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KOMBUCHA MUSHROOM TEA

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Kombucha mushroom tea is produced from a fermentation mixture (e.g., alcohol, ethyl acetate, various amino acids) of yeasts and bacteria prepared by incubating a starter culture in black tea and sugar.

Specific Substances

    1) Chombucha
    2) Combucha
    3) Chambuska
    4) Champagne of life
    5) Dr. Sklenar's Kombucha Mushroom Infusion
    6) Fungus japonicus
    7) Fungo-japon Kombucha
    8) Kombucha mushroom tea
    9) Kombucha tea
    10) Kargasok tea
    11) Kwassan
    12) Manchurian mushroom
    13) Manchurian tea
    14) Kvas
    15) Spumonto
    16) T'chai from the sea
    17) Tea fungus
    18) Tea sponge
    19) Tea wine
    20) Teekwas
    21) Tschambucco
    22) COMBUCHA TEA
    23) MANCHURIAN "FUNGUS"
    24) TEEKWASS
    25) THE SEA T'CHAI

Available Forms Sources

    A) USES
    1) The tea has been used in folk medicine to treat the following:
    1) Arthritis
    2) Cancer
    3) Impaired vision
    4) Decreased libidos
    5) Bronchitis and asthma
    6) Kidney illnesses
    7) Cataracts
    8) Cardiac illnesses
    9) Diabetes
    10) Diarrhea
    11) Gray hair
    12) Herpes
    13) Insomnia
    14) Hypertension
    15) AIDS
    16) Obesity
    17) Peptic ulcer
    18) Motion sickness
    19) Liver disorders
    20) Hemorrhoids

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Kombucha mushroom tea is produced from a fermentation mixture of yeasts and bacteria prepared by incubating a starter culture in black tea and sugar. The tea has been used in folk medicine to treat a variety of conditions such as cancer, impaired vision, decreased libido, asthma, cataracts, AIDS, diabetes, diarrhea, herpes, hypertension, and obesity. Contaminants may include molds, Aspergillus, Saccharomyces cerevisiae, and Candida valida.
    B) TOXICOLOGY: The toxicological mechanism of Kombucha mushroom tea has not been identified. Possibilities include infection by contaminants or accumulation of fermentation products.
    C) EPIDEMIOLOGY: Toxicity is very rare and has only been reported after chronic ingestion.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Rashes, anorexia, abdominal cramping, and fever may occur following the ingestion of Kombucha tea.
    2) SEVERE TOXICITY: Tachycardia, hypertension, metabolic acidosis, cardiovascular collapse, respiratory distress, and hepatotoxicity have also been reported in patients following chronic ingestion of Kombucha tea. An HIV-positive man developed shortness of breath, fever, lactic acidosis, acute renal failure, and mildly elevated liver enzymes after ingesting Kombucha tea. Cutaneous anthrax has been reported as a result of applying Kombucha mushroom to the skin.

Laboratory Monitoring

    A) Monitor vital signs, liver enzymes, and renal function.
    B) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.
    C) Obtain an ECG in symptomatic patients, and institute continuous cardiac monitoring.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate 1 to 2 mEq/kg.
    C) DECONTAMINATION
    1) PREHOSPITAL: Cases of toxicity reported to date have involved chronic ingestion of Kombucha tea. Prehospital gastrointestinal decontamination is generally not recommended.
    2) HOSPITAL: Cases of toxicity reported to date have involved chronic ingestion of Kombucha tea. GI decontamination is generally not warranted.
    D) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in patients with severe allergic reactions or respiratory distress.
    E) ANTIDOTE
    1) None
    F) HYPERSENSITIVITY REACTION
    1) MILD/MODERATE: Antihistamines with or without inhaled beta agonists, corticosteroids or epinephrine. SEVERE: Oxygen, aggressive airway management, antihistamines, epinephrine, corticosteroids, ECG monitoring, and IV fluids.
    G) ACUTE LUNG INJURY
    1) Supplemental oxygen; PEEP and mechanical ventilation may be needed.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    2) OBSERVATION CRITERIA: Patients with a deliberate overdose, and those who are symptomatic should be observed with frequent monitoring of vital signs. Patients that remain asymptomatic can be discharged.
    3) ADMISSION CRITERIA: Patients should be admitted for persistent cardiac dysrhythmias, metabolic acidosis, respiratory failure, and acute renal failure.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    I) PITFALLS
    1) Missing an ingestion of another agent or other possible etiologies for a patient’s symptoms. History of exposure may be difficult to obtain in some settings.
    J) DIFFERENTIAL DIAGNOSIS
    1) Includes other agents that cause hypertension, tachycardia, metabolic acidosis, or hepatotoxicity. Diseases or exposures that produce acute respiratory distress (eg, inhalation of acid or alkaline mists, asthma, COPD). Patients with underlying cardiac dysrhythmias or electrolyte imbalance may develop more severe symptoms.

