Myoglobin released during muscle injury can precipitate acuterenal failure.1,2 There are many causes of rhabdomyolysis, includingexcessive exercise, "crush" injuries, seizures, infections,severe potassium and phosphate depletion, staphylococcal toxins,venoms, and licit and illicit drugs, including ethanol.2,3,4Intoxication with the liqueur absinthe (derived from oil ofwormwood) has not been associated with rhabdomyolysis or acuterenal failure. We report the case of a patient who was hospitalizedafter drinking essential oil of wormwood purchased through theInternet.
Case Report
A 31-year-old man was found at home by his father in an agitated,incoherent, and disoriented state. Paramedics noted tonic andclonic seizures with decorticate posturing. In the emergencyroom, he was lethargic but belligerent. His mental status improvedafter treatment with haloperidol, and he reported finding adescription of the liqueur absinthe at a site on the World WideWeb entitled "What Is Absinthe?" (http://www.gumbopagescom/food/misc/beverages/absinthe.html).5
Later, the man obtained one of the ingredients described onthe Internet, essential oil of wormwood. The oil was purchasedelectronically from a commercial provider of essential oilsused in aromatherapy, a form of alternative medicine. Severalhours before becoming ill, he drank approximately 10 ml of theessential oil, assuming it was absinthe liqueur.
The patient had no history of neuromuscular or kidney diseaseor alcohol dependence or abuse. He was afebrile, his pulse was90 beats per minute, his blood pressure 103/52 mm Hg, with noorthostatic change, and his respiratory rate was 16 per minute.There was a small tongue laceration. The patient was listlessbut communicative and oriented as to person, place, and time.He had no focal neurologic abnormalities, and the remainderof the examination was normal.
Laboratory studies revealed hypernatremia, hypokalemia, andhypobicarbonatemia (Table 1). The patient's arterial-blood gasvalues while breathing oxygen were as follows: pH, 7.27; partialpressure of carbon dioxide, 43 mm Hg; and partial pressure ofoxygen, 133 mm Hg. The results of lumbar puncture were normal,as were those of computed tomography of the head. Toxicologicscreening tests of blood and urine were negative. The urinewas yellow, with a positive (4+) dipstick test for blood. Microscopyshowed tubular casts but no crystals or white or red cells.A urinary ammonium sulfate precipitation assay for myoglobinwas negative. No discoloration of the serum was noted.
Table 1. Biochemical Values in a Patient with Rhabdomyolysis and Acute Renal Failure Associated with Intoxication with Oil of Wormwood.
On the second hospital day, the patient had moderately intense,bilateral soreness of the leg muscles. The serum creatine kinaseconcentration was markedly elevated (Table 1). The patient wastreated with intravenous sodium bicarbonate and saline. Congestiveheart failure developed, which was treated with diuretics, sodiumrestriction, and discontinuation of alkalinization. The serumcreatinine concentration increased to a peak value of 4.4 mgper deciliter (390 µmol per liter) on the third hospitalday and then declined (Table 1). At no time did the patienthave oliguria, hypocalcemia, or hypophosphatemia. His musclesoreness subsided quickly. He had no further symptoms, and hisserum electrolyte, creatine kinase, and creatinine concentrationswere normal on day 17, nine days after discharge.
The manufacturer of the oil the patient had drunk confirmedthat it consisted solely of essential oil of wormwood, unadulteratedwith licorice, glycyrrhizic acid, or anise.
Discussion
This patient's seizure, probably caused by essential oil ofwormwood, apparently led to rhabdomyolysis and subsequent acuterenal failure. The underlying mechanism is unknown. The resultsof the initial studies indicated anion-gap metabolic and respiratoryacidosis. The large anion gap is typical of the early phasesof rhabdomyolysis and was probably due to the accumulation oflactate, ketone bodies, and other intracellular organic intermediatesbecause of muscle injury and renal dysfunction.6 Gas chromatographymassspectrometry performed on the remaining fluid from the patient'sdrink failed to reveal the ingredients, but methanol, ethanol,and ethylene glycol were not present in it or in the patient'sblood or urine. No commercial assay for essential oil of wormwoodis available.
