St John’s wort, derived from the flowering tops of the perennial plant Hypericum perforatum native to Europe and Asia, was brought to North America by European settlers. According to legend, the eponymous St John’s wort arose from the head of John the Baptist after his beheading. Patients may use this herb for its anxiolytic, sedative, bronchodilatory, and antidepressant effects, and as an analgesic for peptic ulcer disease and hemorrhoids [6]. Hyperforin and hypericin are believed to be 2 of the principal active constituents of St John’s wort responsible for its beneficial effects [7]. St John’s wort is available in a variety of preparations to treat various ailments. The suggested dose to treat depression is 300 mg, standardized to 0.3% hypericin, taken orally 3 times daily for 4 to 6 weeks; alternatively, a tea can be brewed from 2 to 4 g of the herb in 1 to 2 cups of water [7].

The mechanism of action of St John’s wort remains unknown, as in vitro and in vivo studies have reached different conclusions: in vitro studies demonstrate inhibition of monoamine oxidase isoforms, whereas in vivo studies demonstrate inhibition of γ-aminobutyric acid (GABA) receptors [8]. The antidepressant effects of the herbal may be a result of GABA inhibition. The potential for undesired side effects with concomitant administration of monoamine oxidase inhibitors (MAOIs), amphetamines, selective serotonin reuptake inhibitors (SSRIs), trazodone, tricyclic antidepressants, narcotics, and cold and flu medications exists [9]. Furthermore, St John’s wort has been implicated in one case of hypertensive crisis in a 41-year-old psychiatric patient [10].

Interactions with β-sympathomimetic agents such as Ma Huang or pseudoephedrine may instigate a hypertensive crisis. St John’s wort, when taken in combination with other SSRIs such as fluoxetine or paroxetine, may cause serotonergic syndrome, which is manifested by tremors, hyperthermia, autonomic dysfunction, hallucinations, myoclonus, and possibly death [11,13]. Photosensitivity is another common side effect of St John’s wort, therefore caution is advised when administering other drugs, such as tetracycline and piroxicam, which have similar adverse effects. In addition, caution is advised with patients concurrently using MAOIs. Further research is needed to elucidate the exact interactions and effects, but caution and awareness should be the rule in the perioperative period.

Echinacea is produced from the dried roots and rhizomes of the Echinacea angustifolia or Echinacea pallida plants. Fresh juice, made from the nonroot portions of the Echinacea purpurea plant, is also available [6]. Patients commonly take this herbal supplement to treat the following ailments: abscesses, eczema, burns, liver cancer [13], colorectal cancer [14], upper respiratory tract infections, urinary tract infections, varicose leg ulcers, and skin wounds [6].

The recommended dosage of echinacea is 6 to 9 mL of juice daily, or 900 to 1000 mg of powder orally 3 times daily, or 0.75 to 1.5 mL of tincture orally 2 to 5 times daily. In addition, echinacea can be brewed as a tea using 4 g of herb brewed in boiling water for 10 minutes. Using echinacea for 10 to 14 days is thought to provide maximal benefit; experts recommend taking this herb for no longer than 8 weeks, as the immune enhancing effects may be decreased by this time [6].

Certain patient populations may not benefit from echinacea therapy: individuals infected with human immunodeficiency virus, patients with AIDS, patients with collagen vascular disease, and patients suffering from multiple sclerosis (echinacea stimulates the immune system [14], therefore autoimmune diseases that are treated with immunosuppressant drugs may have a negative interaction with echinacea).

Echinacea is an inhibitor of the cytochrome P-450 3A4 hepatic microsomal system, one of the key metabolic enzyme pathways involved in drug metabolism. This effect can become a concern in patients concomitantly taking drugs that are metabolized by this system, including phenytoin, rifampin, rocuronium, and local anesthetics; caution is advised because there may be prolonged clinical effects of these agents [15]. Awareness of this interaction is important for anesthesia providers.