Range Of Toxicity

    A) TOXICITY: The range of toxicity of Kombucha mushroom tea has not been established. The majority of case reports describe patients developing adverse effects following 2 weeks to 2 months of ingestion of 4 to 12 ounces of tea daily.

Clinical Effects

Summary Of Exposure

    A) USES: Kombucha mushroom tea is produced from a fermentation mixture of yeasts and bacteria prepared by incubating a starter culture in black tea and sugar. The tea has been used in folk medicine to treat a variety of conditions such as cancer, impaired vision, decreased libido, asthma, cataracts, AIDS, diabetes, diarrhea, herpes, hypertension, and obesity. Contaminants may include molds, Aspergillus, Saccharomyces cerevisiae, and Candida valida.
    B) TOXICOLOGY: The toxicological mechanism of Kombucha mushroom tea has not been identified. Possibilities include infection by contaminants or accumulation of fermentation products.
    C) EPIDEMIOLOGY: Toxicity is very rare and has only been reported after chronic ingestion.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Rashes, anorexia, abdominal cramping, and fever may occur following the ingestion of Kombucha tea.
    2) SEVERE TOXICITY: Tachycardia, hypertension, metabolic acidosis, cardiovascular collapse, respiratory distress, and hepatotoxicity have also been reported in patients following chronic ingestion of Kombucha tea. An HIV-positive man developed shortness of breath, fever, lactic acidosis, acute renal failure, and mildly elevated liver enzymes after ingesting Kombucha tea. Cutaneous anthrax has been reported as a result of applying Kombucha mushroom to the skin.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER: Fever (104.1 degrees F) developed in a 22-year-old HIV-positive man who also experienced shortness of breath, lactic acidosis, elevated liver enzymes, and acute renal failure within 15 hours of sharing a 1-L bottle of unpasteurized Kombucha tea with a friend. Following supportive care, he recovered within 36 hours of ingestion (Sunghee Kole et al, 2009).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 59-year-old woman required resuscitation due to cardiac arrest following ingestion of 4 ounces of Kombucha tea daily for two months prior to onset of fatigue and loss of consciousness. The patient also had intravascular coagulopathy, severe metabolic acidosis, and peritonitis, with pre-existing hypertension, anemia and mild renal insufficiency. Toxicology screens were negative. The patient died two days after hospitalization (CDC, 1995).
    b) CASE REPORT: A second patient presented in respiratory distress to the same emergency department one week later. She suffered cardiac arrest, with severe metabolic acidosis and pulmonary edema, but recovered with resuscitation and supportive treatment. The patient had ingested approximately 4 ounces of Kombucha tea daily for the preceding two months, increasing the quantity of tea ingested from 4 to 12 ounces and the incubation period of the tea from 7 to 14 days immediately prior to the onset of symptoms (CDC, 1995).
    c) Both patients had obtained their Kombucha "mushroom" from the same source. At least 115 others in the area had received Kombucha "mushroom" from the same source but none became ill (CDC, 1995).
    B) TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Tachycardia (heart rate 180 beats/min) and hypertension developed in a 22-year-old HIV-positive man who also experienced shortness of breath, fever, lactic acidosis, elevated liver enzymes, and acute renal failure within 15 hours of sharing a 1-L bottle of unpasteurized Kombucha tea with a friend. Following supportive care, he recovered within 36 hours of ingestion (Sunghee Kole et al, 2009).
    C) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Tachycardia and hypertension (BP 192/105 mm Hg) developed in a 22-year-old HIV-positive man who also experienced shortness of breath, fever, lactic acidosis, elevated liver enzymes, and acute renal failure within 15 hours of sharing a 1-L bottle of unpasteurized Kombucha tea with a friend. Following supportive care, he recovered within 36 hours of ingestion (Sunghee Kole et al, 2009).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 48-year-old woman developed respiratory distress and acute pulmonary edema following daily ingestion of 4 to 12 ounces of Kombucha tea for two months. The incubation of the tea was increased from 7 to 14 days immediately prior to symptom onset. The patient suffered cardiac arrest, was resuscitated and recovered (CDC, 1995).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 22-year-old HIV-positive man presented with shortness of breath and fever after ingesting a 1-L bottle of unpasteurized Kombucha tea with a friend. Within 15 hours of the ingestion, he became combative and confused, and developed lactic acidosis, acute renal failure, and mildly elevated liver enzymes. Following supportive care, he recovered within 36 hours of ingestion (Sunghee Kole et al, 2009).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) LOSS OF APPETITE
    1) WITH POISONING/EXPOSURE
    a) Mild anorexia developed in a patient following two weeks of Kombucha tea ingestion (Perron et al, 1995).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) One patient complained of vague abdominal cramping following 2 weeks of Kombucha tea ingestion (Perron et al, 1995).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANOREXIA
