- Email: [email protected]
How do you like your quail prepared?1
2790
World Literature Review
2. Gorbach SL, Nahas L, Plaut AG, et al. Studies of intestinal microflora V. Fecal microbia ecology in ulcerative colitis and regional enteritis; relationship to severity of disease and chemotherapy. Gastroenterology 1968;54:575– 87. 3. Keighley MRB, Arabi Y, Dimock F, et al. Influence of inflammatory bowel disease on intestinal microflora. Gut 1978;19: 1099 –104. 4. Cooke EM. A quantitative comparison of the faecal flora of patients with ulcerative colitis and that of normal persons. J Pathol Bacteriol 1967;94:439 – 44. 5. Cooke EM. Properties of strains Escherichia coli isolated from the faeces of patients with ulcerative colitis, patients with acute diarrhoea and normal persons. J Pathol Bacteriol 1968;95:101– 13.
How Do You Like Your Quail Prepared? Aparicio R, Onate JM, Atuzean A, et al. Epidemic Rhabdomyolysis Following Quail Ingestion: A Clinical, Epidemiologic and Experimental Study Clin Toxicol 1999;112:143– 6
ABSTRACT A few toxic outbreaks by quail ingestion have been described, none in Spain, and the toxin has not yet been identified. The authors described a toxic outbreak by quail that had ingested Galeopsis ladanum seeds and developed and tested an animal model. A rhabdomyolysis outbreak caused by the eating of contaminated quail was studied clinically and epidemiologically. Quails’ crops were analyzed and patients were studied. An animal model was developed. Alkaloid content in G. ladanum seeds and quail meat was measured. Twenty patients suffered from rhabdomyolysis (myalgia, increase of muscular enzymes, and myoglobinuria) after ingestion of quail that had eaten G. ladanum seeds, as could be seen by their presence in quails’ crops. Six patients needed hospital care, but evolution of the disorder was benign. Rats fed with quail that had eaten G. ladanum seeds had higher creatine kinase levels than control rats (p ⫽ 0.0588). Several alkaloids, including stachydrine, that may have been responsible for the toxicity were detected in seeds. Another unidentified alkaloid was detected in the quail. Quail that have eaten G. ladanum seeds are toxic for human beings, causing rhabdomyolysis. A plant alkaloid may be the toxin involved in inducing the rhabdomyolysis in the outbreak. (Am J Gastroenterol 2001;96: 2790 –2792. © 2001 by Am. Coll. of Gastroenterology)
COMMENTS The authors of this investigation carefully described the clinical and epidemiological features of an epidemic of rhabdomyolysis induced by the ingestion of quail. Second, they have virtually identified the toxin responsible for the rhabdomyolysis on Lesbos (Galeopsis ladanum seeds).
AJG – Vol. 96, No. 9, 2001
Table 1. Prospective Level of Creatine Kinase (U/L) in Rats Fed Quail Group I II III IV V
Diet Standard rat chow Quail fed 1 day with seeds of G. ladanum Quail fed 3 days with G. ladanum Quail fed standard quail diet Quail shot in Valdavia
No. of Creatine Kinase Rats (Mean ⫾ SD) 2 3
158 ⫾ 40 507 ⫾ 94
3
535 ⫾ 300
4 4
367 ⫾ 105 228 ⫾ 123
Third, their experimental design clarifies the pathogenesis of this syndrome. In the clinical description of their study they considered 29 patients to have been at risk, of which 20 (45%) exhibited clinical evidence of rhabdomyolysis. The six patients whose symptoms were so severe that they required hospitalization were included among those with rhabdomyolysis. The investigators noted no significant differences in sex or age, in physical activity, in the amount of quail meat consumed, or in the consumption of alcohol between the symptomatic and asymptomatic groups of patients. The initial symptoms appeared 3–24 h after eating the quail. The myalgias were accompanied by muscle cramps in several patients, by diarrhea in one patient, and by nausea and vomiting in another. The duration of symptoms ranged from 4 to 72 h. In one patient they persisted for 10 days. Contents of the crops of the quail were separately analyzed for quail shot in Los Quinones, the epicenter of