CAFFEINE

Caffeine 250 mg/mL and sodium benzoate 250 mg/mL injection has been used intramuscularly as an analeptic, a stimulant in acute circulatory failure, a diuretic, and intravenously to alleviate headaches following spinal puncture (Kastrup, 1988).
Caffeine has been used in the treatment of prolonged apnea in preterm infants (Gilman et al, 1985).

SOURCES

Caffeine is found in a wide variety of common beverages, foods, and pharmaceuticals. For example, some approximate concentrations of caffeine are (FDA News, 1984; Anon, 1984): PRODUCTAMOUNTCOFFEEbrewed drip coffee60 to 180 mg/5-ounce (oz) cupbrewed percolator coffee40 to 179 mg/5-oz cupinstant coffee30 to 190 mg/5-oz cupdecaffeinated brewed coffee2-5 mg/5-oz cupdecaffeinated instant coffee1 to 5 mg/5-oz cupNescafe-Classic(R) instant coffee63 mg/5-oz cup (Galasko, 1989)Instant Coffee powder57 mg/rounded teaspoonful (1.5 g)Espresso100 mg/serving (1.5 to 2 oz)TEAbrewed commercial tea20 to 90 mg/5-oz cupbrewed imported tea25 to 110 mg/5-oz cupinstant tea2 to 20 mg/5-oz cupiced tea67 to 76 mg/12-oz glassFOODcocoa2 to 20 mg/5-oz cupchocolate milk2 to 7 mg/8 ozmilk chocolate1 to 15 mg/ozdark semi sweet chocolate5 to 35 mg/ozBaker's chocolateaverage 26 mg/ozchocolate syrupaverage 4 mg/ozchocolate cake13.8 mg/92-g serving (1/sixteenth of 9-in cake)candy, chocolate7.7 mg/1-oz barcandy, chocolate-covered2.8 mg/1-oz barchocolate ice cream4.5 mg/two-thirds cupchocolate pudding, instant5.5 mg/one-half cupnut fudge brownie7.7 mg/1 and one-fourth ozSnickers Charged(TM) candy bar60 mg/1.83-oz bar

SOFT DRINKS (Note: The maximum allowable caffeine content is 0.02% which amounts to 72 mg/12 ounces (oz)). All amounts are per 12-oz can (Prod Info, 1988).

Another source determined caffeine content of energy drinks, carbonated sodas, and other beverages (McCusker et al, 2006):

BEVERAGE	SERVING SIZE (OUNCE)	CAFFEINE (MG/SERVING)
ENERGY DRINKS
Red Devil(R)	8.4	41.8
SoBe(R) Adrenaline Rush	8.3	76.7
SoBe(R) No Fear	16	141.1
Hair of the Dog(R)	8.4	none detected
Red Celeste(TM)	8.3	75.2
E Maxx(TM)	8.4	73.6
Amp(TM)	8.4	69.6
Red Bull(R) Sugar-free	8.3	64.7
Red Bull(R)	8.3	66.7
KMX(TM)	8.4	33.3
CARBONATED SODAS
Coca-Cola Classic(R)	12	29.5
Diet Coke(R)	12	38.2
Diet Coke(R) with Lime	12	39.6
Caffeine Free Diet Coke(R)	12	none detected
Vanilla Coke(R)	12	29.5
Pepsi(R)	12	31.7
Diet Pepsi(R)	12	27.4
Mountain Dew(R)	12	45.4
Mountain Dew(R) Live Wire(TM)	12	48.2
Dr Pepper(R)	12	36
Diet Dr Pepper(R)	12	33.8
Sierra Mist(TM)	12	none detected
Celeste(TM) Cola	12	19.4
Sprite(R)	12	none detected
Seagram's(R) Ginger Ale	12	none detected
Barq's(R) Root Beer	12	18
Pibb Xtra(R)	12	34.6
A&W(R) Root Beer	12	none detected
7-UP(R)	12	none detected
OTHER BEVERAGES
Nestea(R) Cool Lemon Iced Tea	12	11.5
Lipton(R) Brisk Lemon Iced Tea	12	6.5
Yoohoo(R) Chocolate Drink	9	less than 2.7
Starbucks Doubleshot(TM)	6.5	105.7
Starbucks Frappuccino(R) Mocha	9.5	71.8
Starbucks Frappuccino(R) Vanilla	9.5	63.8
Velda Farms(R) chocolate milk	16	less than 3.8

CAFFEINE CONTENT OF FOUNTAIN COCA-COLA
LOCATION	SERVING SIZE (OUNCE)	CAFFEINE (MG/SERVING)
Burger King(R)	16	41.5
Wendy's(R)	16	41.5
McDonald's(R)	16	44
Chick-fil-A(R)	16	48.4
Fast Track	16	45.5
Steak N Shake(R)	16	43.5
Atlanta Bread Company(R)	16	40.9
Checkers(R)	16	46.9
Citgo(R) Food Mart	16	48.4

Caffeine also is found in a variety of over-the-counter (OTC) drugs used as stimulants or diuretics.

