Estudio descriptivo del traumatismo máxilofacial en el Hospital de La Serena entre los años 2004-2011 / Maxillofacial injuries: experience in 343 patients

Background: Oral and Maxillofacial injuries are an important problem at public health services, due to the anatomical complexity of the involved areas and committed aesthetic factor. Aim: To determine and analyze the etiology, frequency, location and treatment of patients with maxillofacial trauma at a Chilean regional Hospital between 2004 and 2011. Material and Methods: Review of medical records of 343 patients aged 0 to 87 years (258 males) treated for maxillofacial trauma. Results: Physical aggression was the main etiologic factor in 35 percent of patients, followed by falls and sports injuries in 27 and 16 percent of cases respectively. The most commonly damaged structure was the dentoalveolar area in 43 percent of patients, followed by mandibular and malar lesions in 31 and 12 percent of cases. Twenty two percent of patients required an open reduction with osteosynthesis as treatment. Discussion: Maxillofacial trauma was more common in males. The main etiologic factor was physical aggression and the most affected damaged structure was the dentoalveolar area. Osteosynthesis was required for treatment in 22 percent of cases...

Introducción: Las lesiones máxilofaciales son un problema de relevancia dentro de los servicios hospitalarios dada la complejidad anatómica de las zonas que involucra y el factor estético que compromete. Objetivo: Determinar y analizar la etiología, frecuencia, localización y tratamientos de pacientes con traumatismo máxilofacial en un hospital regional de Chile entre los años 2004-2011. Metodología: En un estudio descriptivo de serie de casos se evaluó registros de 343 pacientes diagnosticados y tratados por trauma máxilofacial. Los datos obtenidos fueron ingresados y analizados en el programa Epi Info y se agruparon en tablas de distribución y gráficos. Resultados: El promedio de edad fue de 27 años y la relación hombre-mujer de 3: 1. L as agresiones se presentaron como la principal causa (3 5 por ciento) y las estructuras más afectadas fueron las dentoalveolares (43 por ciento). Discusión: La mayor proporción de traumatismos máxilofaciales se observó en las primeras décadas de vida y fueron más frecuentes en hombres. El principal factor etiológico fue la agresión y la estructura más dañada, la dentoalveolar, seguida por fracturas mandibulares y cigomáticas. El tratamiento de elección fue la reducción abierta y osteosíntesis con placas y tornillos...

Argumentos de mujeres atendidas en su parto y nacimiento de sus bebés por parteras / Arguments posed by women assisted by midwives at during childbirth

Se describen los argumentos de 5 mujeres que utilizaron los servicios de partera en los últimos 5 años. Se utilizó una entrevista no estructurada de pregunta abierta. Se realizó análisis de contenido de categorías, se calcularon frecuencias y porcentajes. Los argumentos para optar por la atención de parteras entre otros son creencias de bienestar, preferencias de acompañamiento y experiencias con el sector salud, no ser afiliada al sector de salud, la influencia de amigos, la distancia del centro hospitalario, creencia de disminución del riesgo de enfermedad o muerte del recién nacido y las actividades y los procedimientos realizados por la partera a la madre. Los resultados sugieren involucrar, además del componente de género, un enfoque familiar y social en los servicios gineco obstétricos, e incluirlos en los currículos de Medicina y Enfermería para formar profesionales que respondan a las necesidades de esta población.

