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Brain emboli in the lungs of cattle
THE LANCET
Letters to the Editor
Brain emboli in the lungs of cattle
Hyperventilation syndrome
SIR—It would be unfortunate if inaccurate information in Garland’s letter (Aug 31, p 610)1 were to go unchallenged. There is, at present, no evidence that bovine lungs present a source of human exposure to bovine brain tissue in the UK. The type of captive-bolt stunner which injects compressed air into the cranial cavity to disrupt the brain structure is not used on cattle in the UK, and it would be an offence to mince lungs to put into sausages. It is true that lungs are not Specified Bovine Material, but their use in the way described has been prevented by the Meat Products and Spreadable Fish Products Regulations 1984 (SI 1984, no 1566). Since becoming aware some weeks ago of Garland’s claims we have arranged for lungs from ten cattle killed by the usual type of captive-bolt pistol to be examined for brain emboli. None were found, but the study is being repeated using lungs from 200 cattle killed in ten different slaughterhouses.
SIR—Hornsveld and colleagues (July 20, p 154)1 suggest that the term hyperventilation syndrome should be avoided. In this context I report a 19-year-old nurse who had never been seriously ill. While working in our cardiology laboratory she appeared remarkably tired. Her heart rate was 48 beats per min, and her blood pressure was 90/70 mm Hg. She said that she was taking a β-blocker (50 mg metoprolol twice daily). A few months earlier she had been working at an outside hospital where she had had a syncope of about 1 min duration together with tachycardia (heart rate 130 beats per min) and blood pressure of 170/110 mm Hg. The following investigations were unremarkable: complete physical/ neurological examination, routine blood and urine analyses, thyroid hormones, renin activity, ACTH-stimulation, 24-h urinary catecholamines, 24-h electrocardiography, and blood pressure monitoring, ultrasound of abdomen (including kidneys and adrenal glands) and of cerebral vessels, chest radiograph, and computed tomography of head and abdomen. Thus, the cause of her syncope was unexplained. She was maintained on 50 mg metoprolol twice daily because of raised heart rate and blood pressure during her attacks. Under this therapy, further syncopes did not occur, but she felt continuously weak and tired. A firm diagnosis was established by two questions: “Did you breath deeply? Did you experience paraesthesias and cramps in your fingers?” She replied: “Yes, I had a feeling of asphyxiation. There were horrible paraesthesias in my fingers and around my mouth as well as spasms in my legs and fingers”. These answers clearly pointed to a hyperventilation syndrome, probably of psychogenic origin, to which young women aged 15 to 20 years are particularly susceptible. The attacks may mimic cardiac, pulmonary, and neurological diseases with variable symptoms (eg, dyspnoea, abdominal and/or chest pain, agitation, panic, dizziness, seizures, syncope).2,3 Typical features are tachypnoea, paresthesiae, carpopedal spasms, and hyperreflexia up to tetany. Often, tachycardia and hypertension are present. The hyperventilation syndrome is often unrecognised but early diagnosis is important to prevent irrelevant investigations, serious misdiagnoses, and unnecessary therapies.4 I agree with Hornsveld and colleagues1 that the hyperventilation provocation test is invalid as a diagnostic tool. However, the term hyperventilation syndrome does seem to be indispensable. Perhaps its use should be restricted to psychogenic hyperventilation, in which it is pathophysiologically well founded.2,3 The diagnosis rests ultimately on arterial blood gas analysis, which reveals the effects of hyperventilation with decreased pCO2 and raised pH, and is made by exclusion.2,3 In this context, it is especially important to be aware that hyperventilation can unmask Prinzmetal’s angina by triggering spasms of the coronary arteries.5 Therefore, when a patient complains of angina pectoris during hyperventilation, further cardiological investigations are called for.
K C Taylor Ministry of Agriculture, Fisheries and Food, Government Buildings (Toby Jug Site), Hook Rise South, Tolworth, Surbiton, Surrey KT6 7NF, UK
1
Garland T, Bauer N, Bailey M. Brain emboli in the lungs of cattle after stunning. Lancet 1996; 348: 610–11.