DRUGS
Anacin(R)		32 mg
Anacin(R) Maximum Strength		32 mg
Appedrine(R), Maximum strength		100 mg
Aqua-Ban(R)		100 mg
Aspirin-Free Excedrin(R)		65 mg
Cafergot(R) (all forms)		100 mg
Cope(R)		32 mg
Coryban-D(R)		30 mg
Darvon(R) compound		32.4 mg
Dexatrim(R)		200 mg
Dexatrim(R) Extra Strength		200 mg
Dristan(R) cap, tab		16.2 mg
Excedrin(R)		65 mg
Fiorinal(R)		40 mg
Midol(R)		32.4 mg
NoDoz(R)		100 mg
Prolamine(R)		140 mg
Synalgos DC(R)		30 mg
Triaminicin(R) tab		30 mg
Vivarin(R)		200 mg
Wigraine(R) (all forms)		100 mg
NATURAL PRODUCTS
Guarana	3% to 5% (24 to 40 mg per 800 mg tablet) one brand (Zoom(R)) states 20.8 mg per 800 mg tablet
Coffee beans	1% to 2%

GUARANA: To achieve a potential toxic caffeine concentration of 20 mg/L, a 70-kg person would need to consume the caffeine content of 17 g of guarana (containing 5% weight/weight caffeine) (Drew & Dawson, 2000).
CHEWING GUM: A 13-year-old boy became agitated and aggressive, and developed sinus tachycardia, tachypnea, hypertension, increased diuresis, dysuria, and paresthesia of the legs following consumption of 2 packets of stimulant ("energy") chewing gum within a 4-hour period. Each packet reportedly contained 160 mg caffeine (0.57% caffeine per gum pellet) (Natale et al, 2009).
LOOK-ALIKE PRODUCTS

AVAILABILITY: Caffeine was formerly available in combination with phenylpropanolamine and ephedrine in formulations designed to mimic controlled stimulants. (This combination was removed from the market in 1982 by the US Food and Drug Administration (FDA). Caffeine alone is still available.)
COMBINATIONS: Caffeine with either ephedrine, pseudoephedrine, or phenylpropanolamine is no longer being produced.
DOSAGE LIMIT: Since 1989, over-the-counter products labeled as stimulants may not contain more than 200 mg per dose (FDA, 1988).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

USES: Caffeine (1,3,7-trimethylxanthine) is present in coffee, tea, colas, and chocolate. It is also utilized in over-the-counter cough and cold therapies, and in many dietary supplement products used as anorexiants, diuretics, and stimulants. Botanical sources of caffeine include: guarana, yerba mate, and kola nuts. Caffeine is used medicinally for neonatal apnea and postlumbar puncture headache.

PHARMACOLOGY: Caffeine is a trimethylxanthine closely related to theophylline. It acts through nonselective inhibition of adenosine receptors and phosphodiesterase. There is also beta-1 and beta-2 adrenergic stimulation secondary to catecholamine release.

TOXICOLOGY: Caffeine is an adenosine analog and functions primarily as an adenosine antagonist lowering the seizure threshold. It also inhibits phosphodiesterase, resulting in accumulation of cAMP and calcium, causing organ-specific downstream effects such as smooth muscle relaxation, or muscle/cardiac/CNS excitation. Caffeine overdoses result in surges in circulating catecholamines and rennin, as well as increased levels of norepinephrine, dopamine, and serotonin in the brain.

EPIDEMIOLOGY: Caffeine is commonly used; however, severe manifestations of toxicity are rare, and most exposures result in mild toxicity.

