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OBJECTIVE: To determine if insertion of rIVCF for PE prophylaxis in high risk trauma patients could result in a clinically meaningful reduction (>24 h) in time that patients are left unprotected from PEs SUMMARY AND BACKGROUND DATA: Trauma patients are at high risk for the development of pulmonary embolism (PE). Early pharmacologic PE prophylaxis is ideal, however many patients are unable to receive prophylaxis due to concomitant injuries. Current guidelines are conflicting on the role of prophylactic retrievable inferior vena cava filters (rIVCF) for PE prevention in this patient population, and robust data to guide clinicians is lacking. METHODS: In this single center, randomized control trial of adult (age > 18 years) trauma patients at high risk for PE by EAST criteria and unable to receive pharmacologic prophylaxis for at least 72 h, we randomized 42 patients to receive a rIVCF or to not have a rIVCF placed. Our primary endpoints were time left unprotected to PE development and feasibility. RESULTS: The median patient age was 53 years, with a median Injury Severity Score of 33. Randomization to rIVCF reduced the time left unprotected to PE (Control: 78.2 h [53.6-104]; rIVCF: 25.5 h [9.8-44.6], p = 0.0001). Two pulmonary embolisms occurred in the control group, and one in the rIVCF group. Seven deaths occurred in the control group, and 8 in the rIVCF group. CONCLUSION: This feasibility study demonstrates a clinically meaningful reduction in time left unprotected to PE. Further investigations powered to demonstrate a reduction in PE incidence are required. LEVEL OF EVIDENCE: Level 1 Evidence randomized controlled trial.
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Embolia Pulmonar , Filtros de Vena Cava , Adulto , Estudios de Factibilidad , Humanos , Puntaje de Gravedad del Traumatismo , Persona de Mediana Edad , Prevención Primaria , Embolia Pulmonar/prevención & control , Vena Cava InferiorRESUMEN
INTRODUCTION: Upper airway angioedema is a life-threatening emergency department (ED) presentation with increasing incidence. Angiotensin-converting enzyme inhibitor induced angioedema (AAE) is a non-mast cell mediated etiology of angioedema. Accurate diagnosis by clinical examination can optimize patient management and reduce morbidity from inappropriate treatment with epinephrine. The aim of this study is to describe the incidence of angioedema subtypes and the management of AAE. We evaluate the appropriateness of treatments and highlight preventable iatrogenic morbidity. METHODS: We conducted a retrospective chart review of consecutive angioedema patients presenting to two tertiary care EDs between July 2007 and March 2012. RESULTS: Of 1,702 medical records screened, 527 were included. The cause of angioedema was identified in 48.8% (n=257) of cases. The most common identifiable etiology was AAE (33.1%, n=85), with a 60.0% male predominance. The most common AAE management strategies included diphenhydramine (63.5%, n=54), corticosteroids (50.6%, n=43) and ranitidine (31.8%, n=27). Epinephrine was administered in 21.2% (n=18) of AAE patients, five of whom received repeated doses. Four AAE patients required admission (4.7%) and one required endotracheal intubation. Epinephrine induced morbidity in two patients, causing myocardial ischemia or dysrhythmia shortly after administration. CONCLUSION: AAE is the most common identifiable etiology of angioedema and can be accurately diagnosed by physical examination. It is easily confused with anaphylaxis and mismanaged with antihistamines, corticosteroids and epinephrine. There is little physiologic rationale for epinephrine use in AAE and much risk. Improved clinical differentiation of mast cell and non-mast cell mediated angioedema can optimize patient management.
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Obstrucción de las Vías Aéreas/patología , Angioedemas Hereditarios/diagnóstico , Angioedemas Hereditarios/etiología , Inhibidores de la Enzima Convertidora de Angiotensina/efectos adversos , Epinefrina/efectos adversos , Adulto , Anciano , Obstrucción de las Vías Aéreas/complicaciones , Angioedemas Hereditarios/patología , Angioedemas Hereditarios/terapia , Contraindicaciones , Difenhidramina/uso terapéutico , Servicio de Urgencia en Hospital , Femenino , Humanos , Incidencia , Masculino , Ranitidina/uso terapéutico , Estudios Retrospectivos , Factores de RiesgoRESUMEN
CONTEXT: Risk prediction following acetaminophen (paracetamol, APAP) overdose is based on serum APAP, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels. One recently proposed risk stratification tool, the APAPxAT multiplication product, uses either AST or ALT, whichever is higher, yet their interrelation is not well known following APAP-induced hepatic injury. OBJECTIVE: To describe the kinetics of AST and ALT release into and disappearance from the circulation following APAP overdose. MATERIALS AND METHODS: An observational case series of adult patients with peak AST or ALT > 100 IU/L attributable to APAP toxicity. Cases were identified by electronic search of hospital laboratory database and by discharge diagnosis corroborated by structured explicit medical record review. RESULTS: Of 68 cases identified (mean age (SD): 39 (18) years, 63% female, and 21% ethanol co-ingested), 28 (41%) developed hepatotoxicity (peak AST or ALT > 1000 IU/L), 28 (41%) coagulopathy (international normalized ratio or INR > 2), and 21 (31%) both. Three patients (4%) were transferred for liver transplantation and ultimately six (8.8%) died. Serum AST and ALT activity rose in a closely aligned 1:1 AST:ALT ratio, but fell at distinctly different rates: AST activity fell with a half-life (interquartile range [IQR]) of 15.1 (12.2, 19.4) hours, and ALT 39.6 (32.9, 47.6) hours. Using an aminotransferase falling to below 50% of peak as the basis for discontinuing acetylcysteine would have resulted in antidotal treatment being stopped 24 (IQR: 9.6, 40) hours earlier (and in no cases later) using AST rather than ALT. Only six patients had an AST:ALT ratio greater than 2:1 at the time of acetylcysteine administration; of these six, four died and one survivor developed coagulopathy. DISCUSSION: AST and ALT release into the circulation appears tightly linked and numerically similar, except in the sickest patients. Once the aminotransferases peak, AST returns to baseline more quickly. CONCLUSION: Either AST or ALT can be used for early risk stratification tools when only one is known. Any criterion for N-AC discontinuation should be based on the decline of AST rather than ALT, with a potential benefit measured in days.