Prized by Chinese herbalists for centuries, Western interest in ginkgo as a nonpharmacologic treatment of Alzheimer disease has intensified lately as more and more people have become interested in alternative medicines and therapies [16]. Ginkgo extract is derived from the leaves of the kew tree, also known as the maidenhair tree or Ginkgo biloba tree. Patients use Ginkgo to treat such ailments as asthma, dementia, hearing loss, SSRI-induced erectile dysfunction, memory loss, and senile macular degeneration, and to enhance alertness [6]. In France and Germany, ginkgo is among the leading prescriptions for poor circulation and dementia, whereas in the United States ginkgo is available only as an over-the-counter dietary supplement [6]. Ginkgo is among the most popular herbal supplements in the United States, with sales exceeding $150 million [17].

Commonly recommended dosages of ginkgo are, for dementia, 120 to 240 mg orally twice to thrice daily and for poor leg circulation, vertigo, or tinnitus, 120 to 160 mg orally twice to thrice daily [6].

Awareness of possible adverse effects of ginkgo is imperative for the anesthesiologist, as ginkgo is the third best-selling herbal product in the United States [15]. Although relatively safe, possible untoward effects of the herb include nausea, vomiting [18], headache, seizures, and increased risk of bleeding (the maximum recommended dose is 240 mg thrice a day). Furthermore, several case reports detailing morbidities of ginkgo exist: subarachnoid hemorrhage, subdural hematoma, and hyphema [19–22]. The additive effects of ginkgo with aspirin, warfarin, enoxaparin, heparin, abciximab, and other anticoagulant and antiplatelet agents may contraindicate neuraxial anesthetic techniques, as clotting ability may be unpredictable. The terpene lactone components of ginkgo (ginkgolides) inhibit blood clotting via inhibition of platelet aggregation [21,23]. Perioperative physicians may better assess the degree to which a patient is anticoagulated using platelet function analysis and/or coagulation studies. Common drug interactions include a decreased efficacy of anticonvulsants when administered with ginkgo [23]. Also, the seizure threshold is lowered in patients taking tricyclic antidepressants with ginkgo [23]. It is recommended that gingko be discontinued 36 hours before surgery to decrease the risk of side effects [24].

Saw palmetto is harvested from the brown-black berries of the American dwarf palm, Serenoa repens/Sabal serrulata. Historically, saw palmetto was listed as a treatment for genitourinary tract ailments in the National Formulary from 1906 to 1950 [6]. At present, patients use saw palmetto to treat benign prostate hypertrophy (BPH), to decrease gynecomastia [6], to improve libido, to increase sperm production, and to reduce fluid retention.

The recommended dose of the available preparations for BPH is 320 mg orally in 2 equal doses, continued for 3 months [6].

Possible concerns for the anesthesiologist and perioperative physician include an elevation in blood pressure and a theoretical potentiation of blood-thinning agents [6].

Garlic, botanically known as Allium sativum, is one of the most studied medicinal herbs. The use of garlic to treat various maladies has been traced back not only to the ancient China but also to western Europe [25]. Supplements of garlic are prepared from either dried cloves that have been crushed into powder or are made from garlic oil. Of note, products that claim to be “odor-free” may lack medicinal value, because it appears that the beneficial effects of garlic come from the sulfur-containing allicin, the chemical that imparts garlic with its distinctive aroma [6]. Garlic has been used to treat asthma, tinea pedis, constipation, diabetes, fungal infection, heavy-metal poisoning, hypertension, and hypercholesterolemia [6].

The commonly recommended dose of garlic for treating elevated cholesterol is 600 to 900 mg orally once daily [6]. Alternatively, 4 g of fresh garlic or 8 mg of garlic oil can be taken. The World Health Organization (WHO) 1999 monograph recommends these doses: 2 to 5 g fresh garlic, 0.4 to 1.2 g dried powder, 2 to 5 mg oil, 300 to 1000 mg extract, or any other formulation containing 2 to 5 mg allicin [6]. The formulation of garlic most often used in clinical trials is Kwai (Lichtwer Pharma, Köln, Germany); it is available as a nonenteric-coated dehydrated garlic powder formulation standardized for 1.3% allicin.

