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March 6th, 2012 posted by Paul Rega, MD, FACEP March 6, 2012 @ 4:31 pm

C. difficile poses threat across medical facilities

Infections from Clostridium difficile (C. difficile), a bacteria that causes diarrhea and other health issues, is a patient safety concern in all types of medical facilities, not just hospitals as traditionally thought, according to a new Vital Signs report today from the Centers for Disease Control and Prevention. While many health care-associated infections, such as bloodstream infections, declined in the past decade, C. difficile infection rates and deaths climbed to historic highs.

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March 6th, 2012 posted by Paul Rega, MD, FACEP @ 4:28 pm

FDA: Selected AED Recall

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http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm294538.htm?source=govdelivery

Cardiac Science Powerheart, CardioVive, CardioLife; GE Responder and Responder Pro; and Nihon-Kohden Automated External Defibrillators (AEDs): Class I Recall – Defective Component

Affected Models include:

 

[Posted 03/02/2012]

AUDIENCE: Emergency Medicine, Cardiology, Risk Manager

ISSUE: FDA notified healthcare professionals and medical care organizations of the Class 1 recall of the listed AEDs which contain a component that may fail unexpectedly due to a defect. If the component were to fail during a rescue attempt, the AED may not deliver defibrillation therapy, causing serious adverse health consequences, including death. The unit’s self test may not detect the failure or impending failure of the component.

BACKGROUND: These products are used for emergency treatment of victims showing symptoms of sudden cardiac arrest who are unresponsive and not breathing. These AEDs were manufactured and distributed from July 1, 2011 through December 30, 2011.

RECOMMENDATION: Affected customers are advised to contact the firm to arrange for delivery of shipping materials for an immediate return of their AEDs for repair. The affected devices will receive a hardware correction, and the same serial number device will be returned to the customer in most cases.
[03/02/2012 - Recall Notice1 - FDA]
[01/13/2012 - Urgent Voluntary Medical Device Recall Letter2 disclaimer icon 3- Cardiac Science]

 
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March 6th, 2012 posted by Paul Rega, MD, FACEP @ 1:30 am

Nitrogen Dioxide Exposure in an Indoor Ice Arena

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http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6108a2.htm?s_cid=mm6108a2_e

Exposure to Nitrogen Dioxide in an Indoor Ice Arena — New Hampshire, 2011

Weekly

March 2, 2012 / 61(08);139-142

In January 2011, the New Hampshire Department of Health and Human Services (NHDHHS) investigated acute respiratory symptoms in a group of ice hockey players. The symptoms, which included cough, shortness of breath, hemoptysis, and chest pain or tightness, were consistent with exposure to nitrogen dioxide gas (NO2), a byproduct of combustion. Environmental and epidemiologic investigations were begun to determine the source of the exposure and identify potentially exposed persons. This report summarizes the results of those investigations, which implicated a local indoor ice arena that had hosted two hockey practice sessions during a 24-hour period when the arena ventilation system was not functioning. A total of 43 exposed persons were interviewed, of whom 31 (72.1%) reported symptoms consistent with NO2 exposure. The highest attack rate was among the hockey players (87.9%). After repair of the ventilation system, no additional cases were identified. To prevent similar episodes, ice arena operators should ensure ventilation systems and alarms are operating properly and that levels of NO2 and carbon monoxide (CO) are monitored continuously for early detection of increased gas levels.

On January 4, 2011, NHDHHS was notified that a previously healthy male aged 19 years was hospitalized for sudden onset of cough, shortness of breath, and hemoptysis shortly after a team ice hockey practice. His physical examination was notable for crackles heard in both lung bases, and his oxygen saturation was decreased to 88%–91% on room air (normal: >95%). Bilateral infiltrates and nodules were observed on chest computed tomography. Investigation revealed that other members of his team (team A) and at least one player from another local team (team B) were experiencing similar symptoms and independently had been directed to local emergency departments. Both teams had practiced in the same ice arena on the evening of January 3.

