You Have A New Patient!
A 53-year-old male was brought to the Emergency Department by Emergency Medical Services (EMS). The EMS team reported that his wife had called 911 after finding him in the bathroom experiencing a seizure. When paramedics arrived, the seizures had ceased, and the patient was unconscious. En route to the hospital, the EMS team did not report performing any relevant medical procedures.
Upon arrival, the patient was lethargic with a Glasgow Coma Scale (GCS) score of 8, making it impossible to obtain a clinical history. On physical examination, the patient’s respiratory rate was 10 breaths per minute, and he was slightly bradycardic with a heart rate of 52 bpm. He had a fever with a body temperature of 38.3°C, and his blood pressure was 85/50 mmHg. Oxygen saturation on room air was 94%. The pupils were normal.
On auscultation, cardiac sounds were rhythmic and stable, and lung sounds were clear and normal. Neurological examination was unremarkable, showing no evidence of nervous system disorders. Gastrointestinal auscultation revealed no abnormalities in bowel sounds. Laboratory examinations were within normal limits. The electrocardiogram (ECG) showed sinus bradycardia at 50 bpm, with a QRS duration of 122 ms and a normal QTc interval.
The patient’s wife and son later arrived at the hospital and reported his current medications, which included propranolol, benazepril, and as-needed use of metoclopramide and alprazolam.
What Do You Need To Know?
Importance
Beta-adrenergic blocking agents, more commonly known as Beta-Blockers (BBs), are a class of medications used to treat various heart-related conditions, such as arrhythmias, heart failure, and angina. They are also used to prevent and manage symptoms in individuals suffering from migraines and tremors. The first BBs were developed in the early 1960s, and today there are over twenty different BB molecules and numerous commercial formulations available.
It is crucial to recognize, identify, and treat Beta-Blocker intoxication for at least three key reasons:
Widespread Use: BBs are one of the most commonly prescribed classes of drugs in the United States. According to Definitive Healthcare Claims, 20 million people (accounting for 6% of the population) were using BBs in 2022 [1]. Consequently, many individuals are at risk of poisoning, which can lead to severe consequences.
Pediatric Risks: Approximately 30% of cases of pediatric acute intoxications are caused by cardioactive drugs (e.g., BBs, ACE inhibitors, calcium-channel blockers), with a mortality rate ranging between 0.1% and 0.3%. These incidents account for about 7% of emergency pediatric hospitalizations [2]. Such acute intoxications often result from accidental poisoning, as BBs are frequently used by adult family members and may be readily available at home.
Complex Clinical Presentation: Beta-Blocker Intoxication (BBI) can present a challenging and complex situation for clinicians. It often manifests with mixed signs and symptoms that may mimic disorders of the central nervous system or the cardiocirculatory system. This complexity arises from the multiple physiological effects of BBs, which influence critical cardiac, respiratory, and metabolic mechanisms by acting on myocardial cells, vascular endothelial cells, and smooth muscle cells.
Epidemiology
According to the 2021 Annual Report of the National Poison Data System, which analyzed cases of exposure to BBs alone (i.e., not in combination with other drugs), 10,832 cases were reported in the United States in 2021. Among these, 4,268 cases required treatment in healthcare facilities [3].
Unintentional exposure accounted for approximately 78% of all reported cases in 2021 (see Table 1), while intentional poisoning cases represented approximately 18%.
Table 1. Number of Single Exposures Analyzed by Reasons for Exposure [3,4]
Year | No. of Single Exposures | Reason | |||
Unintentional | Intentional | Other | Adverse Drug Reaction | ||
2020 | 10,994 | 8,761 | 1,888 | 3 | 253 |
2021 | 10,832 | 8,482 | 1,978 | 3 | 266 |
With regard to outcomes, no severe consequences were recorded in 32.3% of all cases in 2021. BBI-related deaths accounted for 0.17% of cases in 2021 (see Table 2).
