Blood pressure reduction and stroke1

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Letters to the Editor

CO poisoning even if the patient has been in an open-air environment. Michael Wilson Peter Rosen, MD Emergency Department St. John’s Hospital Jackson, Wyoming PII S0736-4679(01)00395-X

REFERENCES 1. Llano A, Raffin T. Management of carbon monoxide poisoning. Chest 1990;97:165–9. 2. Easley RB. Open air carbon monoxide poisoning in a child swimming behind a boat. South Med J 2000;93:430 –2. 3. Jumbelic MI. Open air carbon monoxide poisoning. J Foren Sci 1998;43:228 –30. 4. Hampson NB, Narkool DM. Carbon monoxide poisoning in children riding in the back of pickup trucks. JAMA 1992;267:538 – 40. 5. Outdoor carbon monoxide poisoning attributed to tractor exhaust—Kentucky, 1997. Morbidity and Mortality Weekly Report 1997;46:1224 –7. 6. Silvers SM, Hampson NB. Carbon monoxide poisoning among recreational boaters. JAMA 1995;274:1614 – 6. 7. Baron R, National Institute for Occupational Safety and Health and the National Park Service as quoted in a Deseret News (Salt Lake City, UT) article December 25, 2000. Doctor hones in on monoxide threat: deaths of 2 boys at Lake Powell spurred research.

e Blood Pressure Reduction and Stroke We read with interest the article by Fischberg et al. regarding stroke precipitated by moderate blood pressure reduction in the November issue of the JEM (1). Stroke, a reduction or cessation of blood supply to a region of the brain that causes neurologic impairment, did occur in the case series of six patients after antihypertensive therapy as noted in their article. Whether there was a causal relationship between exposure (antihypertensive therapy) and outcome (stroke), however, is open to debate. The most important factor in any determination of causality, the correct temporal sequence between exposure and outcome, seems to have been present. At the same time, there is no comparison group to determine whether stroke might have occurred had no treatment been given on initial presentation to a health care professional. Undoubtedly, stroke occurs in patients presenting to a health care professional with elevated blood pressure even if not treated. If the same rate of stroke occurs whether or not antihypertensive treatment is given for the same clinical presentation, this would negate the hypothesis that moderate reductions in blood pressure precipitate stroke per se. This case series was also highly selected in that subjects would only be picked for presentation if they developed a stroke after antihypertensive therapy, with subjects being excluded if no stroke devel-

oped with treatment. The mere fact that the subjects presented to a health care professional suggests that some process was ongoing and may have occurred at the same rate whether or not a moderate reduction in blood pressure occurred from treatment. One definitive way to determine whether moderate or mild reductions in blood pressure facilitate or prevent stroke in patients presenting to a health care professional would be to do a randomized controlled trial of treatment versus no treatment in patients with a predefined clinical presentation and predefined treatment guidelines. As it stands now, it is impossible to be certain whether or not moderate reductions in blood pressure precipitate stroke. As per current consensus guidelines as a substitute for randomized studies, it is probably prudent to initially observe hypertensive patients presenting to the Emergency Department (ED) with an acute stroke or transient ischemic attack if the blood pressure is 220/120 torr or less and there are no competing indications, such as chest pain or congestive heart failure, to lower the blood pressure (2,3). This should be defensible in case the physician is worried about litigation for not treating with the development of a complication because this is considered an acceptable level of care (2– 4). Possibly, future studies might evaluate whether modest reductions in blood pressure would be helpful in this setting. In the age of the information superhighway, when the emergency computed tomography scan can be accessed and read by both the attending radiologist and neurologist from the Internet 24 h a day with the results immediately sent back to the Emergency Department, this is another example of technological advances moving faster in the diagnostic evaluation of medical disease than the clinical studies needed to obtain data on improved treatment of medical maladies such as the one mentioned above. Most likely this always will be the case because well done clinical trials take years to conceptualize, implement, and report on. Gene R. Pesola, MD, MPH Department of Emergency Medicine St. Vincent’s Hospital and New York Medical College New York, New York Jay Avasarala, MD Department of Neurology Washington University School of Medicine St. Louis, Missouri David A. Pesola, MD, FACC Department of Cardiology Marquette General Hospital Marquette, Michigan PII S0736-4679(01)00393-6

