386
Letters to the Editor
prior stroke may be necessary to maintain the validity of the results as originally reported. Although not written with this intent, in 2009 the author group published the data necessary to conduct this reanalysis (5). These newer data show no benefit in the adjusted primary analysis comparing favorable outcome after 90 days between the thrombolytic and placebo groups (odds ratio 1.19; confidence interval 0.89–1.59). Although obscure, this statistical error is not trivial. In the ECASS III trial, the probability that there would be so few patients with a history of stroke in the thrombolytic group (7.7%) compared with the placebo group (14.1%) was 1.5 in 1000. It is unfortunate that the randomization was so abnormally skewed, as a beneficial intravenous therapy would have been welcomed for patients with delayed stroke presentations. Emergency physicians should be aware of this important deficit in the single trial supporting delayed use of thrombolytics in ischemic stroke. Unless future studies refute the data from ECASS III and previous neutral and negative trials, the safest action may be to withhold thrombolytic therapy in stroke after 3 h (6–8). Bradley D. Shy, MD Department of Emergency Medicine Mount Sinai School of Medicine New York, New York http://dx.doi.org/10.1016/j.jemermed.2012.05.014 REFERENCES 1. Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med 2008;359: 1317–29. 2. Hill MD, Yiannakoulias N, Jeerakathil T, et al. The high risk of stroke immediately after transient ischemic attack: a population-based study. Neurology 2004;62:2015. 3. Hier DB, Foulkes MA, Swiontoniowski M, et al. Stroke recurrence within 2 years after ischemic infarction. Stroke 1991;22: 155–61. 4. Yamamoto H, Bogousslavsky J. Mechanisms of second and further strokes. J Neurol Neurosurg Psychiatry 1998;64:771–6. 5. Bluhmki E, Chamorro A, Da´valos A, et al. Stroke treatment with alteplase given 3.0–4.5 h after onset of acute ischaemic stroke (ECASS III): additional outcomes and subgroup analysis of a randomised controlled trial. Lancet Neurol 2009;8:1095–102. 6. The Multicenter Acute Stroke Trial – Europe Study Group. Thrombolytic therapy with streptokinase in acute ischemic stroke. N Engl J Med 1996;335:145–50. 7. Donnan GA, Davis SM, Chambers BR, et al. Streptokinase for acute ischemic stroke with relationship to time of administration: Australian Streptokinase (ASK) Trial Study Group. JAMA 1996;276: 961–6. 8. Clark WM, Wissman S, Albers GW, et al. Recombinant tissue-type plasminogen activator (Alteplase) for ischemic stroke 3 to 5 hours after symptom onset. The ATLANTIS Study: a randomized controlled trial. Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke. JAMA 1999;282:2019–26.
, RE: ACUTE ABDOMEN ASSOCIATED WITH ORGANOPHOSPHATE POISONING , To the Editor: I enjoyed reading the article entitled “Acute abdomen associated with organophosphate poisoning” published in The Journal of Emergency Medicine (1). The authors have prospectively evaluated all patients presenting to their Emergency Department due to carbamate or organophosphate compounds poisoning within a 2-year period, while performing ultrasonographic examination in 22 conscious patients with moderate to severe abdominal pain. Fourteen of them (63.6%) had abdominal free fluid. Only one developed pancreatitis. His abdominal findings persisted despite resolution in muscarinic signs after the treatment. It seems that abdominal pain of the remainder resolved after the treatment of poisoning. They then concluded that the patients with a diagnosis of organophosphate poisoning should be screened for acute abdomen and undergo routine abdominal ultrasonography. The question that arises here is, “How can performance of abdominal ultrasonography influence the patients’ management?” As you know, abdominal pain and free fluid may be due to either the direct toxic effect of organophosphate on the muscarinic receptors or pancreatitis secondary to the cholinergic stimulation, which both resolve with early and proper treatment of poisoning (2,3). Therefore, will the treatment be anything but what is done in the course of organophosphate/carbamate poisoning? It should not be forgotten that the literature suggests a high incidence of silent or elusive pancreatitis in these patients (4). Also, abdominal pain is one of the most frequent symptoms associated with organophosphate poisoning (5–7). With respect to these points, do the authors believe that abdominal ultrasonography is a cost-benefit intervention in every organophosphate- or carbamate-intoxicated patient with abdominal pain? It seems that in these patients it is better that if the abdominal symptoms persist after the treatment of organophosphate or carbamate poisoning and their serum amylase is high, ultrasonography be performed to follow the patients regarding the very unlikely possibility of development of pancreatic necrosis. However, even in this case, abdominal computed tomography is a better choice. Hossein Sanaei-Zadeh, MD Division of Medical Toxicology,