rhabdomyolysis, and in other “control” regions. All of the quail killed in the Los Quinones region had only G. ladanum seeds in their crops, whereas those killed in other regions did not. The single most impressive aspect of this investigation was the controlled comparison of the creatine kinase concentrations in the tissues of five groups of rats that had different types of diets (Table 1). Group I, which contained two rats, had eaten standard rat food. In Group II three rats had consumed quail that had ingested G. ladanum seeds for 1 day, and Group III included four rats that had consumed quail that had been fed G. ladanum seeds for 3 days. In Group IV four rats, which had eaten standard quail food, were studied. Finally, in Group V four rats consumed quail that had been shot in Valdavia, which does not have as high a rate of rhabdomyolysis as Los Quinones. All quail were killed, eviscerated, and ground finely into a homogenous mixture that was fed to the rats in 3-g doses, which is equivalent to 150 –200 g given to a human who weighs 75 kg. The concentrations of creatine kinase in the rat tissues were analyzed using nonparametric statistical methodology (Kruskal-Wallis). Alkaloidal substances were determined in the seeds of G. ladanum and in quail muscle using thin layer chromatography. In the beginning there was the Bible. In Numbers 11: 31–35 the first written report of the plague of quail poisoning appeared. Almost 5000 yr later a 49-yr-old farmer living
AJG – September, 2001
on Lesbos in Greece was referred to the hospital on September 22, 1969 for muscle pains in his thighs and legs (1) of 8 days duration. These symptoms started 6 h after the patient had eaten quail. The amount of quail consumed was not stated. After 2 h the pains subsided and the patient noted a progressive decrease of urinary output to anuric levels (⬍50 ml/24 h). Physical examination was negative. There had been no excessive muscular activity. No tenderness of muscles or of the renal areas was present. His blood pressure was 140/90. His medical history, both recent and remote, was negative. Complete blood count; red blood cell count, 3.8 ⫻ 106; Hb, 11 g/dl; white blood cell count, 7000/mm3; SGOT; and SGPT were normal. Urine specific gravity was 1.010; serum albumin, 2.8 g/dl; BUN, 330 mg/dl; K, 6.4; Na, 125; and Cl, 92 (mEq/L). There was no myoglobin in urine. Peritoneal dialysis started on September 27. On October 2 urine output began to increase until it was ⬎1000 ml/24 h. BUN decreased gradually to normal. An electromyogram on November 4, 1969 was normal. It was postulated by Sergent (2) that the cause of the myoglobinuria was rhabdomyolysis, caused by hemlock (Conium maculatum) ingestion. It was also postulated that the myoglobinuria may have been the consequence of enzyme deficiency of myophosphorylase (3). In 1978 Papapetropoulos reported a 27-yr-old Greek man with muscle pain, stiffness, and weakness in association with myoglobinuria. Although of only several days duration, the patient progressed to acute renal failure. It was postulated that the quail carried an unknown toxin and that the ingestion of quail flesh from Lesbos transmitted a toxic agent that induces rhabdomyolysis. The patient exhibited muscle weakness for 56 h. On recovery serum lactate acid levels, electromyograms, and motor conduction velocity were normal (4). A muscle biopsy specimen showed normal striated muscle fibers, and the two principal histochemical types of nicotinamide adenosine nucleotide dehydrogenase-tetrazolium reductase and adenosine triphosphatase (pH 9.4) were well differentiated. Muscle phosphorylase was present. The muscle weakness in quail poisoning has been reported to be similar to the myopathies of known disorders. They concluded that Coturnism is an acute myoglobinuric syndrome that affects only genetically sensitive individuals after they have eaten quail (Coturnix coturnix). This type of poisoning may be related to two other types of food poisoning—that is, the myoglobinuria caused by fish (Haff disease) and the hemoglobinuria caused by fava beans (favism). As far as is known, only the quail that are native to the Mediterranean basin and that migrate every spring northward to Europe and return every autumn to North and Central Africa cause this syndrome. It had been postulated that the toxins responsible are the seeds of hemlock or hellebore plants. Symptoms start 1–9 h after eating quail (5). Muscular exertion before or after the meal aggravates and accelerates the syndrome. Rest after the meal may avert it completely. First, intense pain of the legs, arms, and trunk may occur,