La prótesis total de rodilla inestable / The unstable knee prosthesis

La inestabilidad protésica es la tercera causa más frecuente de fallo de una prótesis totalde rodilla (PTR). Entre el 10 y el 22% de las revisiones quirúrgicas se deben a esta causa.Además de factores individuales, como inestabilidades o deformidades previas, afecciónneuromuscular concomitante, artritis reumatoide u obesidad, las principales causas se deben a errores en la selección de la prótesis primaria o a defectos en la técnica quirúrgica,como inadecuadas resecciones óseas, no obtener un apropiado balance con espaciosimétrico en extensión y fl exión o producir una laxitud iatrogénica, por lo que pueden serprevenibles. Para obtener un buen resultado en su corrección es imprescindible identifi -car la causa de la inestabilidad a fi n de actuar sobre ella y no repetir los errores que laprodujeron. La mayor›´a de los casos requerirán tratamiento quirúrgico y recambio protésico,por lo que en este artículo realizamos un análisis de los distintos modelos disponibles.Como regla general recomendamos utilizar un modelo de prótesis con la m›´nimaconstricción necesaria para lograr la estabilidad, teniendo en cuenta que una prótesisestabilizada posterior puede solucionar una inestabilidad en fl exión, aunque no compensauna inestabilidad medio-lateral, y que si bien una prótesis altamente constreñidacompensa inicialmente ambas inestabilidades, a largo plazo pueden producir complicacionesmecánicas(AU)

Prosthetic instability is the third most frequent cause for the failure of total kneereplacement (TKR), which leads to between 10% and 22% of surgical revisions. In additionto individual factors such as previous instabilities or deformities, an associatedneuromuscular condition, rheumatoid arthritis or obesity, the main causes for prostheticinstability are related to errors in selecting the primary prosthesis or mistakes in thesurgical technique, i.e. inadequate bone resections, failure to obtain an appropriatejoint balance with symmetrical fl exion and extension gaps, causing a iatrogenic laxity,etc. – all of them easily preventable. In order to successfully correct these instabilities,it is indispensable to identify its causes so as to be able to address and thereby avoidrepeating the same mistakes that provoked them in the fi rst place. As, the majority ofcases will require surgical treatment and prosthetic revision, in this study we carry outan analysis of the different models available. As a general rule, we recommend the useof a prosthetic model with the minimum constraint necessary to achieve stability, takinginto account that a posterostabilized prosthesis may be able to address a fl exioninstability, although it cannot compensate for a medial-lateral instability, and that evenif a highly constrained prosthesis can compensate for both instabilities initially, in thelong term it can lead to mechanical complications(AU)

Efectos respiratorios y hemodinámicos del alfentanilo epidural torácico o lumbar tras la cirugía torácica / Respiratory and hemodynamic effects of thoracic or lumbar epidural alfentanil after chest surgery

OBJETIVOS: Evaluación de la repercusión sobre la función pulmonar y hemodinámica de tres pautas diferentes de analgesia postoracotomía. MATERIAL Y MÉTODOS: Estudio aleatorio y doble ciego de 45 pacientes, ASA II-IV, distribuidos en 3 grupos, sometidos a toracotomía (lobectomías o neumonectomías). Tras una dosis test epidural torácica en T5-7 (grupos T-A y T-AL) o lumbar en L2-3 (grupos L), se administraron 10 µg/Kg de alfentanilo a todos los grupos. Luego se inició una infusión epidural de alfentanilo más lidocaína (T-AL) o alfentanilo (L-A y T-A) durante la cirugía y primeras 24 horas postoperatorias. Todos los grupos disponían de una PCA intravenosa de morfina postoperatoria para analgesia de rescate. Se analizaron los parámetros hemodinámicos, función pulmonar, calidad analgésica y complicaciones respiratorias. El análisis estadístico consistió en los test de ANOVA, Scheffé y Chi cuadrado. RESULTADOS: Los tres grupos resultaron homogéneos en el tipo de población e intervención quirúrgica practicada. Los requerimientos de analgesia de rescate fueron superiores en el grupo L-A respecto a los otros grupos. Los resultados de la PaO2 (6 y 18 horas) y espirometría (12 y 18 horas) fueron mejores en el grupo T-AL (p 0,05). El resto de variables no mostraron diferencias estadísticamente significativas. CONCLUSIÓN: La analgesia epidural torácica mendiante alfentanilo y lidocaína se asoció con mejores resultados de los parámetros respiratorios que los otros grupos. Los requerimientos de analgesia de rescate fueron mayores en el grupo L-A(AU)

Anestesia general combinada con ropivacaína epidural torácica en una neumorreducción por enfisema pulmonar severo / Combined general and thoracic epidural anesthesia with ropivacaine in lung reduction surgery for severe pulmonary emphysema

No disponible

[Respiratory and hemodynamic effects of thoracic or lumbar epidural alfentanyl after thoracic surgery]. / Efectos respiratorios y hemodinámicos del alfentanilo epidural torácico o lumbar tras la cirugía torácica.