Author’s reply SIR—We thoroughly researched our letter. Hantover presented “The Knocker” to the Institute for Food Research (UK) in 1989. The Institute thoroughly tested it and proclaimed it to be wonderful. The UK Humane Slaughter Association has pneumatic stunners listed as being acceptable for use in the UK. Hantover confirmed to us by fax in May, 1996, that “The Knocker” is still sold in the UK. “The Meat Products and Spreadable Fish Products Regulation 1984 (SI 1984 no 1566) states that mammalian lungs may be used in cooked but not uncooked meat products. An e-mail from the Ministry of Agriculture, Fisheries, and Food (MAFF) on June 21, 1996, informed us “In Statutory Instrument 1984/1566 ‘cooked’, in relation to a food, means subjected to a process of cooking throughout the whole food so that the food is sold for consumption without further cooking, and ‘uncooked’ shall be construed accordingly”. Cooked sausages means sausages like frankfurters and pepperonis. The British Veterinary Association faxed to us on May 28, 1996, “Just to confirm that it is perfectly legal for bovine lungs to enter the human food chain, though they are more commonly used in pet feed”. The fax continues, that “Lungs can be legally sold in their fresh state but would normally be minced and perhaps be mixed with sausage meat in order to cheapen the mix”. We suggest that Taylor’s sample size of ten cattle is much too small to find neurological tissue. His proposed study is also too small: he should include at least 100 slaughterhouses. The presence of brain emboli in the lungs of people after non-invasive head trauma has been known for over 60 years. Reason dictates that any method of stunning to the head will result in the likelihood of brain emboli in the lungs or, indeed, other parts of the body. Tam Garland Texas A&M University, Department of Veterinary Physiology & Pharmacology, College of Veterinary Medicine, College Station, Texas 77843-4466, USA
Vol 348 • September 14, 1996
Kurt Stoschitzky Department of Medicine, Division of Cardiology, Karl Franzens University, A-8036 Graz, Austria
1
Hornsveld HK, Garssen B, Fiedeldij Dop MJC, van Spiegel PI, de Haes JCJM. Double-blind placebo-controlled study of the hyperventilation provocation test and the validity of the
749
Letters to the Editor
Brain emboli in the lungs of cattle
Hyperventilation syndrome
SIR—It would be unfortunate if inaccurate information in Garland’s letter (Aug 31, p 610)1 were to go unchallenged. There is, at present, no evidence that bovine lungs present a source of human exposure to bovine brain tissue in the UK. The type of captive-bolt stunner which injects compressed air into the cranial cavity to disrupt the brain structure is not used on cattle in the UK, and it would be an offence to mince lungs to put into sausages. It is true that lungs are not Specified Bovine Material, but their use in the way described has been prevented by the Meat Products and Spreadable Fish Products Regulations 1984 (SI 1984, no 1566). Since becoming aware some weeks ago of Garland’s claims we have arranged for lungs from ten cattle killed by the usual type of captive-bolt pistol to be examined for brain emboli. None were found, but the study is being repeated using lungs from 200 cattle killed in ten different slaughterhouses.