Garlic impairs platelet aggregation and has been associated with reports of bleeding. Based on this fact it should be used cautiously, if at all, in patients with peptic ulcer disease or intracranial bleeding, and in patients receiving concurrent antiplatelet or anticoagulation therapy or nonsteroidal anti-inflammatories, or with other drug-related hemostatic issues [26]. There is a case report of a spontaneous spinal/epidural hematoma in a patient using excessive amounts of garlic [27]. Other important adverse effects of garlic include dizziness, nausea, asthma exacerbations, hypothyroidism, and exacerbation of gastroesophageal reflux disease [6].

Garlic’s effect on platelet aggregation is complex and is caused by several mechanisms: garlic reduces thromboxane formation from arachidonic acid, inhibits phospholipase activity, and inhibits the incorporation of arachidonate into platelet phospholipids [28,29].

The anesthesiologist caring for patients being treated with garlic therapy should be especially cognizant for surgical hemostasis. Physicians should be vigilant perioperatively for the possibility of excessive bleeding both intra- and postoperatively [28]. Furthermore, garlic has been reported to interact with the P450 enzyme system [30], which also may affect concomitant drug metabolism.

Although ginger, Zingiber officinale, has attractive purple-green flowers, herbalists value its root more than any other part of the plant. Ginger may be used to treat common ailments such as arthritis, motion sickness, nausea, muscle pain and swelling, and bacterial infections, due to its property as an antioxidant [6]. In addition, ginger has been demonstrated to be an effective cure for hyperemesis gravidarum in the obstetric population [31].

The dose of ginger depends on indication: the dose for nausea is powdered ginger 500 to 1000 mg orally, or fresh ginger root 1000 mg orally [6].

Despite the possible benefits of ginger therapy, certain concerns exist with the excessive intake of this agent. Ginger is a potent inhibitor of thromboxane synthetase. and may also interfere with platelet aggregation [32,33]; therefore, intake of ginger may increase bleeding time [34] and other tests that evaluate platelet function. In a patient with a history of bleeding or bruising, anesthesiologists should consider evaluating alteration in platelet function status before proceeding with a neuraxial or regional anesthetic technique. Ginger has been implicated as a source of arrhythmia, drowsiness, and excessive sedation, side effects of which perioperative physicians should be aware [6].

For over 2000 years, ginseng has been used in traditional Asian medicine to treat such ailments as depression, diabetes, hypertension, fluid retention, overactive thymus, and insomnia. Ginseng has also been used as an aphrodisiac, as a sedative, and to enhance the body’s stress response [6]. Commercially prepared American ginseng is extracted from the Panax quinquefolius plant, and Asian (Korean and Japanese) varieties are derived from the Panax ginseng plant. The Asian variety undergoes more post-harvest processing to isolate the extract and, because of this, it is more sought after for its medicinal properties. The recommended dose of ginseng is 0.5 to 2 g of dry ginseng root daily, or 200 to 600 mg of ginseng extract daily in 2 divided doses [6].

Ginseng has adaptogenic properties, augmenting adrenal steroid production via a central mechanism [35]. Hypoglycemic properties of ginseng are believed to be due to ginsenoside Rb2 and panaxans I, J, K, and L [36–40]. Ginseng has been known to cause the following adverse effects: impotence, hypertension, chest pain, headache, blurred vision, epistaxis [41], insomnia, nausea, vomiting, nervousness, tachycardia, and vaginal bleeding.

Ginseng abuse syndrome is caused by the combination of ginseng with other stimulants, resulting in diarrhea, hypertension, restlessness, insomnia, depression, poor appetite, swelling, and unusual sense of well-being [6]. Ginseng, oral hypoglycemics, and insulin may interact synergistically [6]; blood glucose levels should be assessed perioperatively. The possibility of an acute manic episode exists when patients undergoing MAOI treatment use ginseng because of the additive effects of ginseng and the MAOIs [42,44]. For the anesthesiologist, it is important to be aware of the hypertensive effects of ginseng as well as its antiplatelet properties. Because many anesthetic agents themselves cause hemodynamic instability, the added variable of ginseng may make hemodynamic management challenging. It has been recommended that ginseng should be discontinued at least 1 week before surgery [45].

Siberian ginseng, Eleutherococcus senticosus, belonging to the same family as panax or Asian ginseng, is used as a treatment for inflammation and insomnia due to anxiety, and to improve exercise tolerance, regulate blood pressure, and stimulate the circulatory and immune systems. The recommended dose is 500 to 2000 mg orally, daily for no more than 3 weeks [6].