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Acetaminofén/envenenamiento , Alanina Transaminasa/sangre , Analgésicos no Narcóticos/envenenamiento , Aspartato Aminotransferasas/sangre , Enfermedad Hepática Inducida por Sustancias y Drogas/diagnóstico , Pruebas Enzimáticas Clínicas , Técnicas de Apoyo para la Decisión , Acetilcisteína/uso terapéutico , Adulto , Anciano , Antídotos/uso terapéutico , Biomarcadores/sangre , Enfermedad Hepática Inducida por Sustancias y Drogas/sangre , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , Enfermedad Hepática Inducida por Sustancias y Drogas/mortalidad , Enfermedad Hepática Inducida por Sustancias y Drogas/terapia , Sobredosis de Droga , Femenino , Humanos , Estimación de Kaplan-Meier , Trasplante de Hígado , Masculino , Persona de Mediana Edad , Modelos Biológicos , Valor Predictivo de las Pruebas , Estudios Retrospectivos , Medición de Riesgo , Factores de Riesgo , Factores de Tiempo , Resultado del Tratamiento , Adulto JovenRESUMEN
Angioedema is a transient, localized swelling caused by two distinct mechanisms, mediated by histamine and bradykinin, respectively, although a proportion of cases remain idiopathic. Studies that characterize undifferentiated angioedema presenting in emergency departments (EDs) are limited. This study investigates the presentation patterns of undifferentiated angioedema in the ED based on the presumed mechanism of swelling. Medical records from all ED visits to two tertiary care hospitals from July 2007 to March 2012 were electronically reviewed. Records with documented visible swelling on general inspection and/or fiberoptic laryngoscopy and a diagnostic code for anaphylactic shock, angioneurotic edema, allergy unspecified, defects in the complement system, or unspecified drug adverse effects were included. Demographic, clinical, and outcome data were collected via a standardized form. Data were analyzed descriptively, including frequencies and percentages for categorical data and means and SDs for continuous data. Predictors for admission were identified using multivariate logistic regression models. ED records from 527 visits for angioedema by 455 patients were included in the study. Annual rate of angioedema was 1 per 1000 ED visits. Urticaria was associated with peripheral (p = 0.008) and lip angioedema (p = 0.001), and the absence of urticaria correlated with tongue angioedema (p = 0.001) and trended toward correlation with pharyngeal angioedema (p = 0.056). Significant predictors of admission included nonsteroidal anti-inflammatory drug-induced angioedema (odds ratio [OR], 15.3), epinephrine treatment (OR, 8.34), hypotension (OR, 15.7), multiple-site angioedema (OR, 4.25), and pharyngeal (OR, 1.23) and tongue angioedema (OR, 4.62). Concomitant urticaria was associated with a significant longer stay in the ED (p < 0.001). The presence of urticaria correlated with the location of angioedema, need for airway management, length of ED visit, and recurrence. A detailed drug and family history, screening blood work for C1 esterase inhibitor deficiency when indicated, and prompt management of angioedema based on presumed mechanism of swelling are crucial steps in managing undifferentiated angioedema in ED.
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Angioedema/diagnóstico , Angioedema/etiología , Servicio de Urgencia en Hospital , Adolescente , Adulto , Angioedema/epidemiología , Comorbilidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Oportunidad Relativa , Admisión del Paciente , Evaluación del Resultado de la Atención al Paciente , Pronóstico , Estudios Retrospectivos , Urticaria , Adulto JovenRESUMEN
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent pulmonary carcinogen found in unburned tobacco and tobacco smoke, and is believed to play an important role in human tobacco-induced cancers. In previous studies, NNK has been reported to induce oxidative DNA damage, and to alter DNA repair processes, effects that could contribute to pulmonary tumorigenesis in rodent models. The goal of this study was to determine the effects of NNK on levels of 8-hydroxydeoxyguanosine (8-OHdG), a biomarker of DNA oxidation, and activity of base excision repair (BER), which repairs oxidative DNA damage. Female A/J mice were treated with a tumorigenic dose of NNK (10µmol) i.p. At 1, 2 and 24h post treatment, there were no statistically significant differences in lung or liver 8-OHdG levels between control and NNK-treated mice (P>0.05). Furthermore, NNK did not alter lung or liver BER activity compared to control at any time point (P>0.05). In summary, acute treatment with a tumorigenic dose of NNK did not stimulate oxidative DNA damage or significantly alter BER activity, and these effects may not be major mechanisms of action of NNK in mouse models.