OBJECTIVES: The aim of this study was to evaluate the effects on pulmonary function and hemodynamics of three different types of analgesia after thoracotomy. MATERIAL AND METHODS: Forty-five ASA II-IV patients undergoing thoracotomy (for lobectomy or pneumonectomy) were randomized to three groups (n = 15 each) for double-blind study. After a test dose into the epidural space at T5-7 (groups T-A and T-AL) or L2-3 (group L-A) interspace, 10 micrograms/Kg of alfentanil was administered in all groups, followed by epidural infusion of 400 micrograms/h of alfentanil (group T-A and L-A) or 400 micrograms/h of alfentanil with 50 mg/h of lidocaine (group T-AL) during surgery and 24 hours postoperatively. The patients also used a patient-controlled analgesia device to administer intravenous morphine postoperatively. During the study period the following variables were recorded: hemodynamic parameters, lung function, quality of analgesia and respiratory complications. ANOVA was performed and Scheffé and Chi-square tests were applied with 0.05 as the level of statistical significance. RESULTS: No differences were found between groups with respect to patient characteristics or type of surgery. Rescue analgesia requirements were higher in group L-A than in the other groups. PaO2 (6 and 18 hours) and spirometric parameters (12 and 18 hours) were significantly higher in group T-AL than in the other groups (p < or = 0.05). No other statistically significant differences were found. CONCLUSIONS: Respiratory parameters were better after thoracic epidural analgesia with alfentanil and lidocaine than after the other analgesic techniques studied. Group L-A patients had greater need for rescue analgesia than did patients in the other groups.

Electrophysiology of ventricular fibrillation and defibrillation.

The survival rate from ventricular fibrillation is very high for short-duration fibrillation (<30 secs) but decreases to approximately 3% to 30% in out-of-hospital conditions. During short-duration fibrillation, action potentials occur rapidly with no intervening period of electrical diastole; a shock defibrillates by interacting with the fibrillation action potential to produce a uniformly long postshock extension of refractoriness. In contrast, during long-duration fibrillation, ischemia-induced degradation of cellular electrophysiology occurs, which causes intervening periods of electrical diastole between fibrillation action potentials and, thus, slowing of fibrillation frequency. A successful defibrillation shock must now not only prolong refractoriness when delivered during the action potential but must also excite cells during the periods of depolarized diastole. Biphasic waveforms enhance both effects by causing premature membrane repolarization with the first pulse, thereby allowing sodium channel recovery from inactivation so that the second pulse produces better-formed responses both during the cellular action potential and during the depolarized diastole. Therefore, biphasic waveforms remain superior to monophasic waveforms for treatment of long-duration fibrillation. Improved understanding of the ischemia-induced changes in cellular electrophysiology will suggest further improvements in both defibrillator waveforms and resuscitation techniques.

Electrophysiologic deterioration after one-minute fibrillation increases relative biphasic defibrillation efficacy.

