Caffeine (1,3,7-trimethylxanthine; see the image below) is the most widely consumed stimulant drug in the world.[1] It is present in a variety of forms: medications, coffee, tea, soft drinks, and chocolate. Because caffeine overdoses, intentional or unintentional, are relatively common in the United States, physicians and other medical personnel must be aware of caffeine toxicity to recognize and treat it appropriately.
View Image
Chemical structure of caffeine.
Signs and symptoms
When acute caffeine ingestion is suspected, the history should address the following:
Use of prescription medications or over-the-counter (OTC) drugs
Use of illicit drugs
Recent caffeine ingestion or recent behavior compatible with such ingestion
When ingested in excessive amounts for extended periods, caffeine produces a specific toxidrome (caffeinism), which consists primarily of the following features:
Central nervous system (CNS) – Headache, lightheadedness, anxiety, agitation, tremulousness, perioral and extremity tingling, confusion, psychosis, seizures
Cardiovascular – Palpitations or racing heart rate, chest pain
CNS findings on physical examination include the following:
Anxiety, agitation
Tremors
Seizures
Altered mental status
Head, eyes, ears, nose, and throat findings
Pupils that are dilated but reactive to light
The thyroid should be examined because thyrotoxicosis may mimic caffeine toxicity.
Cardiovascular findings on physical examination include the following:
Widened pulse pressure
Sinus tachycardia, dysrhythmias
Hypotension
Tachypnea
GI findings on physical examination include the following:
Vomiting
Abdominal cramping
Hyperactive bowel sounds
See Presentation for more detail.
Diagnosis
In hemodynamically stable patients with mild symptoms and a clear history of caffeine ingestion, no laboratory studies are indicated. Laboratory studies are indicated in patients with moderate-to-severe symptoms of caffeine toxicity. The following studies may be helpful:
Complete blood count (CBC)
Serum electrolyte, glucose, blood urea nitrogen (BUN), and creatinine concentrations
Routine screening for other potentially treatable toxins
Total creatine kinase (CK) concentrations
Dipstick urinalysis
Rapid urine drug screen
Serum ethanol concentrations and osmolality (in cases of unknown ingestion or suspected coingestion)
Serum pregnancy test
Thyroid studies
Arterial blood gas analysis
Serum caffeine concentration determinations do not influence management.
In hemodynamically stable patients with only mild symptoms, no diagnostic imaging is required. The following studies may be considered in particular circumstances:
Chest radiograph – In patients with chest pain, fever, altered mental status, or respiratory complaints
Unenhanced computed tomography (CT) of the head – In patients with seizures or altered mental status despite initial resuscitation
Patients with chest pain, palpitations, tachycardia, or an irregular heart rhythm should be evaluated with electrocardiography (ECG) and telemetry monitoring.
See Workup for more detail.
Management
Prehospital care is primarily supportive, and most cases resolve. Emergency management of more severe cases includes the following:
ABCs (Airway, Breathing, Circulation)
Management of hypotension
Correction of dysrhythmias
Management of seizures (with benzodiazepines or barbiturates)
Correction of metabolic disturbances (hypokalemia, rhabdomyolysis, hyperglycemia, metabolic acidosis)
Treatment of prolonged vomiting
Decontamination with activated charcoal, sorbitol, or both
In rare severe cases, hemoperfusion or hemodialysis
Consultations may include a regional poison control center, a medical toxicologist, or a psychiatrist (once the patient is medically stable). Medically unstable patients are admitted for the appropriate level of care, depending on the clinical presentation.
About 85% of adults in the United States drink at least one caffeinated beverage a day,[2] as do 73% of children.[3] Caffeine intake intake in US children and adolescents remained stable from 1999 to 2010, but sources of caffeine changed: the contribution of soda decreased from 62% to 38% while that of coffee increased from 10% to nearly 24% and energy drinks (which did not exist in 1999) increased to nearly 6%.[3] In a 2014 nationally representative cross-sectional survey, nearly nearly two thirds of US adolescents aged 13-17 years reported ever using energy drinks, and 41% had done so in the past 3 months.[4]
A study published by the US Food and Drug Administration (FDA) reported that in 2003-2008, the average adult consumed about 300 mg caffeine/day, with teenagers consuming roughly 100 mg/d.[5] In quantities found in food and beverages, caffeine is unlikely to cause acute medical problems; however, a changing market in which energy drinks are not subject to FDA regulatory standards has raised concerns over caffeine-related health problems.