Table 2. Outcomes of Beta-Blocker Intoxication Cases in 2021 [3,4]
Year | No. of Single Exposures | Outcome | ||||
None | Minor | Moderate | Major | Death | ||
2020 | 10,994 | 3,692 | 738 | 954 | 167 | 18 |
2021 | 10,832 | 3,508 | 731 | 1,094 | 144 | 18 |
Among all BBs, propranolol is the medication most frequently associated with cases of BB toxicity and is the most commonly used in suicide attempts worldwide [5].
Pathophysiology
BB generally have three main effects: 1) a negative inotropic effect through beta-adrenergic receptor blockade; 2) a lusitropic effect (i.e., increasing the rate of myocardial relaxation); and 3) a negative chronotropic effect. BB can be categorized based on various properties or characteristics. For example, BB can be classified into two broad categories—selective and non-selective—depending on whether they specifically block beta-receptors (see Table 3).
Metoprolol, atenolol, bisoprolol, and nebivolol are examples of selective BB, meaning they primarily exert their effects on the heart muscle. In contrast, propranolol, nadolol, and sotalol are examples of non-selective BB. These non-selective BB not only affect the cardiocirculatory system but also have a significant impact on the smooth muscle of the bronchi, causing bronchoconstriction and vasoconstriction. Notably, receptor selectivity diminishes as BB concentrations increase. In other words, selectivity progressively declines as the BB concentration in the bloodstream rises.
Table 3. Beta-Blockers Classification
Pharmacological classification |
Selectivity properties | Selective β receptors.
|
Non-selective β receptors.
| ||
Haemodynamic consequences | Vasodilatation effect | |
Non-dilatation effect | ||
Receptor interaction classification | α1-receptor | α1-receptor antagonism (arteriolar vasodilation). |
β receptor
| Selectivity for β receptors. | |
Non-selectivity for β receptors | ||
Intrinsic sympathomimetic activity | possibility of both agonism and antagonism effects | |
Lipophilicity | Lipophilic: High – Intermediate – Low lipophilicity | |
Lipophobic | ||
BB have varying half-lives, ranging from several minutes to several hours. For this reason, symptoms of BBIs caused by different BBs can have different times of onset. Signs and symptoms of toxicity typically appear within 6 hours of medication intake. However, if the beta-blocker is formulated as a slow-release molecule, symptom onset can be delayed by up to 12 hours.
With regard to BB cardiovascular toxicity, the following effects are most significant:
- Sinus node activity impairment, leading to sinus bradycardia or sinus arrest;
- Atrioventricular node activity impairment, leading to atrioventricular block;
- Peripheral vasodilation, resulting in systemic hypotension;
- QT prolongation, which may lead to torsades de pointes (particularly with sotalol and acebutol).
Hypotension and bradycardia can reduce myocardial contraction and oxygen consumption, resulting in tachypnea and hyperventilation that may further compromise hemodynamic stability. BBs like acebutol exhibit intrinsic sympathomimetic activity (ISA, see Table 3), which may result in a lesser effect on heart rate.
BBI can also present with central nervous system (CNS)-specific symptoms, as highly lipophilic BBs can cross the blood-brain barrier. This mechanism may lead to CNS effects such as delirium, seizures, CNS depression, and coma. Propranolol has the highest lipophilic index among BBs [6]. Furthermore, at very high doses, BBs may block sodium channels, stabilizing membrane fluidity and exacerbating toxicity with manifestations such as seizures, coma, and QRS widening.
BBs may also cause metabolic disturbances. A mild hypokalemia may be observed, and hypoglycemia can occur due to BB-mediated inhibition of glycogenolysis and gluconeogenesis [5].
Medical History [7,8]
In cases of BBI, obtaining a comprehensive medical history may sometimes be challenging due to the patient’s altered state of consciousness. For this reason, or to confirm the information collected, it may be necessary to consult witnesses, family members, EMS personnel, or analyze medical records and the patient’s personal belongings [7].
The following information should be collected whenever possible:
- Type of substance: It is recommended to identify the exact beta-blocker involved to better manage the emergency, given the wide range of molecules and reactions.
- Quantity of substance: Determining the amount of beta-blocker administered is crucial for understanding or predicting the severity of toxicity.
- Drug formulation: Identify whether the drug is slow-release, extended-release, or immediate-release.