WITH POISONING/EXPOSURE

MILD TO MODERATE TOXICITY: The earliest symptoms of acute caffeine poisoning include: anorexia, tremor, and restlessness, followed by nausea, vomiting and tachycardia. Chronic high-dose caffeine intake can lead to "caffeinism" which includes nervousness, twitching, anxiety, tremulousness, insomnia, palpitations, and hyperreflexia.
SEVERE TOXICITY: With serious ingestions hypokalemia, hyperglycemia, metabolic acidosis, rhabdomyolysis, hypotension, confusion, seizures, tachycardia, and nonfatal dysrhythmias may occur.

Editor's Note: An ERG guide with information appropriate to this material does not exist.

ACUTE CLINICAL EFFECTS

SUMMARY

PHARMACOLOGY: Caffeine is a trimethylxanthine closely related to theophylline. It acts through nonselective inhibition of adenosine receptors and phosphodiesterase. There is also beta-1 and beta-2 adrenergic stimulation secondary to catecholamine release.
TOXICOLOGY: Caffeine is an adenosine analog and functions primarily as an adenosine antagonist lowering the seizure threshold. It also inhibits phosphodiesterase, resulting in accumulation of cAMP and calcium, causing organ-specific downstream effects such as smooth muscle relaxation, or muscle/cardiac/CNS excitation. Caffeine overdoses result in surges in circulating catecholamines and rennin, as well as increased levels of norepinephrine, dopamine, and serotonin in the brain.
EPIDEMIOLOGY: Caffeine is commonly used; however, severe manifestations of toxicity are rare, and most exposures result in mild toxicity.
MILD TO MODERATE TOXICITY: The earliest symptoms of acute caffeine poisoning include: anorexia, tremor, and restlessness, followed by nausea, vomiting and tachycardia. Chronic high-dose caffeine intake can lead to "caffeinism" which includes nervousness, twitching, anxiety, tremulousness, insomnia, palpitations, and hyperreflexia.
SEVERE TOXICITY: With serious ingestions hypokalemia, hyperglycemia, metabolic acidosis, rhabdomyolysis, hypotension, confusion, seizures, tachycardia, and nonfatal dysrhythmias may occur.

ACID-BASE

ACIDOSIS: Metabolic acidosis and respiratory alkalosis are typical following acute caffeine poisonings (Vaglio et al, 2011; Rudolph & Knudsen, 2010; Anderson et al, 1999; Rouse et al, 1999).

CARDIOVASCULAR

CONDUCTION DISORDERS OF THE HEART: Bigeminy, paroxysmal atrial tachycardia, premature ventricular contractions (PVCs), ventricular tachycardia, and fibrillation have been reported (Vaglio et al, 2011; Nagesh & Murphy, 1988; Price & Fligner, 1990; Forman et al, 1997). A study of newborns concluded that those children born to mothers who consumed greater than 500 mg/day of caffeine were more likely to have cardiac dysrhythmias than those who consumed less than 250 mg/day of caffeine (Hadeed & Siegel, 1993).
HYPOTENSIVE EPISODE: Cardiovascular collapse following massive overdose has been reported in adults (Josephson & Stine, 1976; Rouse et al, 1999), but may not occur in infants due to their ability to better tolerate tachycardia with decreased propensity to cardiac ischemia (Anderson et al, 1999).
TACHYPHYLAXIS: Continued administration of caffeine resulted in complete tolerance to blood pressure and heart rate changes in 1 to 4 days (Ellenhorn & Barceloux, 1988). Some studies maintain that caffeine does not produce a persistent increase in blood pressure (Myers, 1988; Newcombe et al, 1988).
CARDIAC ARREST: Cardiac arrest, occurring within one hour of massive ingestions, has been reported. In 2 cases, a 20-year-old man and a 40-year-old man ingested 18 g and 22 g, respectively, and developed cardiac arrest within an hour (Rouse et al, 1999).

DERMATOLOGIC

SKIN NECROSIS OF NEWBORN: Skin necrosis developed in a 31-week-gestation neonate who received an estimated 300 mg of caffeine by an IV line that extravasated (Anderson et al, 1999).

FLUID ELECTROLYTE

HYPOKALEMIA: Caffeine may directly produce hypokalemia by activation of sodium-potassium ATPase membrane pumps, as is seen in theophylline intoxication. Hypokalemia has also been reported after massive oral ingestions (Vaglio et al, 2011; Rudolph & Knudsen, 2010; Kapur & Smith, 2009).