    a) Kargasok tea administration resulted in anorexia and weight loss in mice (Kwanashie et al, 1989).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 53-year-old male developed transiently elevated liver function tests following ingestion of 1/2 cup of Kombucha tea daily for 2 weeks. Liver function tests included alkaline phosphatase (168 International Units/L), alanine aminotransferase (283 International Units/L), aspartate aminotransferase (123 International Units/L), and gamma-glutamyltranspeptidase (267 International Units/L). Bilirubin was normal. Liver function tests returned to normal within one month. Other causes of hepatotoxicity were ruled-out (Perron et al, 1995).
    b) CASE REPORT: Elevated AST/ALT (greater than 2000 International Units/L) and lactate dehydrogenase (4000 International Units/L) occurred in an 83-year-old after drinking 1/2 cup of Kombucha tea daily for 3 weeks (RMPDC, 1993). No treatment measures or outcomes were reported.
    c) CASE REPORT: Mildly elevated aspartate aminotransferase (57 Units/L) developed in a 22-year-old HIV-positive man who also experienced shortness of breath, fever, lactic acidosis, and acute renal failure within 15 hours of sharing a 1-L bottle of unpasteurized Kombucha tea with a friend. Following supportive care, he recovered within 36 hours of ingestion (Sunghee Kole et al, 2009).
    B) JAUNDICE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Jaundice of 6 weeks duration and elevated liver enzyme levels were reported in a 55-year-old woman who began drinking 2 glasses of Kombucha mushroom tea daily for the past two months. The patient also had an 8-year history of heavy alcohol consumption. Seven weeks after discontinuation of her tea intake and reduction of her alcohol consumption, the patient's jaundice resolved with normalization of her liver enzyme levels (Srinivasan et al, 1997).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Acute renal failure (serum creatinine 2.1 mg/dL) developed in a 22-year-old HIV-positive man who also experienced shortness of breath, fever, elevated liver enzymes, and lactic acidosis within 15 hours of sharing a 1-L bottle of unpasteurized Kombucha tea with a friend. Following supportive care, he recovered within 36 hours of ingestion (Sunghee Kole et al, 2009).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORTS: Severe metabolic acidosis has been reported in two cases (one fatal) who ingested 4 to 12 ounces of Kombucha tea daily for two months. Respiratory depression occurred in one case and cardiac arrest occurred in both cases (CDC, 1995). Both patients had obtained their Kombucha "mushroom" from the same source. At least 115 other persons received Kombucha "mushroom" from the same source but none became ill.
    b) CASE REPORT: Lactic acidosis (lactate 12.9 mmol/L, pH 7.32, PCO2 31 mm Hg, PO2 446 mm Hg, serum bicarbonate 16 mmol/L, an anion gap of 25) developed in a 22-year-old HIV-positive man who also experienced shortness of breath, fever, mildly elevated liver enzymes, and acute renal failure within 15 hours of sharing a 1-L bottle of unpasteurized Kombucha tea with a friend. Following supportive care, he recovered within 36 hours of ingestion (Sunghee Kole et al, 2009).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) DISSEMINATED INTRAVASCULAR COAGULATION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Symptoms of DIC (details not provided) developed in a 59-yr-old following daily ingestion of 4 ounces of Kombucha tea for two months (CDC, 1995). The cause of the DIC was not determined, but autopsy revealed peritonitis (cause unknown) with fecal contamination of the peritoneal cavity.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) MACULOPAPULAR ERUPTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: One patient developed an erythematous, papular rash over his chest and neck following 2 weeks of Kombucha tea ingestion (Perron et al, 1995).
    B) SKIN NECROSIS
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Twenty people (12 female and 8 male) developed lesion-culture proven cutaneous anthrax after topical application of Kombucha mushroom. The original material had too much bacterial contamination to culture the organism directly, but a sample of uncontaminated Kombucha mushroom and tea were demonstrated to be a good culture media for bacillus anthracis (Sadjadi, 1998).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH POISONING/EXPOSURE
    a) Two patients presented with shaking, dyspnea, tachypnea, throat tightness, hypotension, and tachycardia within hours after consumption of Kombucha mushroom tea. All laboratory values were normal except for an elevated WBC count in one of the two patients. Both patients were treated for a presumed allergic reaction and were discharged one day later (Srinivasan et al, 1997).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, liver enzymes, and renal function.
    B) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.
    C) Obtain an ECG in symptomatic patients, and institute continuous cardiac monitoring.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients should be admitted for persistent cardiac dysrhythmias, metabolic acidosis, respiratory failure, and acute renal failure.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a deliberate overdose, and those who are symptomatic should be observed with frequent monitoring of vital signs. Patients that remain asymptomatic can be discharged.