- Time of intake: Assess how much time has passed since the first administration and the onset of symptoms.
- Route of administration: Determine how the substance was administered (e.g., oral, intravenous).
- Number of people involved (if applicable).
Whenever possible, practitioners should also gather a detailed medical history, including:
- Allergies;
- Previous surgeries;
- Known diseases;
- Previous hospitalizations;
- Current and previous medications;
- Patient’s personal and family history of illnesses (e.g., intentional BB intake or previous suicide attempts);
- Use of drugs, tobacco, or alcohol;
- Last meal.
BBI Symptoms
Pulmonary System: Symptoms involving the pulmonary system in cases of BBI may include breathing difficulties such as dyspnea and gasping. These manifestations can indicate significant respiratory compromise and should be promptly addressed.
Cardiovascular System: Cardiovascular symptoms often include chest pain, faintness (typically resulting from hypotension and bradycardia), dizziness, and fatigue. These signs highlight the impact of BBIs on the heart and circulatory system and may signify underlying hemodynamic instability.
Central Nervous System: The central nervous system is frequently affected in BBI, with symptoms such as weakness, agitation, diaphoresis, drowsiness, confusion, and fever. These presentations underscore the potential for CNS-specific involvement, particularly in highly lipophilic BBs capable of crossing the blood-brain barrier.
Gastrointestinal System: Gastrointestinal symptoms commonly observed in BBI include an “upset” stomach, abdominal pain, and nausea. These manifestations may arise as a secondary consequence of systemic effects or direct drug toxicity.
Sensory System: Sensory system involvement in BBI can present as blurred vision or double vision. These symptoms may accompany more generalized CNS toxicity and reflect impaired sensory processing.
BBI Red Flags
Concurrent Intake of Cardioactive Medications: One significant red flag in cases of BBI is the concurrent intake of other cardioactive medications, such as ACE inhibitors or calcium-channel blockers. The combination of these drugs with BBs can amplify their cardiovascular effects, increasing the risk of severe hypotension, bradycardia, and other toxic effects.
Concurrent Intake of Other Medications: Another important consideration is the simultaneous use of other medications, such as benzodiazepines. The interaction between BBs and these drugs can enhance CNS depression, leading to symptoms such as drowsiness, confusion, or even coma in severe cases.
Comorbidities or Medical Conditions: Certain comorbidities or medical conditions for which BB intake is contraindicated also represent critical red flags. Conditions such as asthma, liver failure, kidney failure, or bradyarrhythmia can exacerbate the severity of BBI, as BBs may worsen bronchoconstriction, impair organ function, or exacerbate existing cardiovascular instability.
Physical Examination
During a physical examination (PE) of a patient with a potential BBI, the following key features should be assessed:
Neurological Signs: Neurological signs arise from the drug’s effects on the CNS and impaired brain perfusion. Mental status during BBI correlates directly with the severity of intoxication. Patients may present with weakness, drowsiness, agitation, or confusion. Levels of consciousness can range from alert and agitated to unconsciousness. Additionally, pupil mydriasis may be observed, particularly following a seizure episode.
Thoracic Assessment: Examination of the thoracic region may reveal an increased respiratory rate due to sympathomimetic effects. Conversely, a decreased respiratory rate may result from lethargy or a pre-coma phase. Lung auscultation in patients without asthma or other pulmonary conditions is typically normal, with regular breath sounds. However, findings may vary depending on the patient’s level of consciousness, airway patency, and respiratory effort. Observing the use of chest and neck accessory muscles can provide critical information about respiratory distress and dyspnea. Wheezing may occur as a clinical indicator of bronchospasm.
Cardiovascular Assessment: Cardiovascular findings may vary widely. Patients may present with tachycardia (e.g., as a compensatory response to hypotension) or bradycardia in more advanced stages of intoxication. A weak pulse can indicate shock, and blood pressure is often low. Heart sounds may be arrhythmic. Capillary refill time should be evaluated to assess perfusion status, providing insight into the body’s acute response to poisoning.
