The patient with rhabdomyolysis: have you considered quail poisoning?

As no other cause of rhabdomyolysis was evident, we believe that quail consumption was the culprit. All 3 cases occurred in autumn, the quail migration period. Previous reports have speculated that the syndrome is caused by a toxin or alkaloid that has a curare-like action and nicotine effects on autonomic ganglia and which is contained in seeds eaten by the quail, most likely from hemlock (Conium maculatum)2 (Fig. 2) or other plants (e.g., red hempnettle, or Galeopsis ladanum)3,4 (Fig. 3). Coniine, the most important alkaloid of C. maculatum, can be lethal in a dose of 150 mg,4 but in smaller doses it produces neurotoxic effects, acute rhabdomyolysis and acute renal failure.5 However, coniine triggers clinical manifestations only in sensitive people; personal susceptibility seems to be a factor common to coturnism and Haff disease.5 The patients described here shared their meals (Fig. 4) with other people who were not affected. Although some investigations have suggested that susceptibility runs in families,1 others have excluded a pre-existing enzyme defect as a cause.6 Our patients did not report any previous attacks or family histories of such events. Patient 1: A 62-year-old woman was admitted with nausea, vomiting, weakness and leg muscle pain. The symptoms had begun 7 hours after a meal of fresh roasted quail. She was not taking any medications, had no allergies to food or medications and did not use alcohol, cigarettes or illicit drugs. Her clinical examination revealed normal cardiopulmonary findings and a temperature of 35.2C. She had muscle weakness of both legs but no muscle atrophy or loss of voluntary movements; her deep tendon reflexes were normal. She passed dark brown urine without urgency or dysuria. Results of routine hematological tests were normal. Her creatine kinase (CK) level was 5500 U/L (this increased to 11 000 U/L the next morning) (normally 30-135 U/L for women) with an MB fraction of < 6%; the levels of other muscle enzymes such as lactate dehydrogenase (1231 U/L), aspartate aminotransferase (200 U/L; this increased to 400 U/L the next day) and alanine aminotransferase (100 U/L) were also elevated. Results of troponin and direct Coombs' tests were negative, and the patient had an elevated myoglobin level (> 500 U/L); total bilirubin levels were normal. Urinalysis revealed myoglobinuria but no hemoglobinuria. The patient was admitted to hospital, and her symptoms were considered to have been caused by quail ingestion. She reste