Monitoring

    A) Monitor vital signs, liver enzymes, and renal function.
    B) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.
    C) Obtain an ECG in symptomatic patients, and institute continuous cardiac monitoring.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Cases of toxicity reported to date have involved chronic ingestion of Kombucha tea. Prehospital gastrointestinal decontamination is generally NOT recommended.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Cases of toxicity reported to date have involved chronic ingestion of Kombucha tea. GI decontamination is generally not warranted. Consider activated charcoal after acute overdose if there are other toxic coingestants involved.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) 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).
    1) 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).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) 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.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor vital signs, liver enzymes, and renal function.
    2) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.
    3) Obtain an ECG in symptomatic patients, and institute continuous cardiac monitoring.
    B) ACUTE LUNG INJURY
    1) Maintain adequate ventilation and oxygenation with close monitoring of arterial blood gases. If pO2 cannot be maintained above 50 mmHg with inspiration of 60 percent oxygen by face mask or mechanical ventilation, then positive-end-expiratory pressure (PEEP) in intubated patients or continuous-positive-airway pressure (CPAP) in non-intubated patients may be necessary.
    C) ACIDOSIS
    1) METABOLIC ACIDOSIS: Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate, 1 to 2 mEq/kg is a reasonable starting dose(Kraut & Madias, 2010). Monitor serum electrolytes and arterial or venous blood gases to guide further therapy.
    D) ACUTE ALLERGIC REACTION
    1) SUMMARY
    a) Mild to moderate allergic reactions may be treated with antihistamines with or without inhaled beta adrenergic agonists, corticosteroids or epinephrine. Treatment of severe anaphylaxis also includes oxygen supplementation, aggressive airway management, epinephrine, ECG monitoring, and IV fluids.
    2) BRONCHOSPASM
    a) ALBUTEROL
    1) ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007). CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 mg/kg (up to 10 mg) every 1 to 4 hours as needed, or 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    3) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm.
    b) PREDNISONE: ADULT: 40 to 80 milligrams/day. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 to 2 divided doses divided twice daily (National Heart,Lung,and Blood Institute, 2007).
    4) MILD CASES
    a) DIPHENHYDRAMINE
    1) SUMMARY: Oral diphenhydramine, as well as other H1 antihistamines can be used as indicated (Lieberman et al, 2010).
    2) ADULT: 50 milligrams orally, or 10 to 50 mg intravenously at a rate not to exceed 25 mg/min or may be given by deep intramuscular injection. A total of 100 mg may be administered if needed. Maximum daily dosage is 400 mg (Prod Info diphenhydramine HCl intravenous injection solution, intramuscular injection solution, 2013).
    3) CHILD: 5 mg/kg/24 hours or 150 mg/m(2)/24 hours. Divided into 4 doses, administered intravenously at a rate not exceeding 25 mg/min or by deep intramuscular injection. Maximum daily dosage is 300 mg (Prod Info diphenhydramine HCl intravenous injection solution, intramuscular injection solution, 2013).
    5) MODERATE CASES
    a) EPINEPHRINE: INJECTABLE SOLUTION: It should be administered early in patients by IM injection. Using a 1:1000 (1 mg/mL) solution of epinephrine. Initial Dose: 0.01 mg/kg intramuscularly with a maximum dose of 0.5 mg in adults and 0.3 mg in children. The dose may be repeated every 5 to 15 minutes, if no clinical improvement. Most patients respond to 1 or 2 doses (Nowak & Macias, 2014).
    6) SEVERE CASES
    a) EPINEPHRINE