Gastrointestinal Assessment: Gastrointestinal auscultation may reveal either increased bowel sounds due to sympathomimetic effects or decreased motility as a consequence of low-level intoxication. Given that BBs are metabolized in the liver and/or kidneys, liver or kidney failure may occur, especially in patients with pre-existing hepatic or renal disease.
Body Inspection: Physical examination may reveal skin color changes indicative of perfusion or metabolic failure, such as cyanosis, jaundice, or other signs of kidney or liver dysfunction. Additional findings may include diaphoresis and pallor as markers of shock, as well as mucosal dryness and fever.
Alternative Diagnoses
In BBI, a detailed clinical history and accurate examination, along with diagnostic tests, can help identify the toxic agent [6,7]. However, alternative diagnoses may present with features similar to those of BBI.
Differential Toxicological Diagnoses:
- Digoxin Intoxication: Patients with digoxin intoxication often exhibit more severe arrhythmias (due to AV node blockage) and gastrointestinal symptoms. Renal failure or electrolyte imbalances are more frequent than in BBI.
- Calcium Channel Blockers Intoxication: These patients typically present with more severe hypotension.
- α2 Agonist Intoxication: Patients may develop CNS depression earlier and often present with miosis and hyporeflexia.
- Organophosphate Poisoning: This condition is characterized by increased salivation and tear production, along with tremors.
- Antidepressant Intoxication: Vision problems, confusion, drowsiness, and high blood pressure are more distinguishing features.
- Cocaine Toxicity: Patients more frequently present with agitation, confusion, tachycardia, dysrhythmia, and hypertension.
- Carbamazepine Intoxication: This condition is associated with ataxia, epileptic seizures, and respiratory arrest.
- Cardiac Glycoside Plant Poisoning: Patients often present with hyperkalemia, renal failure, or ventricular arrhythmia.
Differential Non-Toxicological Diagnoses:
- Neurological Conditions: Other conditions presenting with lethargy or unconsciousness (e.g., emergency epidural hematoma, meningitis) should be considered.
- Metabolic Conditions: Conditions leading to major arrhythmias, such as severe hyperkalemia, must also be ruled out.
Acing Diagnostic Testing
Bedside Tests
- Multiparameter Monitoring: Continuous monitoring of vital parameters such as blood pressure, heart rate, respiratory rate, oxygen blood saturation, and body temperature is essential.
- Blood Glucose Level: Blood glucose measurement is crucial to identify hypoglycemia, a potential consequence of beta-blocker toxicity.
- ECG: A 12-lead ECG is generally recommended in addition to continuous cardiac monitoring. It is important to note that many BBs can block sodium or potassium channels, leading to QRS widening and QTc prolongation. These effects can persist for hours to days, depending on the specific BB involved. Sotalol, in particular, is commonly associated with QTc prolongation. This clinical scenario requires careful medical evaluation, close observation, and the discontinuation of other drugs that may contribute to QTc prolongation.
- Arterial Blood Gases Test (ABG): ABG testing is necessary to assess acid-base balance and oxygenation, which may be affected in cases of severe toxicity.
Laboratory Tests
Laboratory tests are essential for identifying comorbidities and metabolic complications. These include:
- Serum Electrolytes: To assess for imbalances that may arise from beta-blocker intoxication or underlying conditions.
- Complete Blood Count (CBC): To evaluate overall health and detect signs of infection or other hematologic abnormalities.
- Liver Function Tests: Particularly important for patients with a history of liver failure, as beta-blockers are metabolized in the liver.
- Pregnancy Test: To rule out pregnancy in women of childbearing age, as pregnancy may influence treatment decisions.
- Blood Alcohol Level: To check for concurrent alcohol use, which may exacerbate beta-blocker toxicity.
- Plasma Dosage Concentration: Rarely available in the Emergency Department or during emergencies, and generally not recommended since it does not typically alter patient management [6].
- Toxicologic Screening Tests on Blood and Urine: These tests are not always conclusive for evaluation. False positives or false negatives may mislead clinical decision-making and are not predictive of patient outcomes.
Imaging
Chest X-Ray: A chest X-ray is particularly useful for patients with asthma or other pulmonary diseases to rule out complications following the acute phase of poisoning.