The Journal of Emergency Medicine

REFERENCES 1. Fischberg GM, Lozano E, Rajamani K, Ameriso S, Fisher MJ. Stroke precipitated by moderate blood pressure reduction. J Emerg Med 2000;19:339 – 46. 2. Broderick J. Guidelines for medical care and treatment of blood pressure in acute stroke. In: Proceedings of a National Symposium on Rapid Identification and Treatment of Acute Stroke. The National Institute of Neurological Disorders and Stroke. Bethesda, MD: National Institutes of Health; 1997:63– 8. 3. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Dallas, TX: American Heart Association; 2000: I204 –I216. 4. Mathews J. The hypertensive patient in the emergency department. J Emerg Med 2000;19:379.

e Response: It is certainly desirable to have prospective data to identify those at risk for stroke by lowering their blood pressure. Note, however, that there is great heterogeneity of relevant variables, including cerebrovascular anatomy, age, time to presentation, concurrent antithrombotic therapy, and baseline blood pressure. These factors, along with numerous potential variations of blood pressure change, make reliable guidelines difficult to establish by a clinical trial. Nevertheless, efforts to establish more reliable approximations of risks, as well as optimal treatments, are to be encouraged. Glenn Fischberg, MD Department of Neurology University of Southern California Keck School of Medicine Los Angeles, California Mark Fisher, MD Department of Neurology University of California Irvine Medical Center Orange, California PII S0736-4679(01)00394-8

e Central Nervous System Involvement in Childhood Brucellosis Brucellosis caused by organisms of the genus Brucella continues to be a major public health problem worldwide. Humans are accidental hosts and acquire this zoonotic disease from direct contact with an infected animal or consumption of products of an infected animal (1,2). We frequently encounter brucellosis in children in our region, placed in the eastern part of Turkey, because the

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majority of people are farmers and raise domestic animals such as cattle. Particularly in the rural regions, cheese is produced by a combination of fresh milk and specific traditional herbs commonly ingested in our region. Between 1994 and 1998 we followed 103 children with brucellosis in our hospital, only one (0.9%) of whom had central nervous system involvement. Here, we report the findings of this case to draw attention to central nervous system involvement in children with brucellosis. A 6-year-old boy was admitted to our Emergency Department (ED) with a 10-day history of jaundice, abdominal pain, and fever. He was diagnosed with brucellosis and given streptomycine ⫹ co-trimoxazole for 4 days by a physician, but the symptoms did not subside. In the past history, two febrile convulsion attacks at age 1 and 5 years were noted. The father and mother and two siblings were also being followed for brucellosis in our outpatient clinic at the time of hospitalization of this patient. On physical examination, a high fever of 38.5°C and tachycardia were recorded. The weight and height were 15 kg (3rd percentile) and 103 cm (3rd percentile), respectively. He had fatigue, with a toxic appearance and scleraicterus. The enlarged liver was palpable 4 cm below the right costal margin, and the spleen was enlarged to 3 cm below the left costal margin. On laboratory investigation, routine urine analysis was normal. Hemoglobin was 9.6 g/dL, leukocyte count 5900/mm3, platelet count 90,000/mm3, erythrocyte sedimentation rate 7 mm/h. On peripheral blood smear, lymphocytes were predominant, the morphological characteristics of red blood cells were normochromic and normocytoic, and thrombocytopenia was noted. Serum electrolytes and renal function tests were within the normal range. Serum total bilirubin was 8.3 mg/dL, direct bilirubin 4.5 mg/dL, aspartate aminotransferase 300 U/L, alanine aminotransferase 275 U/L, alkaline phosphatase 813 IU/L, and ␥-glutamyltransferase 750 U/L. A chest X-ray study was normal. Abdominal ultrasonography revealed hepatosplenomegaly. Cerebrospinal fluid (CSF) examination showed lymphocytes of 33/mm3, protein of 23 mg/dL, and glucose of 39 mg/dL. Both serum and CSF agglutination tests for brucellosis were positive in 1:1280 titration. Brucella was cultured from blood and bone marrow aspiration cultures. Histopathological examination of the liver was compatible with brucellosis. The patient was hospitalized and rifampin plus co-trimoxazole were initiated. On day 4 of admission, ceftriaxone was added to the treatment regimen because the CSF agglutination test was found to be elevated. A combination of three drugs was given for 15 days. The liver function tests became normal on day 12 of admission and he was discharged from hospital with the regimen of co-trimoxazole ⫹ rifampin, which were used for a 2-month period. At