GASTROINTESTINAL

GASTRITIS: Excessive consumption produces marked gastric irritation, nausea, and emesis (Schmidt & Karlson-Stiber, 2008; Price & Fligner, 1990; Dietrich & Mortensen, 1990). In very severe caffeine intoxication, gastrointestinal hemorrhage can develop.
NAUSEA AND VOMITING: According to a retrospective analysis of clinical data from adult patients who presented to the Royal Infirmary of Edinburgh from January 2000 to December 2008 with acute caffeine poisoning (n=38), nausea and vomiting was the most common adverse event, occurring in 63.2% of patients. The median amount of caffeine ingested was 1040 mg (range, 600 to 1500 mg) (Waring et al, 2009).
ABDOMINAL PAIN: According to a retrospective analysis of clinical data from adult patients who presented to the Royal Infirmary of Edinburgh from January 2000 to December 2008 with acute caffeine poisoning (n=38), abdominal pain was reported in 42.1% of patients. The median amount of caffeine ingested was 1040 mg (range, 600 to 1500 mg) (Waring et al, 2009).

HEMATOLOGIC

LEUKOCYTOSIS has been reported following overdose ingestions of caffeine (Trabulo et al, 2011; Kapur & Smith, 2009; Forman et al, 1997; Chopra & Morrison, 1995).

MUSCULOSKELETAL

RHABDOMYOLYSIS: Massive caffeine overdose may result in rhabdomyolysis and secondary renal failure (Campana et al, 2014; Ernest et al, 2010; Kamijo et al, 1999; Anderson et al, 1999).

NEUROLOGIC

RESTLESSNESS: According to a retrospective analysis of clinical data from adult patients who presented to the Royal Infirmary of Edinburgh from January 2000 to December 2008 with acute caffeine poisoning (n=38), dizziness, tremor, and headaches were each reported in 3 patients (7.9%), and agitation was reported in 1 patient (2.6%). The median amount of caffeine ingested was 1040 mg (range, 600 to 1500 mg) (Waring et al, 2009).
SEIZURES may occur with large doses (Rouse et al, 1999; Shum et al, 1997).
HEADACHE: Following ingestion of large doses of caffeine headache has been reported(Waring et al, 2009).
OPISTHOTONUS: After a 10-fold overdose in a premature infant opisthotonus has been reported (Perrin et al, 1987).

PSYCHIATRIC

DELIRIUM: Caffeine has been associated with delirium and psychosis (Kamijo et al, 1999; Ellenhorn & Barceloux, 1988).
PSYCHOTIC DISORDER: Caffeine has been associated with delirium and psychosis (Kamijo et al, 1999; Ellenhorn & Barceloux, 1988).

RESPIRATORY

APNEA: Acute ingestions of a large quantity of caffeine has been associated with respiratory arrest and subsequent death (Turner & Cravey, 1977).

VITAL SIGNS

FEVER: Fever has been noted following large doses (Perrin et al, 1987).
INCREASE IN PULSE: INCIDENCE: According to a retrospective analysis of clinical data from adult patients who presented to the Royal Infirmary of Edinburgh from January 2000 to December 2008 with acute caffeine poisoning (n=38), heart rate greater than 100 beats per minute occurred in 52.6% of patients. The median amount of caffeine ingested was 1040 mg (range, 600 to 1500 mg) (Waring et al, 2009).

CHRONIC CLINICAL EFFECTS

WITH POISONING/EXPOSURE

Caffeine is a CNS stimulant. Most voluntary exposures to caffeine in foods occur on a chronic basis. Excessive caffeine intake may cause flushing or chills, loss of appetite, irritability, anxiety, headache, dizziness, weakness, tremor, vomiting, fever, chills, seizures, tachycardia, cardiac arrhythmias, coma, and death (Abbott, 1986; Ellenhorn & Barceloux, 1988; Baselt & Cravey, 1989).
Urticaria has been associated with caffeine use (Pola et al, 1988). Ingestion of caffeine or coffee results in increased gastric acid and pepsin secretion and a decrease in the lower esophageal sphincter pressure.
Neurobehavioral effects associated with caffeine use include clearer thoughts, reduced drowsiness, sustained intellectual activity, decreased reaction time, and increased psychomotor activity (Lewin, 1994). It remains unclear whether caffeine improves performance or simply reverses the effects of caffeine withdrawal (Rogers & Dernoncourt, 1998; James, 1998).
Hypokalemia has been reported in a pregnant woman with a history of long-term cola consumption (Matsunami et al, 1993) and in a woman with excessive coffee consumption (Rudy & Lee, 1988). Results of a case-control study in women suggested that heavy coffee consumption increases the risk of myocardial infarction among both smokers and nonsmokers (Palmer et al, 1995).
Habitual users may develop a tolerance to the effects of caffeine, which may gradually lead to increased usage (Abbott, 1986). Withdrawal effects are reported in both adults (Phillips-Bute & Lane, 1997; Rogers & Dernoncourt, 1998) and children (Bernstein et al, 1998). These effects probably serve to perpetuate caffeine use (Rogers & Dernoncourt, 1998; Schuh & Griffiths, 1997).
Symptoms resulting from abrupt withdrawal of caffeine in long-term users may include headache, irritability, an inability to work effectively, nervousness, restlessness, lethargy, drowsiness, yawning, nausea, rhinorrhea, and depression (Abbott, 1986; Bruce, 1990; Lewin, 1994).
Headache, hemihypesthesia, and cerebral edema were associated with caffeine withdrawal in a patient who underwent surgery (Hampl et al, 1994).