Further investigation revealed that on the morning of January 3, the ventilation system circuit board failed while being serviced, making the ventilation system inoperable. Two arena workers then spent 60–90 minutes resurfacing the ice using propane-powered equipment, finishing at approximately 11:30 a.m. The workers later reported observing a yellow haze over the ice, but neither reported any symptoms. Team A’s practice was held from 6:00 to 8:00 p.m., and team B’s practice was from 8:00 to 10:00 pm. The yellow haze was noted by players, coaches, and spectators at both practices. The next morning, January 4, at 9 a.m., the circuit board was replaced, and the ventilation system began operating normally. No other exposures had occurred during the time the ventilation system was not functional.

The arena housed a standard-sized ice hockey rink and was owned by a private school. The rink ice was maintained using propane-powered ice-resurfacing machines. The arena had an air monitoring system for CO and carbon dioxide (CO2), but not for NO2.

On the evening of January 4, NHDHHS staff members began interviewing all 33 players and five coaches who were present at practices on January 3. From these initial interviews, case finding was expanded to include four practice spectators and the two arena workers who operated the resurfacing equipment, for a total of 44 exposed persons. Questionnaires that assessed symptoms, exposures, and environmental observations were administered by NHDHHS staff members in person or by telephone. All but one of the 44 exposed persons completed the questionnaire.

A case was defined as the onset of cough, hemoptysis, chest pain, chest tightening, shortness of breath, headache, dizziness, nausea, or vomiting within 48 hours of being in the ice arena from 11:00 a.m. on Monday, January 3, to 9:00 a.m. on Tuesday, January 4. Illnesses with symptoms consistent with the common cold (e.g., runny nose, fever, and head congestion) were not counted as cases. Using this definition, 31 cases were identified among the 43 persons interviewed: 29 among the 33 players (87.9%) and two among the five coaches (40%). None of the four spectators had illness consistent with the case definition, nor did the one arena worker who completed the questionnaire. Most patients (90.3%) had two or more symptoms (Table 1). Although 10 nonplayers (coaches, spectators, and arena personnel) were exposed, players were nearly four times as likely to become ill (87.9% versus 20.0%, risk ratio [RR] = 4.39, 95% confidence interval [CI] = 1.26–15.28). Compared with nonplayers, players also were more likely to have spent more time on the ice (defined as >1 hour versus ≤1 hour) (84.8% versus 40.0%, RR = 2.12, CI = 0.98–4.59). As time spent on the ice increased, so did the attack rate and amount of hemoptysis (Figure).

On January 5, the New Hampshire Department of Environmental Services (NHDES) and the New Hampshire State Fire Marshal’s Office (NHFMO) inspected the ice arena. Measurements for CO and NO2 were taken before running the resurfacing equipment (baseline conditions) and while operating the equipment, and recorded at breathing zone (where persons on the ice would be exposed) as well as adjacent to the equipment exhaust pipe. Air sampling was performed for NO using a Gastec piston hand pump equipped with Sensidyne colorimetric gas detector tubes. A TSI Q-Trak indoor air quality monitor was used to obtain direct readings for CO. While the ice resurfacer was operating in the arena, the NO2 concentration in the breathing zone increased, reaching 0.5 parts per million, the level at which corrective action must be taken according to regulations in states that regulate indoor air quality in ice arenas (Table 2). These measurements did not simulate actual conditions in the arena on January 3 because the arena ventilation system had been fully functional for approximately 24 hours at the time of sampling.

Beginning January 20, a follow-up questionnaire was administered to exposed persons to assess late-onset and persistent symptoms. Thirty-nine (90.7%) of the original 43 persons interviewed responded to the follow-up questionnaire. No new cases were identified; however, two of the original patients reported late onset of hemoptysis (at 5 days and 21 days postexposure) and were advised to seek medical evaluation. Six patients (20%) reported persistent symptoms: shortness of breath on exertion (four cases), cough (two cases), and fatigue (one case).