The positive tetramethylbenzidine reaction in the urine alsosuggested myoglobinuria, but the ammonium sulfate precipitationtest was negative. False negative results may occur with precipitationtests, in contrast to more accurate immunochemical methods,because of the rapid renal clearance of myoglobin, its poorstability in urine, or its presence in urine at a concentrationbelow the analytic sensitivity of the assay.7,8,9
A French liqueur made from the wormwood plant (Artemisia absinthium,Figure 1), absinthe originated in the 18th century.5 The useof extract of wormwood is recorded in ancient Egypt, and itsingestion to exterminate abdominal tapeworms dates to the MiddleAges.5 In the early 1800s, Henri-Louis Pernod began the productionof absinthe, a distillate of wormwood, alcohol, herbs, and seeds.10Soon thereafter, the drink, known for its tart taste and dazzlingblue-green color, gained widespread popularity in Europe andbecame a favorite of artists and writers such as Vincent vanGogh, Henri de Toulouse-Lautrec,10 and Oscar Wilde.11
Photograph courtesy of Dr. Holly H. Shimizu, U.S. Botanical Garden, Washington, D.C.
Absinthism, a syndrome of hallucinations, sleeplessness, tremors,convulsions, and paralysis, was associated with the long-termingestion of the liqueur.12 The ingredient likely to have causedthese abnormalities was thujone, an aromatic hydrocarbon foundin oil of wormwood.12 Scientific interest in absinthe emergedduring the mid-1800s. In 1864 it was reported that Louis Merceof the Bicêtre Hospital in Paris administered small dosesof essential oil of wormwood to dogs and rabbits,10,13 whichled to "convulsions, involuntary evacuations, abnormal respirations,and foaming at the mouth."10 In 1868, a paper entitled "Experimentsand Observations on Absinth and Absinthism" appeared in theBoston Medical and Surgical Journal, now the New England Journalof Medicine.13 This paper described epileptiform activity, chesteffusion, and reddish urine in a patient hospitalized in Parisfor absinthe intoxication and "kidney congestion" in animalsgiven absinthe. In 1874, Dr. Valentin Magnan described alterationsin consciousness and auditory and visual hallucinations in humansingesting absinthe.14 He also observed seizures in animals givenlarge doses of essential oil of wormwood. The epileptogenicagent identified in these experiments was oil of wormwood.
Despite early warnings about the untoward effects of absinthe,strong economic interest in its production precluded limitingits availability. From the 1870s until 1915, consumption ofthe liqueur increased substantially. Claiming that absinthecontributed to psychosis and suicide, France banned it in 1915,followed by other European nations and the United States.10
This case demonstrates the ease of obtaining substances withtoxic and pharmacologic potential electronically and acrossstate lines. Chinese medicinal herbs, some of which can causeacute renal failure,15,16 are easily procured by means of theInternet.17 Although absinthe liqueur is illegal in the UnitedStates, its ingredients are readily available. Absinthe is alsocurrently a popular drink in the bars of Prague, in the CzechRepublic.18 The essential ingredient in this ancient potionwas purchased in this case by means of up-to-the-minute technology.Should the medical community brace itself for future cases ofInternet-mediated toxic diseases?
We are indebted to Melanie Fall for assistance in the preparationof the manuscript.
Source Information
From the Departments of Medicine (S.D.W., P.L.K.) and Pathology (J.B.S.), George Washington University Medical Center, Washington, D.C.
Address reprint requests to Dr. Kimmel at the Division of Renal Diseases and Hypertension, Department of Medicine, George Washington University Medical Center, 2150 Pennsylvania Ave., NW, Washington, DC 20037.
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