ANIMAL STUDIES: Large doses have caused gastric mucosal erosions in experimental animals (Abbott, 1986; Lewin, 1994).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

EMESIS NOT RECOMMENDED

Pre-hospital decontamination should be avoided. Mild exposures do not require treatment, and severe overdose can result in seizures and aspiration.

ACTIVATED CHARCOAL

PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION

Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).

In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).

CHARCOAL DOSE

Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).

Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).

ADVERSE EFFECTS/CONTRAINDICATIONS

Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

ADULT

A single 1-g dose of caffeine may cause confusion, tremors, tachycardia, pyrexia, vomiting and diarrhea; whereas a lethal dose in an adult is estimated to range between 150 to 210 mg/kg (Peters, 1967; Holmgren et al, 2004). Death was reported after ingestion of 6.5 g in an adult (Alstott et al, 1973) , 18 g in a 19-year-old woman (McGee, 1980), and 10 g in a 21-year-old woman (Rudolph & Knudsen, 2010).
Blood caffeine levels in excess of 80 mcg/mL (8 mg/100 mL) have been associated with death; however, the minimum toxic or lethal dose is not well-established due to inter-patient variability, tolerance, and/or preexisting disease states (Rehrig, 1982).
CASE REPORT: Following an overdose of 20 g of caffeine, a 32-year-old woman experienced multiple seizures during gastric lavage with subsequent cardiac arrest; resuscitation was unsuccessful (Shum et al, 1997).
CASE REPORT: A 20-year-old man ingested 18 g of caffeine and experienced cardiac arrest within one hour of the ingestion. Following resuscitation, his condition declined over the next 8 hours with resultant recurrent ventricular fibrillation refractory to therapy. A normal myocardium was seen on autopsy (Rouse et al, 1999).
CASE REPORT: Ventricular fibrillation and subsequent cardiac arrest occurred in a 44-year-old man after intentionally ingesting 10 grams of pure anhydrous caffeine. Following 30 minutes of cardiopulmonary resuscitation, the patient remained in refractory ventricular fibrillation, and arterio-venous extracorporeal membrane oxygenation (ECMO) was started approximately 2 hours later. Despite efforts, the patient died 13 hours post-ingestion (approximately 4 hours after ECMO) (Poussel et al, 2013).
CASE REPORT: A 25-year-old woman died after consuming 0.7 liters of vodka and approximately 4 to 5 cans of an energy drink containing caffeine. An empty bottle containing dietary supplement capsules, with each capsule consisting of 300 mg caffeine, as well as a variety of natural sources of caffeine, including green tea leaves, yerba mate fruits, guarana seeds, and kola nut seeds, was also found at her bedside. An autopsy revealed internal organ congestion, pulmonary and cerebral edema, degeneration of the liver, and aspiration of gastric contents. Analysis of the patient's blood and body tissues estimated the ingested dose of caffeine to be 8.3 grams (Jantos et al, 2013).
CASE REPORT: A 39-year-old man was found dead at the front door of his residence. A dried white fluid was observed on the man's shirt as well as inside of his vehicle, and an opened container of caffeine anhydrous powder and an empty plastic drink container were also found in the vehicle. Autopsy results revealed pulmonary edema and congestion, and his blood caffeine level was 350 mg/L. Following analysis of the bag contents, it was believed that 22 g of 100% pure anhydrous caffeine had been mixed with a drink for consumption, and that, given the amount of white fluid found on the man and in his vehicle, approximately 50% to 60% of the initial oral dose had been retained after ingestion, suggesting an oral dose of 10 to 12 grams of pure caffeine had been ingested (Jabbar & Hanly, 2013).