    1) INTRAVENOUS BOLUS: ADULT: 1 mg intravenously as a 1:10,000 (0.1 mg/mL) solution; CHILD: 0.01 mL/kg intravenously to a maximum single dose of 1 mg given as a 1:10,000 (0.1 mg/mL) solution. It can be repeated every 3 to 5 minutes as needed. The dose can also be given by the intraosseous route if IV access cannot be established (Lieberman et al, 2015). ALTERNATIVE ROUTE: ENDOTRACHEAL ADMINISTRATION: If IV/IO access is unavailable. DOSE: ADULT: Administer 2 to 2.5 mg of 1:1000 (1 mg/mL) solution diluted in 5 to 10 mL of sterile water via endotracheal tube. CHILD: DOSE: 0.1 mg/kg to a maximum of 2.5 mg administered as a 1:1000 (1 mg/mL) solution diluted in 5 to 10 mL of sterile water via endotracheal tube (Lieberman et al, 2015).
    2) INTRAVENOUS INFUSION: Intravenous administration may be considered in patients poorly responsive to IM or SubQ epinephrine. An epinephrine infusion may be prepared by adding 1 mg (1 mL of 1:1000 (1 mg/mL) solution) to 250 mL D5W, yielding a concentration of 4 mcg/mL, and infuse this solution IV at a rate of 1 mcg/min to 10 mcg/min (maximum rate). CHILD: A dosage of 0.01 mg/kg (0.1 mL/kg of a 1:10,000 (0.1 mg/mL) solution up to 10 mcg/min (maximum dose 0.3 mg) is recommended for children (Lieberman et al, 2010). Careful titration of a continuous infusion of IV epinephrine, based on the severity of the reaction, along with a crystalloid infusion can be considered in the treatment of anaphylactic shock. It appears to be a reasonable alternative to IV boluses, if the patient is not in cardiac arrest (Vanden Hoek,TL,et al).
    7) AIRWAY MANAGEMENT
    a) OXYGEN: 5 to 10 liters/minute via high flow mask.
    b) INTUBATION: Perform early if any stridor or signs of airway obstruction.
    c) CRICOTHYROTOMY: Use if unable to intubate with complete airway obstruction (Vanden Hoek,TL,et al).
    d) BRONCHODILATORS are recommended for mild to severe bronchospasm.
    e) ALBUTEROL: ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007).
    f) ALBUTEROL: CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    8) MONITORING
    a) CARDIAC MONITOR: All complicated cases.
    b) IV ACCESS: Routine in all complicated cases.
    9) HYPOTENSION
    a) If hypotensive give 500 to 2000 milliliters crystalloid initially (20 milliliters/kilogram in children) and titrate to desired effect (stabilization of vital signs, mentation, urine output); adults may require up to 6 to 10 L/24 hours. Central venous or pulmonary artery pressure monitoring is recommended in patients with persistent hypotension.
    1) VASOPRESSORS: Should be used in refractory cases unresponsive to repeated doses of epinephrine and after vigorous intravenous crystalloid rehydration (Lieberman et al, 2010).
    2) DOPAMINE: Initial Dose: 2 to 20 micrograms/kilogram/minute intravenously; titrate to maintain systolic blood pressure greater than 90 mm Hg (Lieberman et al, 2010).
    10) H1 and H2 ANTIHISTAMINES
    a) SUMMARY: Antihistamines are second-line therapy and are used as supportive therapy and should not be used in place of epinephrine (Lieberman et al, 2010).
    1) DIPHENHYDRAMINE: ADULT: 25 to 50 milligrams via a slow intravenous infusion or IM. PEDIATRIC: 1 milligram/kilogram via slow intravenous infusion or IM up to 50 mg in children (Lieberman et al, 2010).
    b) RANITIDINE: ADULT: 1 mg/kg parenterally; CHILD: 12.5 to 50 mg parenterally. If the intravenous route is used, ranitidine should be infused over 10 to 15 minutes or diluted in 5% dextrose to a volume of 20 mL and injected over 5 minutes (Lieberman et al, 2010).
    c) Oral diphenhydramine, as well as other H1 antihistamines, can also be used as indicated (Lieberman et al, 2010).
    11) DYSRHYTHMIAS
    a) Dysrhythmias and cardiac dysfunction may occur primarily or iatrogenically as a result of pharmacologic treatment (epinephrine) (Vanden Hoek,TL,et al). Monitor and correct serum electrolytes, oxygenation and tissue perfusion. Treat with antiarrhythmic agents as indicated.
    12) OTHER THERAPIES
    a) There have been a few reports of patients with anaphylaxis, with or without cardiac arrest, that have responded to vasopressin therapy that did not respond to standard therapy. Although there are no randomized controlled trials, other alternative vasoactive therapies (ie, vasopressin, norepinephrine, methoxamine, and metaraminol) may be considered in patients in cardiac arrest secondary to anaphylaxis that do not respond to epinephrine (Vanden Hoek,TL,et al).