NHDHHS, in consultation with the Northern New England Poison Center, recommended that all exposed persons seek medical evaluation, even if asymptomatic, preferably at a designated occupational health clinic. Ultimately, 39 (90.6%) complied (30 of 31 [96.8%] patients and nine of 12 [75.0%] of persons without symptoms). After these initial medical evaluations, the need for follow-up was determined on a case-by-case basis, dependent on severity. NHDES and NHFMO recommended that the arena include an NO2 sensor in the air monitoring system, establish alarm set points for CO and NO2 in line with air action level recommendations (Table 2), and test this system at least monthly. The arena also was advised to conduct maintenance and tailpipe emissions testing on all ice resurfacing equipment at the beginning of the ice arena season and at least once during the season, and consider installing catalytic converters to reduce emissions. However, the most reliable way to prevent exposure in this setting is to replace propane-powered equipment with electric equipment, which should be considered as a long-term solution.

Editorial Note

Respiratory illness caused by NO2 in indoor hockey rinks has been documented infrequently in the literature. Hazardous levels of NO2 in ice arenas often result from malfunction of propane-fueled ice resurfacing equipment or arena ventilation systems (1–5).

Most ice arenas are designed to minimize natural ventilation in an effort to keep warm air away from the ice surface and the ice temperature near freezing. This can create a thermal inversion in which cold air and gases (especially NO2, which is denser than air) become trapped over the ice (6). The protective glass between spectator stands and the ice rink creates an additional barrier to airflow. In this episode, exposure was made worse by prolonged use of propane-powered ice resurfacers while the ventilation system was off.

Nitrogen dioxide is a yellow to reddish brown gas that irritates the upper and lower respiratory tracts and can cause short-term central nervous system symptoms (6). Severity of symptoms is related to duration of NO2 exposure (5,6), although exertion with increased frequency and depth of respiration might have made the hockey players more susceptible than the spectators or coaches to the effects of the gas. This has been reported during other exposures (4). No specific antidote for NO2 toxicity exists, and therapy is focused on supportive care and prolonged monitoring (6). The long-term consequences of acute NO2 exposure are not well understood, but in this instance, six of 31 persons had persistent symptoms up to 4 weeks postexposure. Other studies document self-reported symptoms several weeks after exposure (4), 6 months postexposure (1), and even 5 years postexposure (7). However, tests of pulmonary function (e.g., spirometry and bronchoprovocation) at 10 days, 2 months, and 6 months postexposure have provided little objective evidence of compromised lung function (1,4). The small but unpredictable potential for delayed development of life-threatening conditions such as bronchiolitis obliterans warrants follow-up of exposed persons (6).

The findings in this report are subject to at least two limitations. First, a broad case definition was used to ensure complete case finding and appropriate follow-up; however, this might have led to inflation of the attack rate. Second, with the exception of the index case, symptom data were based on self-report, which also might have inflated the attack rate.

No federal regulations exist for indoor air quality in ice arenas, and only three states have enacted regulations (Minnesota, Rhode Island, and Massachusetts). Only Minnesota and Massachusetts specify limits for NO2 levels. After this incident, NHFMO sent an informational bulletin to all indoor ice arenas in the state based, in part, on recommendations from the U.S. Environmental Protection Agency and the regulations existing in other states (Table 2). Without legislated regulations, however, direct education of the public about signs and symptoms of NO2 exposure and education of arena staff about the risk of NO2 toxicity is important for prevention.

References

  1. Kahan ES, Martin UJ, Spungen S, Ciccolella D, Criner GJ. Chronic cough and dyspnea in ice hockey players after an acute exposure to combustion products of a faulty ice resurfacer. Lung.2007;185:47–54.
  2. CDC. Nitrogen dioxide and carbon monoxide intoxication in an indoor ice-arena—Wisconsin, 1992. MMWR 1992;41:383–5.
  3. Pelham TW, Holt LE, Moss MA. Exposure to carbon monoxide and nitrogen dioxide in enclosed ice arenas. Occup Environ Med 2002;59:224–33.
  4. Hedberg K, Hedberg CW, Iber C, et al. An outbreak of nitrogen dioxide-induced respiratory illness among ice hockey players. JAMA 1989;262:3014–7.
  5. Rosenlund M, Bluhm G. Health effects resulting from nitrogen dioxide exposure in an indoor ice arena. Arch Environ Health 1999;54:52–7.
  6. Greenberg MI, Hamilton RJ, Phillips SD, McCluskey GJ, eds. Occupational, industrial, and environmental toxicology. 2nd ed. Philadelphia, PA: Mosby; 2003.
  7. Rosenlund M, Jungnelius S, Bluhm G, Svartengren M. A 5-year follow-up of airway symptoms after nitrogen dioxide exposure in an indoor ice arena. Arch Environ Health 2004;59:213–7.