PEDIATRIC

CASE REPORT: A 15-year-old girl experienced sinus tachycardia with multiple premature ventricular contractions and occasional bigeminy after ingestion of 80 tablets of an unknown strength of caffeine. Seizures developed abruptly with subsequent cardiac arrest and death (Shum et al, 1997).

MAXIMUM TOLERATED EXPOSURE

ADULT

SUMMARY: Patients have survived after ingestion of 1 g to 105 g of caffeine (Holstege et al, 2003; Stillner et al, 1978; Benowitz et al, 1982; Nagesh & Murphy, 1988). Two separate individuals, each ingesting 20 g caffeine, survived, but one suffered from myocardial infarction and the other developed complex dysrhythmias (Forman et al, 1997; Chopra & Morrison, 1995).
CASE REPORT: A 41-year-old woman made a complete recovery following a 50 g overdose. Initially, the patient developed several different dysrhythmias (eg, wide complex tachydysrhythmia, ventricular fibrillation, bradyarrhythmia, and asystole) and hypotension (systolic blood pressure in the 50s by doppler only), but responded to vasopressin infusion and hemodialysis. Within 24 hours of admission, the patient was hemodynamically stable, but had a protracted ICU course after developing bilateral pneumonia, rhabdomyolysis, and multisystem organ failure (Holstege et al, 2003).
CASE REPORT: A 40-year-old man survived a 22 g caffeine overdose. Within an hour of ingestion, he experienced seizures and pulseless ventricular tachycardia, which responded to cardiac resuscitation. He recovered following symptomatic therapy and was discharged 6 days postingestion (Rouse et al, 1999).
CASE REPORT: After ingesting 10 to 20 g of caffeine, an 18-year-old man developed irregular narrow complex tachycardia, sinus bradycardia, and pulseless wide complex rhythm that auto-converted (Kapur & Smith, 2009).
CASE REPORT: A 39-year-old man developed severe hypokalemia (1.8 mmol/L) and rhabdomyolysis after ingesting, over a 3-day period, 14,400 mg ibuprofen, 922 mg codeine, and 1920 mg caffeine. The patient recovered with potassium replacement and supportive care (Ernest et al, 2010).
CASE REPORT: A 27-year-old man, with schizophrenia successfully controlled with antipsychotics, developed irritability and recurrent paranoid thoughts after consuming 2 60-mL energy drinks. Each energy drink contained 200 mg of caffeine plus 48 mg guarana (another source of caffeine). One week later, after consuming 3 60-mL energy drinks (at least 600 mg caffeine [4.8 mg/kg]) within 15 minutes, he developed mood swings (initially laughing and talkative, followed by restlessness, withdrawn, and argumentative), tachycardia, insomnia, and paranoid thoughts that continued for the next several hours. The patient recovered with supportive care and remained stable after discontinuing consumption of energy drinks (Menkes, 2011).
According to a retrospective analysis of clinical data from adult patients who presented to the Royal Infirmary of Edinburgh from January 2000 to December 2008 with acute caffeine poisoning (n=38), nausea and vomiting, abdominal pain, dizziness, tremors, headache, agitation, tachycardia, and hypertension occurred after a median ingestion of 1040 mg of caffeine (range, 600 to 1500 mg) (Waring et al, 2009).
CASE REPORT: Acute renal failure, rhabdomyolysis, and elevated liver enzymes were reported in a 42-year-old man after intentionally ingesting 24 g of caffeine 4 days earlier. Laboratory data revealed a BUN of 167 mg/dL, a serum creatinine concentration of 10.2 mg/dL, a creatinine phosphokinase concentration of 59,360 units/L, an ALT of 367 units/L, and an AST of 694 units/L. With supportive therapy, including daily hemodialysis sessions for 9 days, the patient's condition improved and he was transferred for inpatient psychiatric therapy (Campana et al, 2014).
CASE REPORT: A 32-year-old man intentionally ingested 156 caffeine tablets (15.6 g of caffeine) and presented to the emergency department, approximately 1.5 hours later, with sinus tachycardia (116 beats/min). Arterial blood gas revealed mild metabolic acidosis, and his plasma caffeine level was 237 mg/L. Approximately 2 hours postingestion, he developed tonic-clonic seizures, managed with benzodiazepines, and, 0.5 hours later, ventricular tachycardia occurred. Despite administration of lidocaine and magnesium, his ventricular tachycardia persisted, and combined hemodialysis and hemoperfusion therapy was performed approximately 4 hours postingestion. Within 0.5 hours of initiating the combined therapy, his ventricular tachycardia improved with complete resolution within 2 hours. At the end of therapy, the patient's caffeine plasma level was 150 mg/L. Following observation, the patient made a complete recovery without further cardiac symptoms (Ishigaki et al, 2014).
CASE REPORT: A 44-year-old woman presented to the emergency department with nausea, vomiting, palpitations, chest tightness, muscle twitching, and tea-colored urine approximately 6 hours after ingesting 4 cups of black coffee (approximately 1000 mL). Monitoring of vital signs indicated a heart rate of 110 beats/min, blood pressure of 136/92 mmHg, a respiration rate of 20 breaths/minute, temperature of 36.2 degrees C, and an oxygen saturation of 99% on room air. Initially, her laboratory values were normal, with the exception of a mild elevation of hepatic enzymes (AST 45 units/L [reference range 0 to 40 units/L], ALT 108 units/L [reference range 0 to 41 units/L]). However, after 4 hours of observation and administration of IV fluids, repeat laboratory analysis revealed creatine kinase (CK) and CK-MB concentrations of 7315 units/L (reference range 26 to 308 units/L) and 266 units/L (reference range 0 to 25 units/L), respectively. Her initial plasma caffeine concentration was estimated to be 16 mcg/mL (taking into account that the actual plasma caffeine concentration, obtained 10 hours post-ingestion was 4 mcg/mL and the average half-life of caffeine is 5 hours). With continued supportive care for 5 days, the patient completely recovered without neuromuscular sequelae (Chiang et al, 2014).