Abstracts

Case Reports

    A) ACUTE EFFECTS
    1) CARDIAC ARREST: A 59-year-old woman was brought unconscious to the emergency department, where she developed disseminated intravascular coagulopathy, cardiac arrest and was resuscitated. Her condition continued to deteriorate and she died two days following presentation. ABGs indicated severe metabolic acidosis: pH 6.9, pO2 474.9 mmHg, pCO2 39.2 mmHg. Lactic acid was elevated at 9.85 mM. Toxicologic screen was negative. Routine medications included treatment for hypertension, anemia and mild renal insufficiency. The patient had ingested approximately 4 ounces of Kombucha tea daily for the preceding two months. Autopsy findings included peritonitis with fecal contamination. A second patient presented to the same emergency department one week later in respiratory distress. She suffered cardiac arrest but was resuscitated and recovered. ABGs indicated severe metabolic acidosis: pH 6.7, pO2 86 mmHg, pCO2 67 mmHg. Lactic acid was elevated at 12.4 mM. Toxicologic screen was negative. The patient had ingested approximately 4 ounces of Kombucha tea daily for the preceding two months, increasing the quantity of tea ingested from 4 to 12 ounces and the incubation period of the tea from 7 to 14 days immediately prior to the onset of symptoms. Both patients had obtained their Kombucha mushroom from the same source. At least 115 others in the area had received Kombucha mushroom from the same source and none became ill (CDC, 1995).
    B) ADVERSE EFFECTS
    1) HEPATOTOXICITY: A 53-year-old man developed transient hepatotoxicity following ingestion of 1/2 cup of Kombucha tea daily for 2 weeks. Nine days following discontinuation of the tea, he presented to the emergency department complaining of chest tightness, vague abdominal cramps and mild anorexia, accompanied by an erythematous, papular rash over the chest and neck. Liver function tests included elevated alkaline phosphatase (168 International Units/L), alanine aminotransferase (283 International Units/L), aspartate aminotransferase (123 International Units/L), and gamma-glutamyltranspeptidase (267 International Units/L). Bilirubin was normal. Acetaminophen, alcohol and drug use, and hepatitis were eliminated. The patient was followed as an outpatient and received no treatment. Liver enzymes returned to normal over the following month (Perron et al, 1995).