In 1989, the US Food and Drug Administration (FDA) limited the amount of caffeine in OTC products to a maximum of 200 mg/dose. Caffeine is present in concentrated forms in OTC products such as alertness-promoting medications (eg, NoDoz, Vivarin), menstrual aids (eg, Midol), analgesics (eg, Excedrin, Anacin, BC Powder), and diet aids (eg, Dexatrim). Caffeine is also a component of prescription medications (eg, Fioricet, Cafergot) and herbal preparations.The ingestion of such concentrated sources of caffeine is the general cause of acute caffeine toxicity. See the image below for caffeine equivalents of common products.
View Image
Caffeine content of various foods, beverages, medications, and supplements. Caffeine content is approximate for brewed beverages and chocolate).
Caffeine has differing CNS, cardiovascular, and metabolic effects based on the quantity ingested. Average doses of caffeine (85-250 mg, the equivalent of 1-3 cups of coffee) may result in feelings of alertness, decreased fatigue, and eased flow of thought. High doses (250-500 mg) can result in restlessness, nervousness, insomnia, and tremors. In high doses, caffeine can cause a hyperadrenergic syndrome resulting in seizures and cardiovascular instability.
Because caffeine overdoses, intentional or unintentional, are relatively common in the United States, physicians and other medical personnel must be aware of caffeine toxicity to recognize and treat it appropriately.
In cola beverages, caffeine is permitted by the FDA for flavor use at a 0.02% (0.2 mg/mL) concentration, equivalent to 20 mg in a 100-mL beverage or 71 mg in a 12-ounce beverage (Code of Federal Regulations, title 21, sec. 182.1180).[6] Because caffeine is not considered a nutrient, the FDA does not require manufacturers to label the amount of caffeine present in food and beverages, although caffeine must be listed as an ingredient if the manufacturer adds it to their product.[7]
Although caffeine is found in food and over-the-counter products, more than 97% of caffeine consumed by adults and teenagers comes from beverages, including coffee, tea, cola-products, and energy drinks.[5] Unlike cola-beverages, energy drinks and shots are typically classified as dietary supplements; thus, individuals who consume these products are likely unaware of how much caffeine they are actually consuming.[7] See Table 1, below.
Table 1. Reported Caffeine Content of Common Beveragesref4}
View Table
See Table
The caffeine content of dietary supplements is virtually unregulated by the FDA. Prior to the Dietary Supplement Health and Education Act (DSHEA) of 1994, dietary supplements were subject to the same regulatory requirements as other foods; however, after DSHEA, the safety of dietary supplements became the sole responsibility of manufacturers. Consequentially, there are no limitations on the amount of caffeine in dietary supplements and manufacturers are not required to list the caffeine content of their products.
In 2018, the FDA issued a new guidance regulating the sale of "bulk quantities" (packages containing enough powder or liquid for thousands of recommended servings) of pure or highly concentrated caffeine in powder or liquid forms sold directly to consumers. However the FDA did not address preexisting beverages.[8]
The rising popularity of caffeinated energy drinks over the past decade has raised new concerns about their impact on public health. As illustrated above, energy drinks contain substantially more caffeine than conventional cola beverages, with caffeine content ranging from 75-300 mg per serving. Many also contain caffeine-containing ingredients such as guarana, kola nut, or yerba mate. Consequentially, they may contain more caffeine than reported in Table 1 above.[9] These energy drinks are also sold in larger sizes (16-23.5 fl oz). It is not uncommon for individuals to consume multiple caffeinated beverages over the course of a day.
Caffeine has differing CNS, cardiovascular, and metabolic effects based on the quantity ingested. Average doses of caffeine (85-250 mg, the equivalent of 1-3 cups of coffee) may result in feelings of alertness, decreased fatigue, and eased flow of thought. High doses (250-500 mg) can result in restlessness, nervousness, insomnia, and tremors. In high doses, caffeine can cause a hyperadrenergic syndrome resulting in seizures and cardiovascular instability.