PEDIATRIC

Patients have survived after ingestions ranging from 78 mg/kg up to 912 mg/kg. Symptoms included arrhythmias, seizures, pulmonary edema, hypertension, and metabolic disturbances (Mace, 1978; Rowland & Mace, 1976; Perrin et al, 1987; Dietrich & Mortensen, 1990; Fligner & Opheim, 1988).
CASE REPORT: A 17-year-old girl developed nausea, vomiting, tremor, anxiety, hyperventilation, hypokalemia (2.4 mmol/L), and an elevated plasma lactate level of 7 mmol/L with a concomitant decrease in pH to 7.33 after intentionally ingesting 12 g of caffeine (266 mg/kg). The patient recovered with supportive care (Schmidt & Karlson-Stiber, 2008).
CASE REPORT: A 13-year-old boy became agitated and aggressive, and developed sinus tachycardia, tachypnea, hypertension, increased diuresis, dysuria, and paresthesia of the legs following consumption of 2 packets of stimulant ("energy") chewing gum within a 4-hour period. Each packet reportedly contained 160 mg caffeine (0.57% caffeine per gum pellet). With supportive care, the patient recovered (Natale et al, 2009).

INFANT

CAFFEINE CITRATE

GENERAL: Premature infants receiving caffeine citrate have developed toxicity following inadvertent excessive exposure. Following overdose, serum caffeine levels have ranged from approximately 24 mg/L (increased irritability and poor feeding reported) to 350 mg/L, and serious toxicity has been associated with serum levels greater than 50 mg/L (Prod Info Cafcit, 2001).
CASE REPORT: A premature infant received 600 mg caffeine citrate (approximately 322 mg/kg) over 40 minutes, and developed tachycardia, ST depression, respiratory distress, heart failure, gastric distention, acidosis, and a severe extravasation burn with tissue necrosis at the peripheral intravenous injection site (Prod Info Cafcit, 2001).
CASE REPORT: A 32-week premature male (born at 28 weeks) received an inadvertent 300 mg/kg dose (intended dose 3 mg/kg) of caffeine, and developed typical symptoms of acute toxicity (ie, dehydration, tachycardia, electrolyte disturbances, and metabolic acidosis). Following supportive care, laboratory and clinical symptoms normalized within 96 hours; no permanent sequelae was reported (Ergenekon et al, 2001).
CASE REPORT: An IV overdose of 160 mg/kg occurred in a 31-week gestation, 1860-g neonate (estimated dose, 300 mg over 40 minutes) with clinical effects of hyperglycemia, cardiac failure, and gastric dilatation. Resolution of toxic symptoms occurred on days 6 and 7 and were correlated with a drop in serum caffeine concentrations to 60 to 70 mg/L (Anderson et al, 1999).