The Journal of Emergency Medicine
Department of Emergency Medicine, Hazrat Ali-Asghar (p) Hospital, Shiraz University of Medical Sciences, Shiraz, Iran http://dx.doi.org/10.1016/j.jemermed.2013.08.134 REFERENCES 1. Aslan S, Cakir Z, Emet M, et al. Acute abdomen associated with organophosphate poisoning. J Emerg Med 2011;41:507–12. 2. Christoph RA. Organophosphates and carbamates. In: Manual of toxicologic emergencies. Chicago: Year Book; 1989:626–8. 3. Makrides C, Koukouvas M, Achillews G, Tsikkos S, Vounou E, Symeonides M. Methomyl-induced severe acute pancreatitis: possible etiological association. JOP 2005;6:166–71. 4. Lankisch PG, Muller CH, Niederstadt H, Brand A. Painless acute pancreatitis subsequent to anticholinesterase insecticide (Parathion) intoxication. Am J Gastroenterol 1990;85:872–5. 5. Robey W. Insecticides, herbicides, rodenticides. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency medicine: a comprehensive study guide. 6th edn. New York: McGraw-Hill; 2004: 1134–8. 6. Hayes MM, van derWesthuizen NG, Gelfand M. Organophosphate poisoning in Rhodesia. S Afr Med J 1978;54:230–4. 7. Exner CJ, Ayala GU. Organophosphate and carbamate intoxication in La Paz, Bolivia. J Emerg Med 2009;36:348–52.
, RESPONSE TO LETTER , To the Editor: We appreciate the opportunity to respond to the comments regarding our article (1). In the context of costeffectiveness, it is certainly irrational to recommend ultrasound (US) for every patient with organophosphate poisoning (OPI). In the present study, we recommended US for patients with abdominal pain in the course of OPI. It is well known that US is a low-cost and repeatable modality performed easily at the bedside, without untoward radiation in the acute setting. On the other hand, it would be more reasonable to proceed with abdominal computed tomography in patients with persistent vomiting and high serine amylase levels, with a thorough search for pancreatitis. Mustafa Serinken, MD Department of Emergency Medicine Pamukkale University Medical School Denizli, Turkey http://dx.doi.org/10.1016/j.jemermed.2013.09.031 REFERENCE 1. Aslan S, Cakir Z, Emet M, et al. Acute abdomen associated with organophosphate poisoning. J Emerg Med 2011;41:507–12.
387
, COMPLIANCE OF THE AMERICANS WITH DISABILITY ACT , To the Editor: Revolutionary, technological advances have been designed and implemented in our country, which have increased the accessibility for people with disabilities. These technological advances include: Telecommunication Devices for the Deaf (TDD), handicap-accessible parking, cement ramps from entrance of parking lot to the facility, and electronic door openers. On July 22, 1990, President George H.W. Bush signed into law the Americans with Disability Act (ADA) of 1990. Under this law, no individual will be discriminated against on the basis of disability, including deafness. With the passage of this law, the Civil Rights Division of the Department of Justice became integrated into ADA policy to enhance the enactment of the ADA legislation. With the employment freeze of the ADA and the overwhelming number of complaints filed yearly requesting compliance of the ADA, it has been a challenging problem for the ADA to ensure that people with disabilities in our country are not subjected to discrimination. During the last 40 years, leaders in our country have designed and implemented revolutionary, technological advances that have dramatically increased the accessibility for persons with disabilities. These advances include the following four components: Telecommunication Devices, handicap-accessible parking, cement ramps from entrance of parking lot to the facility, and electronic door openers. These components have been carefully integrated into the Americans with Disability Act that ensures implementation in all states. Once the ADA was passed, the Civil Rights Division was integrated into the ADA to ensure optimal enforcement of the law. Dr. Richard Edlich was appointed to Director of the Emergency Department (ED) at the University of Virginia Health Science Center (Charlottesville, VA) in 1974 (1). One of his first accomplishments was to work with the gifted scientist in internal medicine, Dr. Dan Spyker, to develop a Poison Control Center (2). After they developed the Poison Control Center, they naively thought that all Virginia citizens could contact them for guidance and advice regarding drug overdoses and drug reactions. This momentary naive overconfidence was shattered when Dr. Edlich received a handwritten note from a deaf disgruntled mother of a patient. The mother’s note was a cry for help because she could not contact the Poison Control Center for advice regarding her son, whom she suspected had taken an overdose of medication. She indicated that neither the Poison Control Center nor the University of Virginia Health Science Center had a TDD.