Because caffeine overdoses, intentional or unintentional, are relatively common in the United States, physicians and other medical personnel must be aware of caffeine toxicity to recognize and treat it appropriately.
Caffeine, a methylxanthine, is closely related to theophylline. Caffeine is rapidly and completely absorbed from the GI tract; it is detectable in the plasma 5 minutes after ingestion, with peak plasma levels occurring in 30-60 minutes. The volume of distribution in adults is approximately 0.5 L/kg.
Caffeine is primarily metabolized by the cytochrome P450 (CYP) oxidase system in the liver. The plasma half-life of caffeine varies considerably from person to person, with an average half-life of 5-8 hours in healthy, nonsmoking adults. Caffeine clearance is accelerated in smokers; clearance is slowed in pregnancy, in liver disease, and in the presence of some CYP inhibitors (eg, cimetidine, quinolones, erythromycin). In addition, the hepatic enzyme system responsible for caffeine metabolism can become saturated at high levels, resulting in a marked increase in serum concentration with small additional doses.
Various mechanisms mediate the effects of caffeine in the human body. Caffeine directly stimulates respiratory and vasomotor centers of the brain and acts as an adenosine antagonist, resulting in peripheral vasodilatation and CNS stimulation. Caffeine is a potent releaser of catecholamines (norepinephrine and, to a lesser extent, epinephrine) that increases cardiac chronotropic and inotropic activity, bronchodilation, and peripheral vasodilatation. Caffeine is also a phosphodiesterase inhibitor. However, because extremely high concentrations of caffeine are required to inhibit this enzyme, whether this effect contributes to the clinical effects of caffeine in vivo is unknown.
In addition to its cardiovascular effects, caffeine induces a number of metabolic changes, including hyperglycemia (by stimulating gluconeogenesis and glycogenolysis), increased renal filtration, ketosis, and hypokalemia. Caffeine is a potent stimulator of gastric acid secretion and GI motility.
Death from caffeine toxicity is rare, but it has been reported due to dysrhythmias, seizures, and aspiration of emesis. Oral doses of caffeine greater than 10 g can be fatal in adults.[10] A daily intake of 400 mg—about four or five cups of coffee—is considered safe for adults, while 200 mg is considered safe for pregnant women.[7, 11]
Caffeine poisoning is a relatively common toxicologic emergency in the United States, and the number of cases has steadily increased in the past decade. The Substance Abuse and Mental Health Services Administration (SAMHSA) reported a jump in the number of emergency department visits involving energy drinks, increasing roughly 10-fold from 2005 (1128 visits) to 2008 and 2009 (16,053 and 13,114 visits, respectively). More than half of the visits made by patients age 18-25 years involved the combination of energy drinks with alcohol or other drugs.[12] Between 2007 and 2011 the number of energy drink related visits to the emergency room doubled. [13]
The American Association of Poison Control Centers (AAPCC) reported 1122 single exposures to caffeine-containing energy drinks in 2016, with five major outcomes but no deaths. The AAPCC also reported 3702 single exposures to caffeine as a street drug, with 16 major outcomes but no deaths.[14]
Caffeinated alcoholic beverages were a public health concern because caffeine can mask some sensory cues that people might normally rely on to determine their level of intoxication. The US Food and Drug Administration (FDA) banned their sales in 2010.[7] In spite of the ban, mixing alcohol with energy drinks is still common practice and popular. In 2015, 13.0% of students in grades 8, 10, and 12 and 33.5% of young adults aged 19 to 28 reported consuming alcohol mixed with energy drinks at least once in the past year. Furthermore, the CDC reports that drinkers aged 15 to 23 who mix alcohol with energy drinks are 4 times more likely to binge drink at high intensity.[15] It is very important for the physician to inquire about co-ingestion of caffeine-containing drinks when obtaining a history for possible drug overdose or alcohol poisoning.