INTRODUCTION: The probability of survival decreases to 70% after 2 minutes of ventricular fibrillation. Biphasic shocks are more effective than monophasic shocks in terminating short-duration (<30 sec) ventricular fibrillation. We tested the hypotheses that developing ischemia changes the electrophysiologic characteristics of fibrillation and that the relative efficacy of biphasic shocks increases as electrophysiologic characteristics deteriorate. METHODS AND RESULTS: Monophasic (12 msec) and biphasic (6/6 msec) shocks (1 to 4 A) were tested in random order in isolated rabbit hearts after 1-minute ischemic fibrillation. Monophasic action potentials showed only a sporadic occurrence of electrical diastole after 5 seconds of fibrillation (24% of action potentials in the right ventricle and 18% in the left ventricle). After 60 seconds of fibrillation, diastole (17.83+/-1.14 msec in the right ventricle and 21.52+/-1.16 msec in the left ventricle) appeared after almost every action potential (P < 0.0001 compared with 5 sec), despite a lack of change in fibrillation cycle length and dominant frequency. Monophasic I50 was 2.89 A, and biphasic I50 was 1.4 A (77% reduction in energy). Normalized curve width decreased 28%. Retrospective analysis showed that shocks delivered early in the fibrillation action potential had a greater probability of succeeding (89%) than shocks delivered late (30%; P < 0.001). CONCLUSION: After 1-minute ischemic fibrillation, diastolic intervals occur during fibrillation. Therefore, defibrillation shocks have an approximately 29% probability of interacting with the fibrillation action potential during diastole. At this time, biphasic shocks produced a more deterministic defibrillation threshold and became even more efficacious (I50 B/M = 0.48) than at short fibrillation durations (I50 B/M = 0.7).

Electrophysiological deterioration during long-duration ventricular fibrillation.

BACKGROUND: Probability of survival from sudden cardiac arrest caused by ventricular fibrillation (VF) decreases rapidly with fibrillation duration. We hypothesized that cellular ischemia/fibrillation-induced electrophysiological deterioration underlies decreased survival. METHODS AND RESULTS: We determined fibrillation monophasic action potential (MAP) morphology including action potential frequency content, duration, cycle length, developing diastolic intervals, and amplitude as a function of ischemic fibrillation duration in 10 isolated rabbit hearts. We also correlated ECG frequency (used clinically) and MAP amplitude and frequency. Fibrillation cycle length and diastole duration increased, whereas APD(100) shortened significantly with time (P:<0.001). Between 1 and 3 minutes, diastole appeared primarily as the result of APD(100) shortening, with only small changes in cycle length. Between 2 and 5 minutes, diastole increased primarily as the result of increased cycle length. Diastole developed progressively from 5% of VF cycles at 5 seconds to approximately 100% of VF cycles by 120 seconds (P:<0.001). Diastole increased from 1% of cycle length at 5 seconds to 62% at 5 minutes. Its duration increased from 4.7 ms at 5 seconds to 90 ms at 5 minutes (P:<0.001). Both MAP and ECG 1/frequency closely correlated with fibrillation cycle length. CONCLUSIONS: These results show a rapid and progressive electrophysiological deterioration during fibrillation, leading to electrical diastole between fibrillation action potentials. This rapid deterioration may explain the decreased probability of successful resuscitation after prolonged fibrillation. Therefore, a greater understanding of cellular deterioration during fibrillation may lead to improved resuscitation methods, including development of specific defibrillator waveforms for out-of-hospital cardiac arrest.

Probability of induction and stabilization of ventricular fibrillation with epinephrine.

Clinical studies suggest that epinephrine facilitates ventricular fibrillation (VF) although mechanisms remain unclear. We tested the hypothesis that epinephrine increases the probability of inducing VF and stabilizes VF in association with shortening of fibrillation action potential duration. VF was induced in isolated, New Zealand White rabbit hearts (n=16) under control conditions and in the presence of 0.9 micro M/l epinephrine. Monophasic action potentials were recorded during sinus rhythm, pacing, and fibrillation. Epinephrine reduced fibrillation p80 by 80%, from 23+/-4 to 4.6+/-1 V (P<0.05); and reduced fibrillation p90 by 82%, from 29.3+/-5.4 to 5.4+/-1.9 V (P<0.05). Epinephrine also reduced the probability of spontaneous termination of VF during the first 5 s of VF from 29 to 8% (P<0.05). Epinephrine significantly decreased mean fibrillation cycle length from 104.5+/-2 to 75.7+/-2.3 ms (P<0.001). Mean action potential duration (60% repolarization) decreased from 76+/-3 to 40+/-3 ms (P<0.0003). Frequency analysis showed a mean dominant frequency during VF of 10.0+/-0.2 Hz under control conditions and 13. 3+/-0.3 Hz with epinephrine (P<0.0001). These results suggest that epinephrine increases the probability of VF induction and decreases the probability of spontaneous defibrillation. Stabilization of fibrillation is associated with shortening of action potential duration and fibrillation cycle length, which may allow a greater number of fibrillation waves in the ventricle.

