Background Despite the high sensitivity and negative predictive value of contemporary high-sensitivity troponin T assays (hsTnT), creatine kinase (CK) continues to be routinely tested for the diagnosis of acute coronary syndrome (ACS). We conducted a study to identify the clinical utility of routine CK measurement, its relevance in clinical decision making in the era of hsTnT, and the potential cost-savings achievable by limiting its use. Methods We conducted a retrospective review of all adult patients presenting to a tertiary care center in the year 2017. We identified patients presenting with cardiac complaints who had non-diagnostic hsTnT and positive CK. These patients underwent chart review to determine whether a diagnosis of AMI was made. Results A total of 36,251 presentations were reviewed. 9951 had cardiac complaints and 8150 had CK measured. 82% of these patients had hsTnT and CK measured; 2012 of these patients had non-diagnostic hsTnT with positive CK. Of these 2012 patients, only 1 was subsequently diagnosed with AMI (0.012%). CK provided no diagnostic benefit over hsTnT alone in > 99.9% of cases. With a cost for CK of $4/test, we estimated that routine CK testing costs at least $32,000 per year in our center, and over $100,000 per year across the region. Conclusion Routine CK testing does not provide a significant benefit to patient care and therefore represents an unnecessary system cost. Routine CK testing for the diagnosis of AMI should be eliminated from emergency departments in the era of hsTnT assays.
Tetanus is a life-threatening clinical syndrome that commonly presents with muscular spasms, rigidity, and autonomic instability. It is considered rare in industrialized countries, and tetanus occurring secondary to dental abscesses, procedures, or infections has been infrequently reported. We describe the case of a patient inadequately immunized for tetanus, who presented to the emergency department with muscular spasms, rigidity, and autonomic instability in the setting of an odontogenic infection. A clinical diagnosis of tetanus was made and subsequently managed successfully. RÉSUMÉLe tétanos est une maladie clinique, potentiellement mortelle, qui s'accompagne souvent de spasmes musculaires, de rigidité et d'une instabilité du système nerveux autonome. Il s'agit d'une maladie rare dans les pays industrialisés, et les cas de tétanos consécutifs à des abcès dentaires, à une intervention ou à des infections ne font pas souvent l'objet de description dans la documentation médicale. Sera exposé ici un cas de tétanos chez un malade non suffisamment immunisé contre la maladie, qui a consulté un médecin au service des urgences pour des spasmes musculaires, de la rigidité et une instabilité du système nerveux autonome, dans le contexte d'une infection odontogène. Un diagnostic clinique de tétanos a été posé et la maladie a été traitée adéquatement.Keywords: tetanus, dental, immunization CASE REPORTA healthy 32-year-old male presented to the emergency department with generalized body muscular spasms and a 2-week history of right upper-third molar tooth pain due to a recent tooth fracture in the setting of multiple dental caries and baseline poor dentition.He reported 48 hours of intermittent episodes of jaw twitching lasting for approximately 10 minutes, re-occurring every 15 minutes. Thereafter, the spasms spread to involve the neck, shoulder, arms, back, and legs with increasing intensity and duration. He described the spasms as extremely painful.The patient had no other significant past medical history and denied illicit drug use. The patient was a roof mechanic. He denied any recent lacerations. The immunization records revealed that he was inadequately immunized and was last vaccinated against tetanus 12 years previous.Examination revealed moderate swelling and erythema surrounding the right upper-third molar site that was fractured. The spasms involved the majority of facial muscles causing trismus (lockjaw due to spasm of the muscles of mastication), dysphagia, and eyelid closure. Spasms of the neck and back resulted in stiffness, involuntary extension, and arching; and of the upper and lower limbs causing various extension and flexion movements. There was no impairment of consciousness during the patient's entire presentation, and in between episodes he had normal power and sensation throughout; however, he had increased muscular tone and widespread exaggerated reflexes with elicited Babinski reflexes bilaterally. Despite the patient's increased nuchal muscle tone, he did not exhibit other signs of meni...
The information provided by these techniques was invaluable in developing procedures and identifying risk factors to help reduce the effect of future outbreaks within veterinary hospitals.
BACKGROUND: Community-associated methicillin-resistantStaphylococcus aureus(CA-MRSA) differ from health care-associated MRSA (HA-MRSA) in their genotypic and phenotypic characteristics. The purpose of the present study was to compare the demographics, antimicrobial susceptibilities and molecular epidemiology of CA-MRSA and HA-MRSA in Canada. METHODS: In 2007, 385 MRSA isolates were collected from Canadian patients attending hospital clinics, emergency rooms, medical/ surgical wards and intensive care units. Susceptibilities to betalactams, clarithromycin, clindamycin, daptomycin, levofloxacin, linezolid, moxifloxacin, tigecycline, trimethoprim-sulfamethoxazole and vancomycin were determined by Clinical and Laboratory Standards Institute broth microdilution. Strain typing was performed by pulsed-field gel electrophoresis (PFGE) and themecA,nucandpvlgenes were detected by polymerase chain reaction. RESULTS: Of the 385 MRSA, 19.5% were CA-MRSA and 79.2% were HA-MRSA as determined by PFGE. CA-MRSA belonged to PFGE types CMRSA10/USA300 (66.7%) and CMRSA7/USA400 (33.3%); PFGE types identified among HA-MRSA included CMRSA2/USA100/800 (81.6%), CMRSA6 (13.1%), CMRSA1/ USA600 (3.3%), CMRSA5/USA500 (1.3%), CMRSA3 (0.3%) and CMRSA9 (0.3%). Panton-Valentine leukocidin (PVL) was detected in 94.7% of CA-MRSA and 0.7% of HA-MRSA. Resistance rates (CA-MRSA versus HA-MRSA) were 61.3% versus 97.7% to levofloxacin, 73.3% versus 96.7% to clarithromycin, 12.0% versus 74.8% to clindamycin and 0.0% versus 15.4% to trimethoprim-sulfamethoxazole. No MRSA were resistant to vancomycin, linezolid, tigecycline or daptomycin. CONCLUSIONS: CA-MRSA represented 19.5% of all MRSA. CA-MRSA was significantly more susceptible to levofloxacin, clarithromycin, clindamycin and trimethoprim-sulfamethoxazole than HA-MRSA. Of CA-MRSA, 94.7% were PVL-positive while 99.3% of HA-MRSA were PVL-negative. CA-MRSA is an emerging pathogen in Canadian hospitals.
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