Range Of Toxicity

Summary

    A) TOXICITY: The range of toxicity of Kombucha mushroom tea has not been established. The majority of case reports describe patients developing adverse effects following 2 weeks to 2 months of ingestion of 4 to 12 ounces of tea daily.

Minimum Lethal Exposure

    A) CASE REPORT: One patient died following ingestion of 4 ounces Kombucha mushroom tea daily for 2 months. No causal relationship was established (CDC, 1995).

Maximum Tolerated Exposure

    A) CASE REPORT: A 22-year-old HIV-positive man presented with shortness of breath and fever after sharing a 1-L bottle of unpasteurized Kombucha tea with a friend. Within 15 hours of the ingestion, he became combative and confused, and developed lactic acidosis, acute renal failure, and mildly elevated liver enzymes. Following supportive care, he recovered within 36 hours of ingestion. Fungal cultures of the tea grew Candida krusei and Candida glabrata(Sunghee Kole et al, 2009).

Pharmacology Toxicology

Toxicologic Mechanism

    A) The toxicological mechanism of Kombucha mushroom tea has not been identified. Possibilities include infection by contaminants or accumulation of fermentation products.

Physicochemical

Ph

    A) pH may range from neutral to 2.0-3.0.

Molecular Weight

    A) Not applicable

References

General Bibliography

    1) Bauer-Petrovska B & Petrushevska-Tozi L: Mineral and water soluble vitamin content in the Kombucha drink. Intl J Food Sci Tech 2000; 35:201-205.
    2) CDC: Unexplained Severe illness Possibly associated with consumption of Kombucha Tea - Iowa 1995. CDC: MMWR 1995; 44:892-900.
    3) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    4) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    5) FDA: FDA cautions consumers on "Kombucha Mushroom Tea" (News release), US Department of Health and Human Services, Public Health Service, Food and Drug Administration, Washington, DC, 1995.
    6) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    7) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    8) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    9) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    10) Kraut JA & Madias NE: Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol 2010; 6(5):274-285.
    11) Kwanashie HO, Usman H, & Nkim SA: Screening of 'kargasok tea' I: Anorexia and obesity. Biochem Soc Transactions 1989; 17:1132-1133.
    12) Lieberman P, Nicklas R, Randolph C, et al: Anaphylaxis-a practice parameter update 2015. Ann Allergy Asthma Immunol 2015; 115(5):341-384.
    13) Lieberman P, Nicklas RA, Oppenheimer J, et al: The diagnosis and management of anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol 2010; 126(3):477-480.
    14) Mayser P, Fromme S, & Leitzmann C: The yeast spectrum of the 'tea fungus Kombucha'. Mycoses 1995; 38:289-295.
    15) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    16) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    17) Nowak RM & Macias CG : Anaphylaxis on the other front line: perspectives from the emergency department. Am J Med 2014; 127(1 Suppl):S34-S44.
    18) Perron AD, Patterson JA, & Yanofsky NN: Kombucha "mushroom" hepatotoxicity. Ann Emerg Med 1995; 26:660-661.
    19) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    20) Product Information: diphenhydramine HCl intravenous injection solution, intramuscular injection solution, diphenhydramine HCl intravenous injection solution, intramuscular injection solution. Hospira, Inc. (per DailyMed), Lake Forest, IL, 2013.
    21) RMPDC: Case Files: Case number 16026251, submitted to AAPCC meeting, Rocky Mountain Poison and Drug Center, New York, NY, 1993.
    22) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    23) Sadjadi J: Cutaneous anthrax associated with the Kombucha "mushroom" in Iran (letter). J Amer Med Assoc 1998; 280:1567-1568.
    24) Srinivasan R, Smolinske S, & Greenbaum D: Probable gastrointestinal toxicity of Kombucha tea. J Gen Intern Med 1997; 12:643-644.
    25) Sunghee Kole A, Jones HD, Christensen R, et al: A case of kombucha tea toxicity. J Intensive Care Med 2009; 24(3):205-207.
    26) Vanden Hoek,TL; Morrison LJ; Shuster M; et al: Part 12: Cardiac Arrest in Special Situations 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. American Heart Association. Dallas, TX. 2010. Available from URL: http://circ.ahajournals.org/cgi/reprint/122/18_suppl_3/S829. As accessed 2010-10-21.