Letters to the Editor
prior stroke may be necessary to maintain the validity of the results as originally reported. Although not written with this intent, in 2009 the author group published the data necessary to conduct this reanalysis (5). These newer data show no benefit in the adjusted primary analysis comparing favorable outcome after 90 days between the thrombolytic and placebo groups (odds ratio 1.19; confidence interval 0.89–1.59). Although obscure, this statistical error is not trivial. In the ECASS III trial, the probability that there would be so few patients with a history of stroke in the thrombolytic group (7.7%) compared with the placebo group (14.1%) was 1.5 in 1000. It is unfortunate that the randomization was so abnormally skewed, as a beneficial intravenous therapy would have been welcomed for patients with delayed stroke presentations. Emergency physicians should be aware of this important deficit in the single trial supporting delayed use of thrombolytics in ischemic stroke. Unless future studies refute the data from ECASS III and previous neutral and negative trials, the safest action may be to withhold thrombolytic therapy in stroke after 3 h (6–8). Bradley D. Shy, MD Department of Emergency Medicine Mount Sinai School of Medicine New York, New York http://dx.doi.org/10.1016/j.jemermed.2012.05.014 REFERENCES 1. Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med 2008;359: 1317–29. 2. Hill MD, Yiannakoulias N, Jeerakathil T, et al. The high risk of stroke immediately after transient ischemic attack: a population-based study. Neurology 2004;62:2015. 3. Hier DB, Foulkes MA, Swiontoniowski M, et al. Stroke recurrence within 2 years after ischemic infarction. Stroke 1991;22: 155–61. 4. Yamamoto H, Bogousslavsky J. Mechanisms of second and further strokes. J Neurol Neurosurg Psychiatry 1998;64:771–6. 5. Bluhmki E, Chamorro A, Da´valos A, et al. Stroke treatment with alteplase given 3.0–4.5 h after onset of acute ischaemic stroke (ECASS III): additional outcomes and subgroup analysis of a randomised controlled trial. Lancet Neurol 2009;8:1095–102. 6. The Multicenter Acute Stroke Trial – Europe Study Group. Thrombolytic therapy with streptokinase in acute ischemic stroke. N Engl J Med 1996;335:145–50. 7. Donnan GA, Davis SM, Chambers BR, et al. Streptokinase for acute ischemic stroke with relationship to time of administration: Australian Streptokinase (ASK) Trial Study Group. JAMA 1996;276: 961–6. 8. Clark WM, Wissman S, Albers GW, et al. Recombinant tissue-type plasminogen activator (Alteplase) for ischemic stroke 3 to 5 hours after symptom onset. The ATLANTIS Study: a randomized controlled trial. Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke. JAMA 1999;282:2019–26.
, RE: ACUTE ABDOMEN ASSOCIATED WITH ORGANOPHOSPHATE POISONING , To the Editor: I enjoyed reading the article entitled “Acute abdomen associated with organophosphate poisoning” published in The Journal of Emergency Medicine (1). The authors have prospectively evaluated all patients presenting to their Emergency Department due to carbamate or organophosphate compounds poisoning within a 2-year period, while performing ultrasonographic examination in 22 conscious patients with moderate to severe abdominal pain. Fourteen of them (63.6%) had abdominal free fluid. Only one developed pancreatitis. His abdominal findings persisted despite resolution in muscarinic signs after the treatment. It seems that abdominal pain of the remainder resolved after the treatment of poisoning. They then concluded that the patients with a diagnosis of organophosphate poisoning should be screened for acute abdomen and undergo routine abdominal ultrasonography. The question that arises here is, “How can performance of abdominal ultrasonography influence the patients’ management?” As you know, abdominal pain and free fluid may be due to either the direct toxic effect of organophosphate on the muscarinic receptors or pancreatitis secondary to the cholinergic stimulation, which both resolve with early and proper treatment of poisoning (2,3). Therefore, will the treatment be anything but what is done in the course of organophosphate/carbamate poisoning? It should not be forgotten that the literature suggests a high incidence of silent or elusive pancreatitis in these patients (4). Also, abdominal pain is one of the most frequent symptoms associated with organophosphate poisoning (5–7). With respect to these points, do the authors believe that abdominal ultrasonography is a cost-benefit intervention in every organophosphate- or carbamate-intoxicated patient with abdominal pain? It seems that in these patients it is better that if the abdominal symptoms persist after the treatment of organophosphate or carbamate poisoning and their serum amylase is high, ultrasonography be performed to follow the patients regarding the very unlikely possibility of development of pancreatic necrosis. However, even in this case, abdominal computed tomography is a better choice. Hossein Sanaei-Zadeh, MD Division of Medical Toxicology,