World Literature Review
2791
usually in muscles that have been utilized. Muscular weakness or paralysis may precede or coexist with the pain. Brown or red urine, which may be associated with oliguria, anuria, and azotemia, is usually present. The involved muscles are tender to palpation. SGOT may be as high as 40 times the upper limit of normal (i.e., circa 2,000 IU/L). Lactic dehydrogenase may be 10 times the upper limit of normal and creatine kinase may be 100 times normal. Levels of 20,000 U are not uncommon. Because myoglobin does not combine with haptoglobin, the presence of haptoglobin and a positive benzidine test suggest that myoglobinuria rather than hemoglobinuria is responsible. The myoglobinuria may persist for 8 –28 h. Albuminuria may persist for a week or more. Lesbos, where 120 patients with quail poisoning have been observed between 1950 and 1977, appears to be the epicenter of quail-induced poisoning. No case was reported during this period on other Aegean islands. Four cases of skylark-induced myoglobinuria have also been reported (6). This report by Aparicio and his associates in Palencia, Spain establishes how quail-induced rhabdomyolysis occurs in species that develop quail poisoning. It confirms that quail are the vector and that the actual toxins (or toxinogens) are seeds that are ingested by the quail during their passage from the north to southern Spain, France, or Algeria. They provide data to show that quail poisoning appears at almost the same time each year—the second week of September in sunny Spain, when these plants are in fruition. It had previously been postulated that hemlock seeds were the culprit (7), but the report of Aparicio establishes that G. ladanum seeds can be responsible, and that the disease is not seen in areas in which these seeds do not grow or, perhaps, at times that these seeds are not ripe. It is conceivable that different plants may pollinate different species of birds and/or at different times. It will be fascinating to learn how the seeds are converted to toxic alkaloids and to identify the nature and specificity of the alkaloids. It is known that hemlock seeds can also induce rhabdomyolysis (7). It is fortunate that the fatality rate of this type of quail poisoning is relatively low. Actually, Aparicio et al. indicated that the areas of involvement may be quite specific and surprisingly small. This observation provides the hope that effective public health measures may be possible if the disease becomes a greater problem. Harold Conn, M.D. Yale University New Haven, Connecticut
REFERENCES 1. Bullis AG, Kastanakis S, Giamarbrelou H, Diaros GK. Acute renal failure after a meal of quail. Lancet 1971;2:1702 (correspondence). 2. Sergent E. Les cailles empoisoneuses. Arch Inst Pasteur d’Algerie 1948;26:249 –51.
2792
World Literature Review
3. Sergent E. Les cailles empoisoneuses. Arch Inst Pasteur d’Algerie 1942;2:162–70. 4. Ouzounellis T. Some notes on quail poisoning. JAMA 1970; 211:1887–95. 5. Ouzounellis T. Quail poisoning (Coturnism). In: Recheigl M Jr, ed. CRC handbook of naturally occurring food toxicants. Boca Raton, FL: CRC Press, 1971:313–9. 6. Rutecki GW, Ognibene AJ, Gelb D. Rhabdomyolysis in antiquity. Pharos Spring 1998;15–22. 7. Rizzi D, Basile C, DiMaggio A, et al. Clinical spectrum of accidental hemlock poisoning: Neurotoxic manifestations, rhabdomyolysis and acute tubular necrosis. Nephrol Dial Transplant 1991;6:939 – 43.