Risk Stratification
The main risk factors for a worse outcome in BBI can be investigated through medical history, physical examination, and laboratory tests.
Risk Factors in Medical History
Co-ingestion of Other Medications: Many drugs potentiate beta-blocker toxicity, exacerbate acute symptoms, mask clinical signs or laboratory abnormalities, and complicate stabilization. It is essential to determine whether the patient has taken other medications to administer an appropriate antagonist. Specific co-ingested medications to consider include:
- Other antihypertensive drugs (e.g., diuretics, ACE inhibitors, calcium channel blockers);
- Medications for chronic arrhythmia, such as amiodarone or flecainide;
- Drugs that indirectly lower blood pressure (e.g., nitrates, muscle relaxants);
- Medications for asthma or chronic obstructive pulmonary disease (COPD);
- Diabetes medications, especially insulin;
- Allergy medications, including ephedrine, noradrenaline, or adrenaline;
- Non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen.
- Particular attention should be given to psychotropic drugs like tricyclic antidepressants and antipsychotics, as these pose significant risks when combined with beta-blockers.
Pre-existing Diseases: Cardiovascular and pulmonary conditions (e.g., heart failure, valve defects, asthma, COPD) can rapidly deteriorate in time-sensitive, critical situations, leading to worse outcomes for patients.
Other Medical Conditions Incompatible with Beta-Blocker Use:
- Allergy to beta-blockers;
- Pre-existing low blood pressure or conditions that compromise cardiac rhythm;
- Metabolic acidosis.
Risk Factors in Physical Examination
The earlier the onset of severe signs and symptoms, the greater the likelihood of a worse outcome. Key indicators include:
- Unconsciousness or coma;
- Severe dyspnea;
- Arrhythmias;
- Severe hypotension and/or signs of shock.
Risk Factors Identified in Diagnostic Tests
Laboratory and diagnostic tests indicating organ failure or worsening vital parameters are critical markers for a poor prognosis.
Diagnostic Tests
Diagnostic tests that reveal signs of organ failure or worsening vital parameters are critical indicators of a poor prognosis.
Management
Initial Management
Since BBs do not have any specific antidote or antagonist, the primary aim of management is to reduce the effects of BBI and its consequences.
Management Options in Unstable Patients [6,7]
Following an ABCDE approach, the management of BBI in unstable patients focuses on maintaining the perfusion of vital organs by increasing heart rate and myocardial contractility.
Airway
- CNS depression may occur, making early airway management critical to maintaining airway patency. Blood glucose measurements are necessary for patients with altered mental status.
- In children, intubation may provoke additive bradycardia due to vagal stimulation during laryngeal manipulation. The use of atropine may be necessary to prevent this.
Breathing
- Supplemental oxygen and inhaled bronchodilators can help manage BBI-related pulmonary complications, such as bronchospasm.
Circulation
- Ensure venous access and initiate multiparametric monitoring, including blood pressure (BP), heart rate (HR), respiratory rate (RR), oxygen saturation (FiO2), body temperature, and ECG.
- In cases of hypotension, fluid resuscitation with crystalloids should be considered.
- Ventricular arrhythmias and other cardiac resuscitation issues must be addressed according to Advanced Cardiac Life Support (ACLS) protocols.
Disabilities
- For seizures caused by intoxication, benzodiazepines are the first-line medication treatment.
Exposure
- No specific exposure protocols are recommended for BBI.
Medications [6,7]
If patients present to the Emergency Department at an early stage following substantial BB intake and/or exhibit severe symptoms, gastrointestinal decontamination is recommended. This may include gastric lavage, administration of activated charcoal, and/or bowel irrigation.
Contraindications for Gastric Lavage:
- Unprotected airways;
- Concurrent ingestion of caustic substances or hydrocarbons;
- Tablets or pills too large to pass through the probe’s suction holes.
Multiple doses of activated charcoal, hemoperfusion, and hemodialysis may be beneficial for BBs that are water-soluble or excreted primarily through kidney metabolism.