The Journal of Emergency Medicine
Department of Emergency Medicine, Hazrat Ali-Asghar (p) Hospital, Shiraz University of Medical Sciences, Shiraz, Iran http://dx.doi.org/10.1016/j.jemermed.2013.08.134 REFERENCES 1. Aslan S, Cakir Z, Emet M, et al. Acute abdomen associated with organophosphate poisoning. J Emerg Med 2011;41:507–12. 2. Christoph RA. Organophosphates and carbamates. In: Manual of toxicologic emergencies. Chicago: Year Book; 1989:626–8. 3. Makrides C, Koukouvas M, Achillews G, Tsikkos S, Vounou E, Symeonides M. Methomyl-induced severe acute pancreatitis: possible etiological association. JOP 2005;6:166–71. 4. Lankisch PG, Muller CH, Niederstadt H, Brand A. Painless acute pancreatitis subsequent to anticholinesterase insecticide (Parathion) intoxication. Am J Gastroenterol 1990;85:872–5. 5. Robey W. Insecticides, herbicides, rodenticides. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency medicine: a comprehensive study guide. 6th edn. New York: McGraw-Hill; 2004: 1134–8. 6. Hayes MM, van derWesthuizen NG, Gelfand M. Organophosphate poisoning in Rhodesia. S Afr Med J 1978;54:230–4. 7. Exner CJ, Ayala GU. Organophosphate and carbamate intoxication in La Paz, Bolivia. J Emerg Med 2009;36:348–52.
, RESPONSE TO LETTER , To the Editor: We appreciate the opportunity to respond to the comments regarding our article (1). In the context of costeffectiveness, it is certainly irrational to recommend ultrasound (US) for every patient with organophosphate poisoning (OPI). In the present study, we recommended US for patients with abdominal pain in the course of OPI. It is well known that US is a low-cost and repeatable modality performed easily at the bedside, without untoward radiation in the acute setting. On the other hand, it would be more reasonable to proceed with abdominal computed tomography in patients with persistent vomiting and high serine amylase levels, with a thorough search for pancreatitis. Mustafa Serinken, MD Department of Emergency Medicine Pamukkale University Medical School Denizli, Turkey http://dx.doi.org/10.1016/j.jemermed.2013.09.031 REFERENCE 1. Aslan S, Cakir Z, Emet M, et al. Acute abdomen associated with organophosphate poisoning. J Emerg Med 2011;41:507–12.
387
, COMPLIANCE OF THE AMERICANS WITH DISABILITY ACT , To the Editor: Revolutionary, technological advances have been designed and implemented in our country, which have increased the accessibility for people with disabilities. These technological advances include: Telecommunication Devices for the Deaf (TDD), handicap-accessible parking, cement ramps from entrance of parking lot to the facility, and electronic door openers. On July 22, 1990, President George H.W. Bush signed into law the Americans with Disability Act (ADA) of 1990. Under this law, no individual will be discriminated against on the basis of disability, including deafness. With the passage of this law, the Civil Rights Division of the Department of Justice became integrated into ADA policy to enhance the enactment of the ADA legislation. With the employment freeze of the ADA and the overwhelming number of complaints filed yearly requesting compliance of the ADA, it has been a challenging problem for the ADA to ensure that people with disabilities in our country are not subjected to discrimination. During the last 40 years, leaders in our country have designed and implemented revolutionary, technological advances that have dramatically increased the accessibility for persons with disabilities. These advances include the following four components: Telecommunication Devices, handicap-accessible parking, cement ramps from entrance of parking lot to the facility, and electronic door openers. These components have been carefully integrated into the Americans with Disability Act that ensures implementation in all states. Once the ADA was passed, the Civil Rights Division was integrated into the ADA to ensure optimal enforcement of the law. Dr. Richard Edlich was appointed to Director of the Emergency Department (ED) at the University of Virginia Health Science Center (Charlottesville, VA) in 1974 (1). One of his first accomplishments was to work with the gifted scientist in internal medicine, Dr. Dan Spyker, to develop a Poison Control Center (2). After they developed the Poison Control Center, they naively thought that all Virginia citizens could contact them for guidance and advice regarding drug overdoses and drug reactions. This momentary naive overconfidence was shattered when Dr. Edlich received a handwritten note from a deaf disgruntled mother of a patient. The mother’s note was a cry for help because she could not contact the Poison Control Center for advice regarding her son, whom she suspected had taken an overdose of medication. She indicated that neither the Poison Control Center nor the University of Virginia Health Science Center had a TDD.