Sonography of Sigmoid Diverticulitis: Does Sound Make Sense in This Diagnosis? Hollerweger A, Rettenbacher T, Macheiner P, et al. Sigmoid Diverticulitis: Value of Transrectal Sonography in Addition to Transabdominal Sonography AJR 2000;175:1155– 60
ABSTRACT The purpose of this study was to determine the value of sonographic assessment of the sigmoid colon using transrectal and transabdominal sonography for evaluation of sigmoid diverticulitis. Overlying intestinal gas often impairs transabdominal sonographic assessment of the lower sigmoid colon, which can be better visualized and with higher resolution using transrectal ultrasound. In this investigation, 86 consecutive patients with suspected acute sigmoid diverticulitis were referred for transabdominal sonography as the initial imaging method. In 46 patients, transrectal ultrasound was performed in addition to transabdominal sonography if pain was localized to the mid–lower abdomen and if a disease process could not be visualized or only partially visualized on transabdominal examination. An end-firing 5- to 9-MHz endocavitary probe was used for the transrectal examinations. A final diagnosis of sigmoid diverticulitis was made in 50 patients; 34 of these patients had both transabdominal and transrectal sonography. In 20 patients, transrectal sonography showed relevant additional information; six diagnoses of sigmoid diverticulitis were established on transrectal examination alone. Transrectal sonography revealed one perforation, five abscesses, and three fistulous complications that were not shown on transabdominal sonography. In the remaining five patients, correct diagnoses were supported on transabdominal examinations, but only transrectal sonography could show an inflamed diverticulum. In 10 patients, transrectal sonography revealed signs of diverticulitis but no relevant information in addition to results from transabdominal evaluation. Four false negative and two false positive results occurred with transrectal sonography. The authors conclude that transrectal sonography is accurate for confirming clinically suspected acute colonic diverticulitis when the lower sigmoid colon is affected. Com-
AJG – Vol. 96, No. 9, 2001
pared to the transabdominal approach, transrectal sonography avoids false negative results and better defines the severity of disease in the lower sigmoid colon. In summary, transrectal sonography increases the sensitivity of sonographic diagnosis of sigmoid diverticulitis. (Am J Gastroenterol 2001;96:2792–2793. © 2001 by Am. Coll. of Gastroenterology)
COMMENT Acute colonic diverticulitis is predominantly an extramucosal inflammatory disease, nearly always a result of a microperforation of a single diverticulum (1). Accurate imaging is necessary for establishing the correct diagnosis of sigmoid diverticulitis and for staging the severity of disease, which impacts on treatment options (2– 4). Cross-sectional imaging techniques, such as CT and sonography, are increasingly being used for the diagnosis of this disease and for the determination of alternative diagnoses that may not be evident clinically. The choice between CT and sonography as the initial method for evaluating potential diverticulitis largely depends on institutional preferences and available experience using these techniques; in addition, these preferences are in part geographic, with CT often preferred in the United States and sonography the first method chosen in Europe (this study was done in Austria). Various CT and sonographic studies have shown comparable results in assessing acute diverticulitis of the colon (2– 8). Sonography is widely available and noninvasive, and different layers of the bowel wall can be seen; however, problems such as excessive bowel gas and obesity can limit the use of the technique. The addition of transrectal sonography eliminates some of these problems. CT examination may be less available on an emergent basis and is more costly and invasive (i.e., oral and i.v. contrast material), but has fewer limitations in visualizing the bowel and in offering alternate differential diagnoses. The study by Hollerweger and colleagues not only provides further data on the use of transabdominal ultrasound in evaluating patients with suspected acute sigmoid diverticulitis, but also offers new information on the use of transrectal sonography to supplement the sonographic evaluation of this disease. Depending on the criteria used, the sensitivities of transabdominal and transrectal sonography for the diagnosis of acute diverticulitis were 76% and 88%, respectively, whereas the combined sensitivity of both procedures was 94%. The overall specificity of both procedures was 83%, and their positive and negative predictive values were 94% and 83%, respectively. David J. Ott, M.D., F.A.C.G. Department of Radiology Wake Forest University School of Medicine Winston-Salem, North Carolina
World Literature Review
2. Gorbach SL, Nahas L, Plaut AG, et al. Studies of intestinal microflora V. Fecal microbia ecology in ulcerative colitis and regional enteritis; relationship to severity of disease and chemotherapy. Gastroenterology 1968;54:575– 87. 3. Keighley MRB, Arabi Y, Dimock F, et al. Influence of inflammatory bowel disease on intestinal microflora. Gut 1978;19: 1099 –104. 4. Cooke EM. A quantitative comparison of the faecal flora of patients with ulcerative colitis and that of normal persons. J Pathol Bacteriol 1967;94:439 – 44. 5. Cooke EM. Properties of strains Escherichia coli isolated from the faeces of patients with ulcerative colitis, patients with acute diarrhoea and normal persons. J Pathol Bacteriol 1968;95:101– 13.