Table 4. Medications for Gastrointestinal Decontamination
Drug name | Function / Effect | Dose | Frequency | Cautions |
Activated Charcoal | substance absorption in GI system | 1g/kg | one-off |
|
Polyethylene glycol | Bowel irrigation | Adult: 1,5-2,0 L/h, Children 6-12 y.o. : 1,0-1,5 L/h, Infants <6 y.o.: 0,5 L/h | one-off |
|
Glucagon is one of the most commonly used medications for intoxication due to its chronotropic and inotropic effects. While no comprehensive studies or trials conclusively prove glucagon’s efficacy in management, its use has been empirically validated in BBI management protocols over the years for its demonstrated usefulness.
Table 5. Glucagon Therapy for Cardiac Stabilization
Function / Effect | Protocol / Doses | Cautions / Comments |
Heart rhythm and contraction stabilization | Bolus: 3-5 mg IV [0,05 mg/kg] Continuous Administration: 1-10 mg/h | Side effects: hypocalcemia, hyperglycemia and vomiting. |
High-dose insulin therapy has also been reported to be effective in counteracting the negative inotropic effects of beta blockers. The complete therapeutic treatment for euglycemia in BBI is described below. Serum potassium and glucose levels should be checked immediately.
Table 6. Euglycemia Therapy
Function / Effect | Protocol / Doses | Cautions / Comments |
Therapy in case of BBI-induced hypoglycemia |
|
|
Vasopressors should be considered when hypotension proves refractory to fluid administration. The clinical picture, medical history, and physical examination are crucial in guiding the selection of an appropriate vasopressor.
Table 7. BP and HR Increase
Drug name | Function / Effect | Dose | Frequency | Cautions |
Calcium gluconate/ Calcium chloride | BP increase and stabilization | 10 ml at 10%, 0,15 ml/kg | one-off |
|
Atropine | Increase of heart rate | 0,5-1 mg IV (0,02 mg/kg, total dose not inferior at a 0,1 mg) | one-off |
|
Lipid emulsion therapy has emerged as a promising treatment modality for BB toxicity, particularly in cases of severe cardiovascular compromise [8]. The underlying mechanism is thought to involve the “lipid sink” effect, where the lipid emulsion binds to lipophilic drugs, reducing their bioavailability and facilitating their elimination from the body. Clinical evidence suggests that intravenous lipid emulsions can improve hemodynamic stability and restore cardiac function in patients experiencing life-threatening beta blocker overdose [9,10]. A systematic review highlighted the positive outcomes associated with lipid emulsion therapy in various cases of drug toxicity, including beta blockers, emphasizing its role as an adjunctive treatment [11]. However, while lipid emulsion therapy shows promise, it is essential to consider it as part of a comprehensive treatment approach, including standard resuscitation measures and specific antidotes when available [12].
Propranolol and other BB toxic effects are associated with QRS widening. Early recognition of QRS widening and QTc interval prolongation is critical. This should be followed by the administration of sodium bicarbonate for QRS widening and magnesium sulfate for QTc prolongation.
In cases of refractory bradycardia, cardiac pacing should be considered.
Severe poisoning cases may require external mechanical life support, such as extracorporeal membrane oxygenation (ECMO), which may be necessary until the xenobiotic effect subsides.
Special Patient Groups
With regard to age groups exposed to BB, data analysis shows a peak in early childhood (≤5 years old), accounting for 22.6% of total single exposure cases in 2021 (see Table 8) [3]. The largest age group exposed comprises individuals aged 20 years and older, representing 63.5% of exposures.
In younger age groups, exposures are more often unintentional. Among the 13–19 age group, exposures are frequently associated with suicide attempts. In individuals over 20 years of age, the intentionality of exposure varies significantly due to numerous contributing factors.