Death is an uncommon result of caffeine poisoning, but may be due to caffeine-related dysrhythmias, seizures, and aspiration of emesis. Oral doses of caffeine greater than 10 g can be fatal in adults.[10]
The AAPC reported no deaths related to caffeine in 2016.[14] The FDA’s Center for Food Safety and Applied Nutrition (CFSAN) Adverse Event Reporting System (CAERS) reported 29 deaths related solely to Monster, 5-Hour Energy, and Rockstar energy drinks from 2004-2013.[16]
Race-, Sex- and Age-related Variance
Caffeine is the most commonly used drug in the world, and its use is prevalent in essentially all races and ethnic groups.[1] No scientific data have demonstrated that the outcomes of caffeine exposure differ on the basis of race or sex.[17]
Whether or not the effects of caffeine on adults can be generalized to children is unclear; however, studies suggest that children are differently affected by caffeine. One study comparing the effects of caffeine in men and boys found that the same dose of caffeine raised blood pressure in both groups but only decreased heart rate in boys. They also found that boys exhibited increased motor activity and speech rates and decreased reaction time compared with men.[18]
Another study found that an intake of 5 mg/kg body weight leads to elevated blood pressure and lower heart rate, without concomitant changes in energy metabolism in children aged 9-11 years. This amounts to 160 mg caffeine/day in a 10-year-old child weighing 30 kg, which is equivalent to the caffeine content of a single 16-oz Monster or Rockstar energy drink.[19]
In 2016, the AAPCC reported that the most exposures to caffeinated energy drinks were in children younger than 6 years. The second highest number of exposures were in adults aged 20 years and older.[14]
Additional age-related concerns arise from the fact that many energy drinks are marketed toward youth and youth-related activities, such as extreme sports. Students and athletes often drink them to enhance performance. A survey of 496 college students found that 51% of those surveyed drank more than 1 energy drink per month, with the majority of students drinking several energy drinks per week. The main impetus was the desire for increased energy and concentration, with the most common complaint being insufficient sleep or a disruption in their regular sleep cycles.[20]
If acute caffeine ingestion is suspected, patients or their family members should be questioned about their use of prescription medications, over-the-counter (OTC) drugs, and illicit drugs. Patients and family members should be queried about the use of any of the following drugs:
Cocaine
Amphetamines
Methamphetamine
Phencyclidine (PCP)
Antidepressants
Asthma medications
Thyroid medications
Anticholinergics (eg, OTC allergy medications)
The patient and family members or friends may be able to give a history of recent caffeine ingestion (eg, ingestion of alertness-promoting OTC medications, caffeinated beverages, or diet medications) or a history of recent behavior compatible with such use (eg, the patient was trying to lose weight or taking stimulants to aid in working or studying). In an acute overdose, pill bottles found at the scene may provide a clue to what the patient ingested.
When ingested chronically in excessive amounts, caffeine produces a specific toxidrome (caffeinism), which consists of primarily central nervous system (CNS), cardiovascular, and gastrointestinal (GI) hyperstimulation.
CNS features include the following:
Headache
Lightheadedness
Anxiety, agitation
Tremulousness, perioral and extremity tingling (resulting from tachypnea-induced respiratory alkalosis)
Vital signs may include tachypnea and tachycardia. On blood pressure measurement, a characteristic finding is widened pulse pressure due to the positive inotropic effect as well as the vasodilatory effect of caffeine. Hypotension may be present.
CNS findings on physical examination include the following:
Anxiety, agitation
Tremors
Seizures
Altered mental status
The pupils are dilated but reactive to light. The thyroid should be examined because thyrotoxicosis may mimic caffeine toxicity.
Chronic toxicity is generally encountered in people who have ingested higher doses of caffeine-containing compounds (alone or in combination) for various reasons. Patients may be unaware that some products contain caffeine or that high doses of caffeine can be harmful. Patients may ingest caffeine-containing analgesics for headaches, OTC caffeine-containing medications for dieting, or OTC medications for improving alertness while studying or working. In addition, people may drink caffeine in beverages such as coffee, tea, soft drinks,[21] or energy drinks (eg, Red Bull, AMP Energy Drink, Rockstar, Monster) or take caffeine in herbal preparations[22] .