How Do You Like Your Quail Prepared? Aparicio R, Onate JM, Atuzean A, et al. Epidemic Rhabdomyolysis Following Quail Ingestion: A Clinical, Epidemiologic and Experimental Study Clin Toxicol 1999;112:143– 6
ABSTRACT A few toxic outbreaks by quail ingestion have been described, none in Spain, and the toxin has not yet been identified. The authors described a toxic outbreak by quail that had ingested Galeopsis ladanum seeds and developed and tested an animal model. A rhabdomyolysis outbreak caused by the eating of contaminated quail was studied clinically and epidemiologically. Quails’ crops were analyzed and patients were studied. An animal model was developed. Alkaloid content in G. ladanum seeds and quail meat was measured. Twenty patients suffered from rhabdomyolysis (myalgia, increase of muscular enzymes, and myoglobinuria) after ingestion of quail that had eaten G. ladanum seeds, as could be seen by their presence in quails’ crops. Six patients needed hospital care, but evolution of the disorder was benign. Rats fed with quail that had eaten G. ladanum seeds had higher creatine kinase levels than control rats (p ⫽ 0.0588). Several alkaloids, including stachydrine, that may have been responsible for the toxicity were detected in seeds. Another unidentified alkaloid was detected in the quail. Quail that have eaten G. ladanum seeds are toxic for human beings, causing rhabdomyolysis. A plant alkaloid may be the toxin involved in inducing the rhabdomyolysis in the outbreak. (Am J Gastroenterol 2001;96: 2790 –2792. © 2001 by Am. Coll. of Gastroenterology)
COMMENTS The authors of this investigation carefully described the clinical and epidemiological features of an epidemic of rhabdomyolysis induced by the ingestion of quail. Second, they have virtually identified the toxin responsible for the rhabdomyolysis on Lesbos (Galeopsis ladanum seeds).
AJG – Vol. 96, No. 9, 2001
Table 1. Prospective Level of Creatine Kinase (U/L) in Rats Fed Quail Group I II III IV V
Diet Standard rat chow Quail fed 1 day with seeds of G. ladanum Quail fed 3 days with G. ladanum Quail fed standard quail diet Quail shot in Valdavia
No. of Creatine Kinase Rats (Mean ⫾ SD) 2 3
158 ⫾ 40 507 ⫾ 94
3
535 ⫾ 300
4 4
367 ⫾ 105 228 ⫾ 123
Third, their experimental design clarifies the pathogenesis of this syndrome. In the clinical description of their study they considered 29 patients to have been at risk, of which 20 (45%) exhibited clinical evidence of rhabdomyolysis. The six patients whose symptoms were so severe that they required hospitalization were included among those with rhabdomyolysis. The investigators noted no significant differences in sex or age, in physical activity, in the amount of quail meat consumed, or in the consumption of alcohol between the symptomatic and asymptomatic groups of patients. The initial symptoms appeared 3–24 h after eating the quail. The myalgias were accompanied by muscle cramps in several patients, by diarrhea in one patient, and by nausea and vomiting in another. The duration of symptoms ranged from 4 to 72 h. In one patient they persisted for 10 days. Contents of the crops of the quail were separately analyzed for quail shot in Los Quinones, the epicenter of rhabdomyolysis, and in other “control” regions. All of the quail killed in the Los Quinones region had only G. ladanum seeds in their crops, whereas those killed in other regions did not. The single most impressive aspect of this investigation was the controlled comparison of the creatine kinase concentrations in the tissues of five groups of rats that had different types of diets (Table 1). Group I, which contained two rats, had eaten standard rat food. In Group II three rats had consumed quail that had ingested G. ladanum seeds for 1 day, and