardiac monitoring and pulse oximetry
IV access.
Medical Management:
Glucagon: first-line antidote for severe bradycardia and hypotension
Administer as an IV bolus (e.g., 0.05-0.1 mg/kg, max 5-10 mg) followed by a continuous infusion (e.g., 0.05-0.1 mg/kg/hr, max 5 mg/hr)
Mechanism: stimulates adenylate cyclase, bypassing beta-adrenergic receptors
Atropine: may be tried for bradycardia but often ineffective in beta-blocker overdose due to blockade of vagal tone
Epinephrine: can be used for hypotension and bradycardia, but may exacerbate dysrhythmias
Calcium salts (e.g., calcium chloride, calcium gluconate): may be beneficial in some cases, particularly with sodium channel blockade effects
Sodium bicarbonate: indicated for QRS widening or hypotension associated with sodium channel blockade
Vasopressors (e.g., norepinephrine, dopamine): for refractory hypotension
Lipid emulsion therapy: considered for refractory cardiovascular collapse, especially if lipid-soluble beta-blockers are involved.
Surgical Management:
Generally not indicated for beta-blocker overdose itself
However, emergent procedures like transcutaneous or transvenous pacing may be required for refractory bradycardia and hemodynamic instability.
Supportive Care:
Intensive care unit (ICU) admission for continuous monitoring
Mechanical ventilation if respiratory failure occurs
Management of hypoglycemia with IV dextrose
Correction of electrolyte abnormalities
Control of seizures if present
Nursing care focused on hemodynamic stability and close observation.
Complications
Early Complications:
Refractory hypotension and bradycardia
Cardiogenic shock
Pulmonary edema
Seizures
Coma
Hypoglycemia
Bronchospasm
Cardiac arrest.
Late Complications:
Prolonged neurological deficits if hypoxia occurred
Myocardial dysfunction
Recurrent arrhythmias
Psychosocial issues related to intentional overdose.
Prevention Strategies:
Secure storage of medications away from children
Prescription of smaller quantities of beta-blockers when appropriate
Patient and family education on safe use and disposal of medications
Awareness among healthcare providers regarding the risks of beta-blocker toxicity in adolescents.
Prognosis
Factors Affecting Prognosis:
Severity of overdose (amount ingested, specific beta-blocker)
Time to initiation of appropriate therapy
Presence of co-ingestions
Underlying cardiac or medical conditions
Development of complications like shock or cardiac arrest.
Outcomes:
With prompt and aggressive management, including glucagon therapy, most adolescents can recover fully
However, severe cases can lead to significant morbidity or mortality
Survivors may require prolonged hospital stays and rehabilitation.
Follow Up:
Regular cardiology follow-up may be recommended, especially if significant cardiac abnormalities were noted during the acute phase
Psychological assessment and support are crucial for adolescents who have intentionally overdosed.
Key Points
Exam Focus:
Glucagon is the antidote of choice for severe beta-blocker toxicity causing bradycardia and hypotension
Dose: 0.05-0.1 mg/kg IV bolus, followed by infusion
Mechanism: cAMP mediated, bypasses beta-receptors
Consider atropine, epinephrine, calcium, and sodium bicarbonate for refractory cases
Lipid emulsion therapy is a salvage option
Continuous ECG and hemodynamic monitoring are paramount.
Clinical Pearls:
Remember that some beta-blockers (e.g., propranolol, metoprolol) are more lipophilic and have greater CNS penetration, potentially leading to more severe symptoms
The response to glucagon can be rapid but may be transient, necessitating a continuous infusion
Always consider and rule out co-ingestions, as they can significantly alter management
Hypotension in beta-blocker overdose is often catecholamine-resistant.
Common Mistakes:
Delaying glucagon administration in the presence of severe bradycardia and hypotension
Over-reliance on atropine, which is often ineffective
Inadequate supportive care and monitoring
Failure to consider lipid emulsion therapy in profoundly unresponsive cases
Underestimating the severity of overdose in seemingly stable patients.