Table 8. Number of Single Exposures Analyzed by Age of Exposure [3,4]
Year | No. of Single Exposures | Age* | |||
< =5 | 6-12 | 13-19 | > =20 | ||
2020 | 10,994 | 2,524 | 314 | 534 | 7,100 |
2021 | 10,832 | 2,452 | 355 | 611 | 6,894 |
*2020 – Unknown child: 3 /Unknown adult: 473 / Unknown age: 46 *2021 – Unknown child: 0 /Unknown adult: 473 / Unknown age: 47 | |||||
Pediatrics
Pediatric patients have a lower tolerance threshold to beta-blockers due to underdeveloped cardiovascular homeostasis mechanisms. Although various studies have been conducted on infants and children, no comprehensive literature exists, leaving the risk of toxicity from beta-blocking drugs uncertain. Consequently, toddler exposure to BB remains undefined in terms of specific risk factors and criteria.
The most common scenario involves the ingestion of a few tablets. In children without concurrent risk factors, the likelihood of mortality or significant morbidity can generally be ruled out [13-15].
Pregnant Patients
During pregnancy, BB are among the most commonly prescribed medications, particularly labetalol and metoprolol, for treating hypertension and other cardiac conditions. Data indicate no toxicity consequences for the mother or fetus when used at prescribed dosages.
During breastfeeding, low levels of BB may be present in the mother’s milk. Therefore, it is recommended to monitor the baby for any changes in behavior or symptoms [16-18].
Geriatrics
In the elderly, BB toxicity may be exacerbated by interactions with other medications (e.g., antihypertensives, benzodiazepines). Additionally, organ system failure (e.g., kidney and liver failure) and CNS-related symptoms tend to be more pronounced in this population [19,20].
When To Admit This Patient
In BBI, the criteria for deciding whether to admit a patient are as follows [6,7]:
- Observation for Immediate-Release BBs: Stable patients with intoxication from rapid- or immediate-release BBs should be kept under observation for at least 6 hours.
- Observation for Extended-Release BBs: Patients with extended-release or modified-release BB intoxication require longer observation. The situation is considered safe when no signs or symptoms are evident, depending on the specific half-life of the BB.
- Post-Invasive Procedures: Patients who have undergone invasive life-saving procedures must remain under observation.
- Clinical Instability: Patients presenting with clinically unstable parameters, such as bradycardia, hypotension, heart conduction abnormalities, or mental status alterations, should be admitted to the ICU.
- Intentional Intake: Patients suspected of or confirmed to have intentionally ingested BBs, regardless of the severity of intoxication, must not be discharged before undergoing a psychiatric evaluation.
In all cases, consultation with a Poison Control Center or a Toxicology Specialist should be considered.
Discharge Criteria
Before discharge, a thorough re-evaluation of physical symptoms, clinical signs, and vital parameters is mandatory. If necessary, diagnostic tests should be repeated prior to discharge.
If the patient is deemed suitable for discharge:
- Ensure the patient understands all medical advice related to their condition following the intoxication episode, including self-care measures, follow-up checkups, and, if applicable, continuation of medical therapies.
- Provide guidance on reducing BB risk factors.
- Educate the patient on the symptoms and signs of BB poisoning or overdose to facilitate early recognition in the future.
Whenever possible, establish direct communication with the patient’s family doctor to coordinate follow-up care.
Special Considerations
- In pediatric intoxications, involving social workers may be appropriate.
- For non-self-sufficient patients or minors, ensure that family members, caregivers, or legal guardians fully understand the medical advice provided.
Revisiting Your Patient
A 53-year-old male was brought to the emergency room by EMS. The EMS team reported that his wife had called 911 after finding him in the bathroom experiencing a seizure. When paramedics arrived, the seizures had stopped, and the patient was unconscious. On the way to the hospital, the EMS team did not report performing any relevant medical procedures.
The patient was lethargic upon arrival with a Glasgow Coma Scale (GCS) score of 8, making it impossible to obtain a clinical history. On physical examination, the patient’s respiratory rate was 10 breaths per minute, and he was slightly bradycardic with a heart rate of 52 bpm. He had a fever with a stable body temperature of 38.3°C, and his blood pressure was 85/50 mmHg. Oxygen saturation on room air was 94%. Pupils were normal. On auscultation, cardiac sounds were rhythmic and stable, and lung sounds were clear and normal. Neurological examination revealed no nervous system abnormalities, and gastrointestinal auscultation showed no altered bowel sounds. Laboratory results were within normal limits. The ECG showed sinus bradycardia at 50 bpm, with a QRS duration of 122 ms and a normal QTc interval.