SIR—Hornsveld and colleagues (July 20, p 154)1 suggest that the term hyperventilation syndrome should be avoided. In this context I report a 19-year-old nurse who had never been seriously ill. While working in our cardiology laboratory she appeared remarkably tired. Her heart rate was 48 beats per min, and her blood pressure was 90/70 mm Hg. She said that she was taking a β-blocker (50 mg metoprolol twice daily). A few months earlier she had been working at an outside hospital where she had had a syncope of about 1 min duration together with tachycardia (heart rate 130 beats per min) and blood pressure of 170/110 mm Hg. The following investigations were unremarkable: complete physical/ neurological examination, routine blood and urine analyses, thyroid hormones, renin activity, ACTH-stimulation, 24-h urinary catecholamines, 24-h electrocardiography, and blood pressure monitoring, ultrasound of abdomen (including kidneys and adrenal glands) and of cerebral vessels, chest radiograph, and computed tomography of head and abdomen. Thus, the cause of her syncope was unexplained. She was maintained on 50 mg metoprolol twice daily because of raised heart rate and blood pressure during her attacks. Under this therapy, further syncopes did not occur, but she felt continuously weak and tired. A firm diagnosis was established by two questions: “Did you breath deeply? Did you experience paraesthesias and cramps in your fingers?” She replied: “Yes, I had a feeling of asphyxiation. There were horrible paraesthesias in my fingers and around my mouth as well as spasms in my legs and fingers”. These answers clearly pointed to a hyperventilation syndrome, probably of psychogenic origin, to which young women aged 15 to 20 years are particularly susceptible. The attacks may mimic cardiac, pulmonary, and neurological diseases with variable symptoms (eg, dyspnoea, abdominal and/or chest pain, agitation, panic, dizziness, seizures, syncope).2,3 Typical features are tachypnoea, paresthesiae, carpopedal spasms, and hyperreflexia up to tetany. Often, tachycardia and hypertension are present. The hyperventilation syndrome is often unrecognised but early diagnosis is important to prevent irrelevant investigations, serious misdiagnoses, and unnecessary therapies.4 I agree with Hornsveld and colleagues1 that the hyperventilation provocation test is invalid as a diagnostic tool. However, the term hyperventilation syndrome does seem to be indispensable. Perhaps its use should be restricted to psychogenic hyperventilation, in which it is pathophysiologically well founded.2,3 The diagnosis rests ultimately on arterial blood gas analysis, which reveals the effects of hyperventilation with decreased pCO2 and raised pH, and is made by exclusion.2,3 In this context, it is especially important to be aware that hyperventilation can unmask Prinzmetal’s angina by triggering spasms of the coronary arteries.5 Therefore, when a patient complains of angina pectoris during hyperventilation, further cardiological investigations are called for.
K C Taylor Ministry of Agriculture, Fisheries and Food, Government Buildings (Toby Jug Site), Hook Rise South, Tolworth, Surbiton, Surrey KT6 7NF, UK
1
Garland T, Bauer N, Bailey M. Brain emboli in the lungs of cattle after stunning. Lancet 1996; 348: 610–11.
Author’s reply SIR—We thoroughly researched our letter. Hantover presented “The Knocker” to the Institute for Food Research (UK) in 1989. The Institute thoroughly tested it and proclaimed it to be wonderful. The UK Humane Slaughter Association has pneumatic stunners listed as being acceptable for use in the UK. Hantover confirmed to us by fax in May, 1996, that “The Knocker” is still sold in the UK. “The Meat Products and Spreadable Fish Products Regulation 1984 (SI 1984 no 1566) states that mammalian lungs may be used in cooked but not uncooked meat products. An e-mail from the Ministry of Agriculture, Fisheries, and Food (MAFF) on June 21, 1996, informed us “In Statutory Instrument 1984/1566 ‘cooked’, in relation to a food, means subjected to a process of cooking throughout the whole food so that the food is sold for consumption without further cooking, and ‘uncooked’ shall be construed accordingly”. Cooked sausages means sausages like frankfurters and pepperonis. The British Veterinary Association faxed to us on May 28, 1996, “Just to confirm that it is perfectly legal for bovine lungs to enter the human food chain, though they are more commonly used in pet feed”. The fax continues, that “Lungs can be legally sold in their fresh state but would normally be minced and perhaps be mixed with sausage meat in order to cheapen the mix”. We suggest that Taylor’s sample size of ten cattle is much too small to find neurological tissue. His proposed study is also too small: he should include at least 100 slaughterhouses. The presence of brain emboli in the lungs of people after non-invasive head trauma has been known for over 60 years. Reason dictates that any method of stunning to the head will result in the likelihood of brain emboli in the lungs or, indeed, other parts of the body. Tam Garland Texas A&M University, Department of Veterinary Physiology & Pharmacology, College of Veterinary Medicine, College Station, Texas 77843-4466, USA
Vol 348 • September 14, 1996
Kurt Stoschitzky Department of Medicine, Division of Cardiology, Karl Franzens University, A-8036 Graz, Austria
1
Hornsveld HK, Garssen B, Fiedeldij Dop MJC, van Spiegel PI, de Haes JCJM. Double-blind placebo-controlled study of the hyperventilation provocation test and the validity of the
749