Considerations include the following:
Acute toxicity can occur after intentional or unintentional ingestion. OTC alertness-promoting medications are often implicated in intentional overdoses.
Certain medications, such as cytochrome inhibitors (eg, cimetidine) and oral contraceptives, impair caffeine metabolism.[23]
Caffeine clearance is reduced in patients with chronic liver disease, in pregnant women, and in infants.
Caffeine clearance is increased in smokers. With smoking cessation, serum caffeine concentrations can double even if caffeine consumption remains stable.
The patient's signs and symptoms should guide the use of laboratory studies. In hemodynamically stable patients with mild symptoms who give a clear history of caffeine ingestion, no laboratory studies are indicated.
The following laboratory studies are indicated in patients with moderate-to-severe symptoms of caffeine toxicity (ie, hemodynamic instability, dysrhythmias, seizures, altered mental status).
A complete blood cell count (CBC) should be checked to evaluate for infection. Mild leukocytosis (11-16 × 109 L [11,000-16,000/mL]) can be present in caffeine toxicity; however, infectious processes should be excluded.
Serum electrolyte, glucose, blood urea nitrogen (BUN), and creatinine concentrations should be checked. Pay particular attention to potassium concentrations and the anion gap. Hypokalemia is a classic feature of caffeine overdose. An increased anion gap (resulting from lactic acidosis) and hyperglycemia are also common findings in severe toxicity.
Routine screening for other potentially treatable toxins (eg, acetaminophen, salicylate) is recommended. Such testing is essential if the patient ingested analgesic medications containing caffeine combined with other drugs (eg, Excedrin, Cafergot, Fiorinal or Fioricet, Midol, Anacin).
Measure total creatine kinase (CK) concentrations to check for rhabdomyolysis, which is occasionally associated with severe caffeine toxicity. A CK concentration greater than 5 times the upper limit of normal indicates clinically significant rhabdomyolysis. Include the CK-MB fraction and troponin level if myocardial ischemia is suspected.
Results of dipstick urinalysis may give a rapid indication of rhabdomyolysis, myoglobinuria, or both. Glucosuria and ketonuria are also common findings.
A rapid urine drug screen may help in identifying co-ingested substances. Illicit drugs, such as ecstasy or methamphetamine, often contain caffeine as a substitute or co-ingredient. Standard urine drug tests usually cannot detect ecstasy or methamphetamines.
Consider checking serum ethanol concentrations and osmolality in cases of unknown ingestion or suspected co-ingestion.
A serum pregnancy test is indicated in all women of childbearing age.
Thyroid studies should be considered because thyrotoxicosis can mimic caffeine toxicity.
Arterial blood gas analysis is indicated in patients with respiratory compromise, with altered mental status, or with a need for mechanical ventilation.
Serum caffeine concentration determinations do not influence management. Consider the following:
Caffeine tests are generally available only at reference or research laboratories and are not clinically useful.
Serum theophylline concentrations are more rapidly and widely available than caffeine determinations. Because theophylline is a minor metabolite of caffeine, a positive theophylline assay may be helpful in confirming suspected caffeine toxicity.[24]
Patients with severe caffeine toxicity have had serum theophylline concentrations in the therapeutic range (10-20 mg/L).
Patients with chest pain, palpitations, tachycardia, or an irregular heart rhythm should be evaluated with an electrocardiogram (ECG) and telemetry monitoring.
Prehospital care is primarily supportive, as follows:
Address airway, breathing, and circulation (ABCs): Administer oxygen, obtain intravenous access, attach cardiac monitors (if available), and frequently assess vital signs and consciousness (eg, by using the alert, responds to voice, responds to pain, and unresponsive [AVPU] or Glasgow Coma scale).
Check blood glucose level.
Patients with anxiety, severe agitation, or seizures may require a short-acting benzodiazepine (eg, lorazepam) given intravenously or intramuscularly.
Although most patients with caffeine toxicity improve with supportive care, life-threatening complications can result from severe overdoses. Fatalities are generally related to cardiac dysrhythmias. Other factors contributing to mortality include seizures, myocardial infarction, hypotension, electrolyte disturbances, rhabdomyolysis, and aspiration (secondary to an inability to protect the airway).