Group III included four rats that had consumed quail that had been fed G. ladanum seeds for 3 days. In Group IV four rats, which had eaten standard quail food, were studied. Finally, in Group V four rats consumed quail that had been shot in Valdavia, which does not have as high a rate of rhabdomyolysis as Los Quinones. All quail were killed, eviscerated, and ground finely into a homogenous mixture that was fed to the rats in 3-g doses, which is equivalent to 150 –200 g given to a human who weighs 75 kg. The concentrations of creatine kinase in the rat tissues were analyzed using nonparametric statistical methodology (Kruskal-Wallis). Alkaloidal substances were determined in the seeds of G. ladanum and in quail muscle using thin layer chromatography. In the beginning there was the Bible. In Numbers 11: 31–35 the first written report of the plague of quail poisoning appeared. Almost 5000 yr later a 49-yr-old farmer living
AJG – September, 2001
on Lesbos in Greece was referred to the hospital on September 22, 1969 for muscle pains in his thighs and legs (1) of 8 days duration. These symptoms started 6 h after the patient had eaten quail. The amount of quail consumed was not stated. After 2 h the pains subsided and the patient noted a progressive decrease of urinary output to anuric levels (⬍50 ml/24 h). Physical examination was negative. There had been no excessive muscular activity. No tenderness of muscles or of the renal areas was present. His blood pressure was 140/90. His medical history, both recent and remote, was negative. Complete blood count; red blood cell count, 3.8 ⫻ 106; Hb, 11 g/dl; white blood cell count, 7000/mm3; SGOT; and SGPT were normal. Urine specific gravity was 1.010; serum albumin, 2.8 g/dl; BUN, 330 mg/dl; K, 6.4; Na, 125; and Cl, 92 (mEq/L). There was no myoglobin in urine. Peritoneal dialysis started on September 27. On October 2 urine output began to increase until it was ⬎1000 ml/24 h. BUN decreased gradually to normal. An electromyogram on November 4, 1969 was normal. It was postulated by Sergent (2) that the cause of the myoglobinuria was rhabdomyolysis, caused by hemlock (Conium maculatum) ingestion. It was also postulated that the myoglobinuria may have been the consequence of enzyme deficiency of myophosphorylase (3). In 1978 Papapetropoulos reported a 27-yr-old Greek man with muscle pain, stiffness, and weakness in association with myoglobinuria. Although of only several days duration, the patient progressed to acute renal failure. It was postulated that the quail carried an unknown toxin and that the ingestion of quail flesh from Lesbos transmitted a toxic agent that induces rhabdomyolysis. The patient exhibited muscle weakness for 56 h. On recovery serum lactate acid levels, electromyograms, and motor conduction velocity were normal (4). A muscle biopsy specimen showed normal striated muscle fibers, and the two principal histochemical types of nicotinamide adenosine nucleotide dehydrogenase-tetrazolium reductase and adenosine triphosphatase (pH 9.4) were well differentiated. Muscle phosphorylase was present. The muscle weakness in quail poisoning has been reported to be similar to the myopathies of known disorders. They concluded that Coturnism is an acute myoglobinuric syndrome that affects only genetically sensitive individuals after they have eaten quail (Coturnix coturnix). This type of poisoning may be related to two other types of food poisoning—that is, the myoglobinuria caused by fish (Haff disease) and the hemoglobinuria caused by fava beans (favism). As far as is known, only the quail that are native to the Mediterranean basin and that migrate every spring northward to Europe and return every autumn to North and Central Africa cause this syndrome. It had been postulated that the toxins responsible are the seeds of hemlock or hellebore plants. Symptoms start 1–9 h after eating quail (5). Muscular exertion before or after the meal aggravates and accelerates the syndrome. Rest after the meal may avert it completely. First, intense pain of the legs, arms, and trunk may occur,