OTHER

COINGESTION

The combination of caffeine and phenylpropanolamine will result in pharmacologic additive action of each drug (Ekins & Spoerke, 1983).
A 5-month study of 19 patients aged 9 months to 2 years reported that an average total dose of 460 mg (40 mg/kg) caffeine resulted in symptoms; all of these cases involved coingested phenylpropanolamine (average 10.5 mg/kg) (Ekins & Spoerke, 1983).

Carcinogenicity Ratings for CAS58-08-2 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
EPA (U.S. Environmental Protection Agency, 2011): Not Listed
IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Caffeine

3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
MAK (DFG, 2002): Not Listed
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS58-08-2 (U.S. Environmental Protection Agency, 2011):

Not Listed

TOXICITY VALUES

LD50- (ORAL)DOG:
- 140 mg/kg (RTECS, 2004)
LD50- (SUBCUTANEOUS)DOG:
- 100 mg/kg (RTECS, 2004)
LD50- (ORAL)GUINEA_PIG:
- 230 mg/kg (RTECS, 2004)
LD50- (ORAL)HAMSTER:
- 230 mg/kg (RTECS, 2004)
LD50- (INTRAPERITONEAL)MOUSE:
- 168 mg/kg (RTECS, 2004)
LD50- (INTRAVENOUS)MOUSE:
- 62 mg/kg (RTECS, 2004)
LD50- (ORAL)MOUSE:
- 127 mg/kg (RTECS, 2004)
LD50- (SUBCUTANEOUS)MOUSE:
- 242 mg/kg (RTECS, 2004)
LD50- (INTRAVENOUS)RABBIT:
- 58 mg/kg (RTECS, 2004)
LD50- (ORAL)RABBIT:
- 224 mg/kg (RTECS, 2004)
LD50- (INTRAPERITONEAL)RAT:
- 240 mg/kg (RTECS, 2004)
LD50- (INTRAVENOUS)RAT:
- 105 mg/kg (RTECS, 2004)
LD50- (ORAL)RAT:
- 192 mg/kg (RTECS, 2004)
LD50- (SUBCUTANEOUS)RAT:
- 170 mg/kg (RTECS, 2004)

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS58-08-2 (American Conference of Governmental Industrial Hygienists, 2010):

Not Listed

AIHA WEEL Values for CAS58-08-2 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS58-08-2 (National Institute for Occupational Safety and Health, 2007):

Not Listed

OSHA PEL Values for CAS58-08-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS58-08-2 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS58-08-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS58-08-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS58-08-2 (U.S. Environmental Protection Agency, 2010b):

Not Listed
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS58-08-2 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS58-08-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Not Listed

DOT List of Marine Pollutants for CAS58-08-2 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS58-08-2 (EPA, 2005):

Listed as: 1H-Purine-2,6-dione, 3,7-dihydro-1,3,7-trimethyl-

LABELS

NFPA

NFPA Hazard Ratings for CAS58-08-2 (NFPA, 2002):

Not Listed

-PERSONAL PROTECTION

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 58-08-2.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS58-08-2 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

Editor's Note: An ERG guide with information appropriate to this material does not exist.

NFPA Extinguishing Methods for CAS58-08-2 (NFPA, 2002):

Not Listed

EVACUATION PROCEDURES

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

AIHA ERPG Values for CAS58-08-2 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS58-08-2 (U.S. Department of Energy, Office of Emergency Management, 2010):

Not Listed

AEGL Values for CAS58-08-2 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS58-08-2 (National Institute for Occupational Safety and Health, 2007):

Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

Editor's Note: An ERG guide with information appropriate to this material does not exist.

SMALL LEAK/SPILL

Editor's Note: An ERG guide with information appropriate to this material does not exist.

LARGE LEAK/SPILL

Editor's Note: An ERG guide with information appropriate to this material does not exist.

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

CAFFEINE CITRATE: 386.31 (Prod Info CAFCIT(R) IV injection, oral solution, 2008)

DESCRIPTION/PHYSICAL STATE

Caffeine is an odorless, crystalline powder or granule with a bitter taste that is sparingly soluble in water and ethanol at room temperature (Prod Info CAFCIT(R) IV injection, oral solution, 2008).

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