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March 6th, 2012 posted by Paul Rega, MD, FACEP @ 1:23 am

Amantadine for Severe Traumatic Brain Injury

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http://www.nejm.org/doi/full/10.1056/NEJMoa1102609?query=emergency-medicine

Placebo-Controlled Trial of Amantadine for Severe Traumatic Brain Injury

Joseph T. Giacino, Ph.D., John Whyte, M.D., Ph.D., Emilia Bagiella, Ph.D., Kathleen Kalmar, Ph.D., Nancy Childs, M.D., Allen Khademi, M.D., Bernd Eifert, M.D., David Long, M.D., Douglas I. Katz, M.D., Sooja Cho, M.D., Stuart A. Yablon, M.D., Marianne Luther, M.D., Flora M. Hammond, M.D., Annette Nordenbo, M.D., Paul Novak, O.T.R., Walt Mercer, Ph.D., Petra Maurer-Karattup, Dr.Rer.Nat., and Mark Sherer, Ph.D.

N Engl J Med 2012; 366:819-826March 1, 2012

Amantadine hydrochloride is one of the most commonly prescribed medications for patients with prolonged disorders of consciousness after traumatic brain injury. Preliminary studies have suggested that amantadine may promote functional recovery.

 Results:  Amantadine accelerated the pace of functional recovery during active treatment in patients with post-traumatic disorders of consciousness.


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March 6th, 2012 posted by Paul Rega, MD, FACEP @ 1:06 am

Phone triage worked for pregnant women during H1N1

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http://www.sciencedirect.com/science/article/pii/S000293781200186X

Telephone triage: Protocols and clinical judgment are not mutually exclusive
Journal of Emergency Nursing, Volume 26, Issue 3, June 2000, Page 203
Coreen Arioto

Of the 230 women who were evaluated, 41% were treated as outpatients and 59% were seen in the evaluation unit. Of those treated as outpatients, 9% were eventually seen in the evaluation unit and only 4% were ultimately admitted, with a maximum hospitalization of 4 days.



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March 6th, 2012 posted by Paul Rega, MD, FACEP @ 1:01 am

Bangladesh: 3 human H5N1 cases

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http://bdnews24.com/details.php?id=219613&cid=2

Nurul Islam Hasib
bdnews24.com Senior Correspondent

Dhaka, Mar 5 (bdnews24.com)—”Detection of three new human infections with the deadly H5NI strain of bird flu in a week has set alarm bells ringing as scientists have found evidence of the virus in the live-bird market in crowded Dhaka….”



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March 6th, 2012 posted by Paul Rega, MD, FACEP @ 12:57 am

Avian influenza – situation in Viet Nam

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http://www.who.int/csr/don/2012_03_05/en/index.html

5 March 2012 -The Ministry of Health has reported a confirmed case of human infection with avian influenza A (H5N1) virus.

The case is a 22 year-old male from Thanh Hoa province who lived and worked in Binh Duong province. He developed symptoms on 17 February 2012 and first sought medical care on 21 February 2012. He was admitted to the intensive care unit of the Hospital for Tropical Diseases on 23 February 2012 and received Oseltamivir upon admission. He is currently still in hospital.

Confirmatory test results for influenza A (H5N1) were obtained on 25 February 2012 by the Pasteur Institute Ho Chi Minh City, a WHO National influenza Centre.

Epidemiological investigation indicates that the man was involved in the slaughter and consumption of ducks. Pasteur Institute in Ho Chi Minh City and the local health sector are conducting the investigation and response. Close contacts of the case with fever have received prophylaxis and are being monitored; all have been confirmed as negative for H5N1 by PCR.

To date, of the 122 confirmed cases in Viet Nam, 61 have been fatal.



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