Emergency department management consists of restoring cardiovascular stability and addressing the other factors that may contribute to mortality.
Address ABCs, as follows:
Endotracheal intubation is indicated in patients who are unable to maintain an airway because of altered mental status, severe cardiovascular depression, or seizures.
Administer oxygen and obtain intravenous access (if not already obtained) and attach cardiac monitors.
An electrocardiogram (ECG) and initial laboratory studies should be performed at this time.
Caffeine acts as a bronchodilator and generally does not result in respiratory compromise if the patient can protect his or her airway.
Hypotension can occur in caffeine toxicity. It is related to volume depletion, excessive catecholamine stimulation of beta2-adrenergic receptors, or both. Vasopressors (eg, dopamine, phenylephrine) may be required if hypotension is refractory to intravenous fluid boluses. Phenylephrine is a good choice because it is a pure alpha-agonist, although norepinephrine can be used as well.
The treatment of dysrhythmias depends on the nature of the dysrhythmia and the patient's clinical presentation. Dehydration, hypoxemia, metabolic acidosis, and electrolyte disturbances may contribute to morbidity and should be corrected as the patient's dysrhythmia is addressed. Management is as follows:
Patients with supraventricular tachycardia (SVT) and adequate blood pressure and no ECG evidence of ischemia can be treated with supportive care.
Patients with persistent SVT, hypotension, or evidence of cardiac ischemia require intervention to control their heart rate or to restore a sinus rhythm. Initial treatment of caffeine-induced SVT should include administration of benzodiazepines in order to reduce CNS stimulation and release of catecholamines. A short-acting cardioselective beta-blocker (eg, esmolol) or a calcium channel blocker (eg, diltiazem) may be used to control the heart rate. Caution should be exercised since these agents may contribute to hypotension.
Adenosine, often used in the treatment of paroxysmal SVT, is unlikely to be effective in patients with caffeine overdose because caffeine antagonizes adenosine receptors.
In the hemodynamically stable patient, amiodarone or lidocaine may be used to treat ventricular tachycardia (VT).
Electrical cardioversion may be used in hemodynamically unstable patients or in patients whose condition is refractory to pharmacologic intervention.
Because caffeine overdose is a situation of catecholamine excess, the use of beta-blockers raises the theoretical concern that unopposed alpha stimulation could precipitate a hypertensive crisis (similar to beta-blockade in patients with pheochromocytoma). In practice, a hypertensive crisis as a consequence of unopposed alpha stimulation has never been reported in cases of caffeine toxicity, and alpha-agonists (eg, phenylephrine) may be needed to support blood pressure in hypotensive patients. In theory, beta-blockade can be beneficial in patients with refractory hypotension and could be used in consultation with the regional poison control center or board-certified toxicologist.
Seizures should be treated with benzodiazepines (eg, lorazepam). Barbiturates are second-line agents. Animal studies demonstrated that phenytoin is not useful in controlling seizures induced by methylxanthines and that they may actually increase mortality.[25]
Caffeine produces a number of metabolic disturbances. Hypokalemia should be sought for and aggressively treated with intravenous potassium replacement. Rhabdomyolysis should be treated with intravenous fluids to prevent renal failure. Other metabolic complications, such as hyperglycemia and metabolic acidosis, generally resolve with supportive care.
Additional treatment considerations include the following:
Prolonged vomiting should be treated with antiemetic agents.
Because caffeine is absorbed rapidly, gastric lavage is unlikely to be useful in patients who present longer than 1 hour after the ingestion.
Activated charcoal is effective in limiting gut absorption of methylxanthines and is recommended early in treatment.
In rare cases, hemoperfusion or hemodialysis is used in severe caffeine overdose.
A case report describes the use of lidocaine, phenylephrine, and hemodialysis to stabilize cardiovascular collapse in a patient with massive caffeine ingestion.[26]
A case report describes a patient with multiple episodes of pulseless VT who achieved return of spontaneous circulation after defibrillation, intubation, and amiodarone administration.[27]
The objectives of pharmacotherapeutic intervention of caffeine toxicity include (1) stabilization of heart rate and blood pressure; (2) seizure control with benzodiazepines; (3) decontamination with activated charcoal, sorbitol, or both; and (4) correction of electrolyte disturbances.