World Literature Review
2791
usually in muscles that have been utilized. Muscular weakness or paralysis may precede or coexist with the pain. Brown or red urine, which may be associated with oliguria, anuria, and azotemia, is usually present. The involved muscles are tender to palpation. SGOT may be as high as 40 times the upper limit of normal (i.e., circa 2,000 IU/L). Lactic dehydrogenase may be 10 times the upper limit of normal and creatine kinase may be 100 times normal. Levels of 20,000 U are not uncommon. Because myoglobin does not combine with haptoglobin, the presence of haptoglobin and a positive benzidine test suggest that myoglobinuria rather than hemoglobinuria is responsible. The myoglobinuria may persist for 8 –28 h. Albuminuria may persist for a week or more. Lesbos, where 120 patients with quail poisoning have been observed between 1950 and 1977, appears to be the epicenter of quail-induced poisoning. No case was reported during this period on other Aegean islands. Four cases of skylark-induced myoglobinuria have also been reported (6). This report by Aparicio and his associates in Palencia, Spain establishes how quail-induced rhabdomyolysis occurs in species that develop quail poisoning. It confirms that quail are the vector and that the actual toxins (or toxinogens) are seeds that are ingested by the quail during their passage from the north to southern Spain, France, or Algeria. They provide data to show that quail poisoning appears at almost the same time each year—the second week of September in sunny Spain, when these plants are in fruition. It had previously been postulated that hemlock seeds were the culprit (7), but the report of Aparicio establishes that G. ladanum seeds can be responsible, and that the disease is not seen in areas in which these seeds do not grow or, perhaps, at times that these seeds are not ripe. It is conceivable that different plants may pollinate different species of birds and/or at different times. It will be fascinating to learn how the seeds are converted to toxic alkaloids and to identify the nature and specificity of the alkaloids. It is known that hemlock seeds can also induce rhabdomyolysis (7). It is fortunate that the fatality rate of this type of quail poisoning is relatively low. Actually, Aparicio et al. indicated that the areas of involvement may be quite specific and surprisingly small. This observation provides the hope that effective public health measures may be possible if the disease becomes a greater problem. Harold Conn, M.D. Yale University New Haven, Connecticut
REFERENCES 1. Bullis AG, Kastanakis S, Giamarbrelou H, Diaros GK. Acute renal failure after a meal of quail. Lancet 1971;2:1702 (correspondence). 2. Sergent E. Les cailles empoisoneuses. Arch Inst Pasteur d’Algerie 1948;26:249 –51.
2792
World Literature Review
3. Sergent E. Les cailles empoisoneuses. Arch Inst Pasteur d’Algerie 1942;2:162–70. 4. Ouzounellis T. Some notes on quail poisoning. JAMA 1970; 211:1887–95. 5. Ouzounellis T. Quail poisoning (Coturnism). In: Recheigl M Jr, ed. CRC handbook of naturally occurring food toxicants. Boca Raton, FL: CRC Press, 1971:313–9. 6. Rutecki GW, Ognibene AJ, Gelb D. Rhabdomyolysis in antiquity. Pharos Spring 1998;15–22. 7. Rizzi D, Basile C, DiMaggio A, et al. Clinical spectrum of accidental hemlock poisoning: Neurotoxic manifestations, rhabdomyolysis and acute tubular necrosis. Nephrol Dial Transplant 1991;6:939 – 43.