Can shocks timed to action potentials in low-gradient regions improve both internal and out-of-hospital defibrillation?

During the first minute of fibrillation, circulating wavefronts excite new fibrillation action potentials almost immediately following termination of the preceding action potential. The extension of refractoriness hypothesis states that a successful defibrillating shock must produce a uniform postshock refractoriness of a specific optimal duration throughout the ventricle, which blocks these wavefronts and terminates fibrillation. We hypothesized that, if shocks are appropriately timed early in the fibrillation action potential in low-voltage-gradient regions, postshock refractoriness will already be long and the shock need not be strong enough to further extend it. This will result in a lower defibrillation threshold (DFT). This hypothesis was tested in the isolated rabbit heart model. Shocks were synchronized to monophasic action potentials recorded from a low-intensity region. An up/down protocol was used. I50 for early shocks was 17% lower than that for late shocks (31% decrease in E50). Standard deviation of I50 was reduced from 32% for late shocks to 18% for early shocks. Therefore, shock synchronization improves both DFT and intersubject variability during early fibrillation. As fibrillation duration increases, action potential frequency decreases and periods of diastole occur. Because of these ischemic changes, it is uncertain whether shock timing can produce similar improvements in defibrillation under out-of-hospital conditions.

Epinephrine facilitates cardiac fibrillation by shortening action potential refractoriness.

Epinephrine released during ventricular tachycardia (VT) or early fibrillation (VF) appears to be instrumental in stabilizing fibrillation. However, mechanisms remain unclear. Effects of epinephrine on refractory period at normal sinus rates depend on basic cycle length, but effects at short cycle lengths, typical of VT/VF, are unknown. Therefore, the goal of this study was to determine whether epinephrine shortens action potential duration and refractoriness at these short cycle lengths. To simulate early VT/VF, myocardial cell aggregates (n = 35) were paced using field stimulation (5 ms rectangular waveform) at cycle lengths of 200, 180, 160 and 140 ms, which occur during in situ fibrillation: normal sinus rhythm was simulated by pacing at 600 and 400 ms intervals. Action potentials and excitation threshold were recorded with intracellular microelectrodes under control conditions, with 0.9 microM/l epinephrine, and with 0.9 microM/l epinephrine and 0.5 microM/l propranolol. At short cycle lengths, epinephrine significantly shortened action potential duration and refractoriness compared to control. At a cycle length of 160 ms, action potential duration was reduced by 14 ms at 60% repolarization (P < 0.0002) and stimulation threshold by 18% (P < 0.02). Epinephrine also allowed pacing at a cycle length of 140 ms, not achievable under control conditions. Because epinephrine decreases action potential duration at short cycle length in situ, re-entry wavefronts are less likely to encounter refractory tissue: fibrillation is more likely to occur and to remain stabilised. Reduction in action potential duration and excitation threshold were reversed by propranolol, suggesting that epinephrine effects are produced by beta-stimulation.

Relationship between "extension of refractoriness" and probability of successful defibrillation.

The "extension of refractoriness" hypothesis, which suggests that the shock halts fibrillation by extending the refractory period, has not been directly tested. Defibrillation (5 isolated rabbit hearts; 111 episodes) was attempted by 8-ms pulses (65% tilt) delivered through epicardial patches. Monophasic action potentials were recorded in a low current density region (6.3 V/cm at 90% success). Fifty shocks failed to convert; 61 shocks successfully defibrillated. Postshock response duration (from shock to repolarization) was significantly longer for successful type A (with no postshock activations) defibrillation (102.3 +/- 7.5 ms) than for unsuccessful defibrillation (47.6 +/- 4.3 ms; P < 0.0001) for shocks occurring during the last 40% of the fibrillation action potential. Probability of success and postshock response duration both increased with current intensity. However, at each intensity, response durations for successful defibrillation were significantly longer than those for unsuccessful defibrillation. A minimum prolongation of 75 ms was associated with type A defibrillation. These results suggest that shock-induced response duration correlates with successful defibrillation and that a response of 75 ms is required to completely block fibrillation wavefronts.