His wife and son arrived at the hospital and reported that he was taking propranolol, benazepril, and, as needed, metoclopramide and alprazolam. The family brought the drug boxes to the hospital, and it was noted that the propranolol box was almost empty. His son mentioned that the medication had been purchased the day before.
Management and Treatment
The approach began with airway management, followed by preventive therapy with naloxone, glucose, and thiamine. Since the family reported alprazolam use, flumazenil therapy was administered to rule out worsening of possible benzodiazepine intoxication. Intravenous (IV) fluids were provided to address hypotension. Blood glucose levels were normal. The patient did not respond to the initial treatment.
Based on the medical history, physical examination, and clinical presentation, a BBI management protocol was initiated. Glucagon (3 mg IV) and dopamine (5 mcg/min IV) were administered, along with activated charcoal to reduce bowel absorption. Following this, the patient began responding to the treatment. Blood pressure increased to 110/70 mmHg, the ECG showed a sinus rhythm at 86 bpm, and the QRS duration narrowed to 90 ms. Oxygen saturation improved to 98% on room air. Glucagon infusion was continued at 1–10 mg/h.
The patient was transferred to the acute observation room. After one hour, he was conscious, breathing spontaneously, and his vital parameters were stable. Since the propranolol formulation was immediate-release, observation lasted 8 hours.
Discharge and Follow-Up
After the observation period, nephrology and psychiatry consultations were requested to ensure a safe discharge. Repeat physical examination and laboratory tests confirmed stability, and the patient was safely discharged into his family’s care.
Authors
Alessandro Lamberti-Castronuovo
Alessandro Lamberti-Castronuovo is a physician with over 15 years of clinical experience specialized in emergency and internal medicine, with further work in cardiology and diagnostic ultrasound. He is an Emergency Medicine Consultant at the Emergency Department of the Sant’Andrea Hospital in Vercelli Italy, where he is in charge both of the training of resident doctors and of the Hospital Major Incident Planning. Alessandro is also a global health researcher focusing on issues surrounding access to care, and an advocate for ensuring health delivery to vulnerable populations. His main focus of interest is strengthening health systems in order to improve access to care, essentially by building integrated and people-centred health systems based on principles of equity and social justice through a primary health care approach. His projects focus on 1) strengthening access to primary care and continuity of care for vulnerable populations and 2) strengthening emergency department's surge capacity, ultimately bolstering the integration of all health actors in a so-called "whole-of-health-system" approach. After completing his MSc in International Health at the Charité University in Berlin with a thesis project on community health workers in refugee camps, he joined CRIMEDIM (Center for Research and Training in Disaster Medicine, Humanitarian Aid and Global Health) where he is currently pursuing a joint PhD in global health, humanitarian aid and disaster medicine at the University of Eastern Piedmont and University of Bruxelles. His research work focuses on integrating primary care into the health emergency and disaster risk management and on enhancing the preparedness for disasters of whole communities especially the most marginalized parts.
Filippo Pedretti Magli
Filippo Pedretti Magli is a medical student at University of Ferrara. He is also an emergency medical technician, serving in pre-hospital ambulances for emergency medical service. Filippo is a university medical student’s trainer in the field of Disaster Medicine for CRIMEDIM. He recently took part as co-teacher in Infectious risk-management master program for doctors and nurses in Parma, focusing on the analysis with disaster medicine criteria of data about Covid-19 impact on primary health care and health system. He deepened his medical education with several training sessions and courses in the emergency department, achieving certificates in E-FAST ultrasonographic protocol and advanced difficult intubation and intraosseous access procedures.
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References
- Definitive Healthcare. Beta-blocker prescription patterns. Definitive Healthcare Blog. Published March 23, 2022. Accessed December 25, 2024. https://www.definitivehc.com/blog/beta-blocker-prescription-patterns.
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Reviewed and Edited By
Arif Alper Cevik, MD, FEMAT, FIFEM
Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.