Tachydysrhythmias may be treated with calcium channel blockers or beta-blockers (preferred) for rate control or with antidysrhythmics, depending on the rhythm disturbance.
Clinical Context:
Sedative hypnotic with short onset of action and relatively long half-life. Increases action of gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in brain.
Clinical Context:
Naturally occurring endogenous catecholamine that stimulates dopaminergic, beta1-adrenergic, and alpha1-adrenergic receptors in dose-dependent fashion. At 2-5 mcg/kg/min, acts on dopaminergic receptors in renal and splanchnic vascular beds, causing their vasodilation. At 5-15 mcg/kg/min, acts on beta-adrenergic receptors to increase heart rate and contractility. At 15-20 mcg/kg/min, acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise BP.
Clinical Context:
Ultrashort action. Selectively blocks beta1-receptors with little or no effect on beta2-receptors. Useful in patients at risk for complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate left ventricular (LV) dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.
These drugs are used for rate control in cases of atrial fibrillation or another SVT. They should not be used to treat hypertension in the setting of caffeine or sympathomimetic overdose.
Clinical Context:
Decreases conduction velocity in AV node and increases refractory period by blocking calcium influx, converting SVT or slowing rate in atrial fibrillation. Also has vasodilator activity but may be less potent than other agents.
These drugs are used for rate control in atrial fibrillation or another SVT. They should not be used to treat hypertension in the setting of caffeine or sympathomimetic overdose.
Clinical Context:
Class III antiarrhythmic. May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Effective in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence. Before administration, control ventricular rate with another agent (eg, calcium channel blocker). Drug of choice for life-threatening ventricular arrhythmias, except for disorders of prolonged repolarization (eg, long-QT syndrome [LQTS]).
Clinical Context:
Second-line drug for VT or VF. Class IB antiarrhythmic that increases electrical stimulation threshold of ventricle, suppressing automaticity of conduction through the tissue.
These substances adsorb caffeine after acute injections and limit the absorption of caffeine into the systemic circulation. They are most effective when administered within 1 hour of ingestion.
Outpatient follow-up with a psychiatrist is compulsory for any patient after an intentional caffeine overdose.
Outpatient follow-up with a psychiatrist may also be considered for patients who have a comorbid psychiatric illness (eg, depression) or extenuating circumstances (eg, excessive life stress) that may have contributed to their caffeine toxicity.
Intensive care unit (ICU) admission is warranted for patients with seizures, clinically significant dysrhythmias, hemodynamic instability, or other signs of severe caffeine toxicity.
Patients who require ICU admission for caffeine toxicity should receive close hemodynamic monitoring as well as serial measurement of electrolyte levels, with particular attention to serum potassium levels.
Patients with mild symptoms of caffeine toxicity may be admitted to a general medical ward for observation.
Telemetric monitoring should be considered for all patients admitted for caffeine toxicity.
For stable patients with intentional overdoses, consider admission to a psychiatric unit.
Patients may require transfer to a psychiatric facility for evaluation and treatment after an intentional ingestion if they are hemodynamically stable and if they have no evidence of CNS complications.
Patients may require transfer to a toxicology treatment facility for further evaluation and treatment if severe symptoms are present or expected. Transfer with appropriate precautions and only after discussion with the receiving medical toxicologist.
Rare cases of caffeine-induced ventricular dysrhythmias refractory to advanced cardiac life support (ACLS) protocols are reported. In general, however, the prognosis is excellent for patients with caffeine toxicity who reach a medical facility and who can be supported through the acute phase.
Patients may be unaware of the caffeine content of various products (energy drinks, herbal medications, alertness-promoting medications) or of the ill effects related to these medications. Patients in the emergency department or in other health care settings who appear to have effects related to caffeine ingestion should be counseled to limit their caffeine intake and to avoid concentrated sources of caffeine.