Sonography of Sigmoid Diverticulitis: Does Sound Make Sense in This Diagnosis? Hollerweger A, Rettenbacher T, Macheiner P, et al. Sigmoid Diverticulitis: Value of Transrectal Sonography in Addition to Transabdominal Sonography AJR 2000;175:1155– 60
ABSTRACT The purpose of this study was to determine the value of sonographic assessment of the sigmoid colon using transrectal and transabdominal sonography for evaluation of sigmoid diverticulitis. Overlying intestinal gas often impairs transabdominal sonographic assessment of the lower sigmoid colon, which can be better visualized and with higher resolution using transrectal ultrasound. In this investigation, 86 consecutive patients with suspected acute sigmoid diverticulitis were referred for transabdominal sonography as the initial imaging method. In 46 patients, transrectal ultrasound was performed in addition to transabdominal sonography if pain was localized to the mid–lower abdomen and if a disease process could not be visualized or only partially visualized on transabdominal examination. An end-firing 5- to 9-MHz endocavitary probe was used for the transrectal examinations. A final diagnosis of sigmoid diverticulitis was made in 50 patients; 34 of these patients had both transabdominal and transrectal sonography. In 20 patients, transrectal sonography showed relevant additional information; six diagnoses of sigmoid diverticulitis were established on transrectal examination alone. Transrectal sonography revealed one perforation, five abscesses, and three fistulous complications that were not shown on transabdominal sonography. In the remaining five patients, correct diagnoses were supported on transabdominal examinations, but only transrectal sonography could show an inflamed diverticulum. In 10 patients, transrectal sonography revealed signs of diverticulitis but no relevant information in addition to results from transabdominal evaluation. Four false negative and two false positive results occurred with transrectal sonography. The authors conclude that transrectal sonography is accurate for confirming clinically suspected acute colonic diverticulitis when the lower sigmoid colon is affected. Com-
AJG – Vol. 96, No. 9, 2001
pared to the transabdominal approach, transrectal sonography avoids false negative results and better defines the severity of disease in the lower sigmoid colon. In summary, transrectal sonography increases the sensitivity of sonographic diagnosis of sigmoid diverticulitis. (Am J Gastroenterol 2001;96:2792–2793. © 2001 by Am. Coll. of Gastroenterology)
COMMENT Acute colonic diverticulitis is predominantly an extramucosal inflammatory disease, nearly always a result of a microperforation of a single diverticulum (1). Accurate imaging is necessary for establishing the correct diagnosis of sigmoid diverticulitis and for staging the severity of disease, which impacts on treatment options (2– 4). Cross-sectional imaging techniques, such as CT and sonography, are increasingly being used for the diagnosis of this disease and for the determination of alternative diagnoses that may not be evident clinically. The choice between CT and sonography as the initial method for evaluating potential diverticulitis largely depends on institutional preferences and available experience using these techniques; in addition, these preferences are in part geographic, with CT often preferred in the United States and sonography the first method chosen in Europe (this study was done in Austria). Various CT and sonographic studies have shown comparable results in assessing acute diverticulitis of the colon (2– 8). Sonography is widely available and noninvasive, and different layers of the bowel wall can be seen; however, problems such as excessive bowel gas and obesity can limit the use of the technique. The addition of transrectal sonography eliminates some of these problems. CT examination may be less available on an emergent basis and is more costly and invasive (i.e., oral and i.v. contrast material), but has fewer limitations in visualizing the bowel and in offering alternate differential diagnoses. The study by Hollerweger and colleagues not only provides further data on the use of transabdominal ultrasound in evaluating patients with suspected acute sigmoid diverticulitis, but also offers new information on the use of transrectal sonography to supplement the sonographic evaluation of this disease. Depending on the criteria used, the sensitivities of transabdominal and transrectal sonography for the diagnosis of acute diverticulitis were 76% and 88%, respectively, whereas the combined sensitivity of both procedures was 94%. The overall specificity of both procedures was 83%, and their positive and negative predictive values were 94% and 83%, respectively. David J. Ott, M.D., F.A.C.G. Department of Radiology Wake Forest University School of Medicine Winston-Salem, North Carolina