[Prolonged bradyarrhythmias after coronary revascularization surgery]. / Bradiarritmias prolongadas después de cirugía de revascularización coronaria.

The authors report four cases of prolonged bradyarrhythmias after isolated coronary artery bypass graft surgery. All the four patients required permanent pacemaker implantation. Etiologic factors of conduction disturbances after coronary artery bypass and long term follow-up are discussed.

Biphasic defibrillation waveforms reduce shock-induced response duration dispersion between low and high shock intensities.

Mechanisms underlying defibrillation threshold reduction with biphasic waveforms remain unclear. The interaction of local shock-induced voltage gradients, which change with distance from the shocking electrode, and the state of membrane repolarization results in different cellular responses that may influence the success of defibrillation. We used intracellular microelectrodes and S1S2 pacing protocols in myocardial cell aggregates to determine the effects of shock intensity and waveform on refractory period responses during simulated fibrillation (3 s of S1 pacing at 180-ms cycle length). We simulated defibrillation by electric field stimulation S2 using 8-ms monophasic (MS2) and 4/4 biphasic (BS2) waveforms (65% total tilt) delivered at intensities of 1.5, 3, and 5 times S1 diastolic threshold, or approximately 2 to 7 V/cm. Responses following MS2 varied with S2 intensity and coupling interval (P < .001). When averaged over the last 10 ms of the refractory period, MS2 produced a negligible response (8.8 +/- 1.4 ms) at 1.5 times diastolic threshold and a prolonged response (53.0 +/- 3.1 ms) at 5 times diastolic threshold (P < .01). In contrast, BS2 response duration did not change significantly (P - NS) between 1.5 times diastolic threshold (35.1 +/- 12.6 ms) and 5 times diastolic threshold (46.2 +/- 2.7 ms). Our results suggest that biphasic waveforms not only prolong response duration at low shock intensity but reduce dispersion of refractoriness produced by differing local potential gradients generated by defibrillation shocks compared with monophasic waveforms. Preventing dispersion of refractoriness and prolonging shock-induced responses may improve biphasic waveform efficacy at low shock intensity.

Threshold reduction with biphasic defibrillator waveforms. Role of charge balance.

Mechanism underlying improved defibrillation efficacy of biphasic waveforms at low shock intensities remain poorly understood. Recent studies suggest that biphasic waveforms produce a longer mean postshock response throughout the ventricle. This prolongs the cellular refractory period, blocks fibrillation wave fronts, and causes fibrillation to cease. Previous studies showed that hyperpolarizing monophasic waveforms, delivered during the refractory period, can shorten action potential duration (APD90), which would be deleterious for defibrillation. This study tested the hypothesis that a balanced-charge biphasic waveform produces a longer mean total mean APD than a comparable monophasic waveform by preventing this shortening in hyperpolarized regions as well as by prolonging APD in depolarized regions. To test this hypothesis, the authors examined transmembrane potential changes produced by hyperpolarizing and depolarizing monophasic and balanced-charge symmetrical biphasic waveforms using a computer model of the ventricular action potential. Shock intensities within the low-intensity "window," where biphasic waveforms defibrillate with higher efficacy than monophasic waveforms (1.5-3 times diastolic threshold), were used. Results show that biphasic S2 produced a significantly longer response both under hyperpolarizing and depolarizing conditions. The hyperpolarizing/depolarizing biphasic S2 produced a prolonged response with a well-defined plateau. Following the depolarizing/hyperpolarizing S2, APD90 did not shorten as with the hyperpolarizing monophasic S2. Rather, repolarization continued near the original S1 times course, but with slight prolongation of S1 APD90. These results suggest that biphasic waveforms enhance the prolonged refractory periods required for defibrillation throughout the heart, including regions exposed to both anodal and cathodal stimulation.