Possible adverse effects of Siberian ginseng include diarrhea, difficulty in concentrating, dizziness, hypertension, nervousness, and an unusual sense of well-being. Siberian ginseng has an adverse interaction with digoxin, barbiturates, and vitamins B1, B2, and C. Siberian ginseng, just as American and Asian ginseng, has a potent hypoglycemic effect [6]. Blood glucose levels should be ascertained before any procedure.

Ephedra is a herbal supplement that has been used in Chinese medicine to promote weight loss and to increase energy, and as a treatment for asthma and bronchitis [45]. Ephedra contains a combination of adrenergic alkaloids including ephedrine, pseudoephedrine, norephedrine, methylephedrine, and norpseudoephedrine [46]. Ephedrine is a noncatecholamine sympathomimetic agent with α-1, β-1, and β-2 activity acting at adrenergic receptors and releasing endogenous norepinephrine [45]. Patients chronically taking ephedra may be catecholamine depleted. Although ephedrine is safely administered by trained anesthesiologists intraoperatively as perioperative therapy for hypotension, unsupervised use by untrained laypersons is potentially dangerous because of the possibility of vasospasm of coronary and cerebral arteries and other sympathomimetic effects, including myocardial infarction and thrombotic stroke [47]. In addition, ephedra has been implicated in hypersensitivity myocarditis characterized by cardiomyopathy with lymphocytic and eosinophilic infiltrates [48]. The elimination half-life of ephedra is 5.2 hours, with 70% to 80% of the herb excreted unchanged in the urine; therefore, it should be discontinued at least 24 hours before surgery [49,50].

Although now of historical significance due to the sporadic use of halothane anesthesia, special consideration should be paid to patients undergoing halothane general anesthesia, because halothane sensitizes the myocardium to exogenous catecholamines, and ventricular arrhythmias may develop [51]. Theoretically, a similar concern exists in patients taking ephedra who receive high doses of desflurane and experience an increase in circulating catecholamines. Furthermore, long-term ephedra use results in tachyphylaxis of its sympathomimetic effects secondary to depletion of endogenous catecholamine stores, which may contribute to perioperative hemodynamic instability. Therefore, direct-acting sympathomimetics are the preferred agents to treat hypotension and bradycardia in these circumstances [45].

Despite the FDA ban on the sale of supplements containing ephedra, this supplement is reported as being readily available from various international Web sites [52].

Tribesmen have traditionally used Hoodia gordonii, a cactus native to Southeastern Africa, during times of starvation to ease their hunger [53]. For the same reason, currently it is a popular weight loss supplement in the United States. Its pharmacologically active constituents include steroidal glycosides (P57AS3 or P57), and steroidal derivates: gordonosides, and calogenin glycosides [53]. MacLean and Luo [54] studied P57 isolated from hoodia, and determined in a rat model that cerebroventricular administration of P57 resulted in an increase in the adenosine triphosphate concentrations of hypothalamic neurons; this in turn was the hypothesized mechanism of appetite reduction. Human research is lacking, and there are few data concerning its efficacy or safety profile. P57 has also been shown to inhibit CYP3A4 activity, which may affect drug metabolism within the liver [55].

Green tea, Camellia sinensis, has been enjoyed in Asia for centuries and recently, green tea and its purified extract has been used in Western medicine as adjuvant treatment of obesity, hyperlipidemia, hypertension, and atherosclerosis [6]. Epigallocatechin-3-gallate (EGCG) is the principal active agent in green tea and is credited for providing an anticancer effect; it accounts for 40% of its total polyphenol content [56]. Other constituents of green tea that may affect the anesthetic management of patients include caffeine, theophylline, and proanthocyanidins (tannins) [57].

Specific doses of green tea to obtain maximal benefits have not been established, because most investigations have studied brewed green tea rather than an extract tablet (tablets vary from 100 to 750 mg of green tea extract) [58]. One cup of tea contains approximately 80 to 100 mg of polyphenols and approximately 50 mg of caffeine [58].