What is caffeine?What is the focus of clinical history for caffeine toxicity?What are the signs and symptoms of caffeine toxicity?Which CNS findings are characteristic of caffeine toxicity?Which cardiovascular findings are characteristic of caffeine toxicity?Which GI findings are characteristic of caffeine toxicity?Which lab tests are performed in the workup of caffeine toxicity?Which imaging studies are performed in the workup of caffeine toxicity?What is included in the prehospital care of severe caffeine toxicity?Which specialist consultations are beneficial in the treatment of caffeine toxicity?What amount of caffeine causes acute toxicity?What are the effects of caffeine in the body?What are the physical effects of caffeine toxicity?How much caffeine is contained in common beverages and supplements?What is the pathophysiology of caffeine toxicity?What is the prevalence of caffeine toxicity in the US?What is the mortality and morbidity associated with caffeine toxicity?Which patient groups are at highest risk for caffeine toxicity?What is included in the clinical history for caffeine toxicity?Which clinical history findings are characteristic of caffeine toxicity?What are CNS signs and symptoms of caffeine toxicity?What are the cardiovascular signs and symptoms of caffeine toxicity?What are the GI signs and symptoms of caffeine toxicity?What are vital sign findings characteristic of caffeine toxicity?Which CNS findings are characteristic of caffeine toxicity?Which GI findings are characteristic of caffeine toxicity?What causes caffeine toxicity?What are the differential diagnoses for Caffeine Toxicity?What is the role of lab testing in the diagnosis of caffeine toxicity?What is the role of serum caffeine concentration is the diagnosis and treatment of caffeine toxicity?What is the role of imaging studies in the diagnosis of caffeine toxicity?What is the role of ECG in the diagnosis of caffeine toxicity?What is included in prehospital care for caffeine toxicity?How is caffeine toxicity treated in the emergency department (ED)?What is the role of vasopressors in the ED treatment of caffeine toxicity?What is the ED treatment for dysrhythmias in caffeine toxicity?What is the role of beta-blockers in the ED treatment of caffeine toxicity?What is the ED treatment for seizures in caffeine toxicity?What is the ED treatment of metabolic complications of caffeine toxicity?What are the less common treatments for caffeine toxicity?Which specialist consultations are beneficial to patients with caffeine toxicity?What medications are used in the treatment of caffeine toxicity?Which medications in the drug class GI decontaminants are used in the treatment of Caffeine Toxicity?Which medications in the drug class Antidysrhythmics are used in the treatment of Caffeine Toxicity?Which medications in the drug class Calcium channel blockers are used in the treatment of Caffeine Toxicity?Which medications in the drug class Beta-blockers are used in the treatment of Caffeine Toxicity?Which medications in the drug class Vasopressors are used in the treatment of Caffeine Toxicity?Which medications in the drug class Benzodiazepines are used in the treatment of Caffeine Toxicity?What is included in long-term monitoring of caffeine toxicity?What is included in inpatient care for caffeine toxicity?When is patient transfer indicated for the treatment of caffeine toxicity?What is the prognosis of caffeine toxicity?What is included in the patient education about caffeine toxicity?
David Yew, MD, Assistant Clinical Professor, Department of Surgery, University of Hawaii, John A Burns School of Medicine; Medical Director and Flight Physician, Hawaii Life Flight, AirMed International
Disclosure: Nothing to disclose.
Coauthor(s)
Sophie Kim, Boston College
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
John G Benitez, MD, MPH, Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center
Disclosure: Nothing to disclose.
Chief Editor
Michael A Miller, MD, Clinical Professor of Emergency Medicine, Medical Toxicologist, Department of Emergency Medicine, Texas A&M Health Sciences Center; CHRISTUS Spohn Emergency Medicine Residency Program
Disclosure: Nothing to disclose.
Additional Contributors
China N Byrns, Department of Cell and Molecular Biology, University of Hawaii at Manoa
Disclosure: Nothing to disclose.
James E Keany, MD, FACEP, Associate Medical Director, Emergency Services, Mission Hospital Regional Medical Center, Children's Hospital of Orange County at Mission
Disclosure: Nothing to disclose.
Acknowledgements
Jeffrey T Laczek, MD Gastroentology Fellow, Walter Reed Army Medical Center
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