Most of the adverse effects of green tea are attributed to its caffeine content, therefore some experts recommend drinking decaffeinated green tea rather than green tea in its natural form. However, it is unknown whether decaffeinated tea has the same health benefits as natural green tea [59,60]. Caffeine is a central nervous system stimulant and a diuretic, increasing urine volume as well as urine sodium and potassium concentrations, thus potentially decreasing sodium and potassium concentrations in the blood. Furthermore, caffeine may worsen incontinence, may increase the production of stomach acid, and may exacerbate peptic ulcer symptoms [58]. Therefore, persons with concurrent advanced liver disease should use caffeine and green tea cautiously, as blood caffeine concentrations may accumulate [57]. In laboratory and animal studies, caffeine has been found to hinder blood clotting because it raises prothrombin time and partial thromboplastin time [58,59]. Furthermore, the tannins in green tea may reduce absorption and bioavailability of codeine, atropine, and iron supplements [44]. Use of green tea in infants has been associated with impaired iron metabolism and microcytic anemia [58]. Furthermore, the tannin content of green tea may inhibit the hemodynamic effects of adenosine [59].

Derived from either plant or fish sources, omega-3 polyunsaturated fatty acids are used primarily to treat elevated cholesterol levels. Typical dietary sources of these fatty acids include salmon, mackerel, sardines, albacore tuna, herring, soy, tofu, flax seed, walnuts, and canola oil. Because Alaskan and Greenland Inuits had favorable lipid profiles and a lower incidence of coronary artery disease as compared with non-Inuit cohorts, it was postulated that their diet, which is high in omega-3 fatty acids, was responsible for this difference. Subsequent studies addressing this fact demonstrated that people who ate fish weekly did in fact have lower mortality from coronary artery disease [61,62].

In the United States, 2 servings of fish per week is the current recommendation for people to reap the benefits of omega-3 fatty acids. It has been postulated that fish oils have several mechanisms of cardiac protection including antiarrhythmic effects, a reduction in serum triglyceride levels, decreased platelet aggregation, an anti-inflammatory effect via enhanced production of nitric oxide (endothelium-derived relaxing factor), and a modest decrease in blood pressure [63,64].

Although further study is necessary to validate these positive effects, many patients take fish oils for these perceived benefits, therefore knowledge of the effects of omega-3 oils is important for the anesthesiologist. Hemostasis can be an issue during surgery as well as planning for regional or neuraxial techniques. Coagulation studies should be obtained before any neuraxial or regional procedure in a patient who has a history of bleeding and bruising and concomitant use of omega-3 oils.

Kava kava has been a popular beverage in the South Pacific for its ability to induce a tranquil, euphoric state and for its sociable effects [65]. Historically, women chewed the leaves, mixing the chewed leaves with coconut milk or other fruit juices [6]. For children diagnosed with attention-deficit/hyperactivity disorder a liquid extract is given orally (1:1 weight/volume fresh plant or 1:4 weight/volume dry plant) in a recommended dose of 5 to 15 drops diluted in their favorite beverage 2 to 3 times daily. The adult dose for anxiety is 100 to 250 mg 1 to 3 times per day as needed, standardized to contain 30% kavalactones per dose. When used solely as a sleep aid, 250 to 500 mg at bedtime is the recommended dose [6].

Kava kava may cause hallucinations, dermopathy, and visual changes [66,68]. Kava kava can also produce antinociceptive effects mediated through nonopioid-dependent pathways [69,70]. In addition, anesthesiologists should be aware that the use of kava kava may potentiate barbiturates and benzodiazepines, leading to excessive sedation [71].

Valerian comes from the perennial plant Valeriana officinalis, which is native to Eurasia and cultivated worldwide. Valerian is used as a sleep aid, as treatment of muscle spasms (particularly in Europe), and to treat restlessness [6].

For sleep disorders, the recommended dosage is 400 to 900 mg of standardized valerian extract 30 to 60 minutes before bedtime. Doses greater than 2.5 g may result in liver injury [6].

Adverse effects of valerian include blurry vision, excitability, headache, insomnia, arrhythmia, and nausea. Producing dose-dependent sedation and hypnosis via GABA receptors, valerian may potentiate the effects of central nervous system depressants and sedative hypnotics [72].