panamerican journal of trauma - Sociedad Panamericana de Trauma
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panamerican journal of trauma - Sociedad Panamericana de Trauma
PANAMERICAN JOURNAL OF TRAUMA INSTRUCTIONS FOR AUTHORS INSTRUCCIONES PARA LOS AUTORES Manuscripts and related correspondence should be sent to either Panamerican Trauma Society or Dr. Ricardo Ferrada MD to the following addresses: Juliana M. Ramírez de Sánchez Panamerican Trauma Society Coordinator E-mail: [email protected] or www.panamtrauma.org Los manuscritos y la correspondencia se deben enviar a Ricardo Ferrada MD o a la Sociedad Panamericana de Trauma a las siguientes direcciones: Ricardo Ferrada MD Editor, Panamerican Journal of Trauma [email protected] 1. Title Page must be first page of manuscript. Provide title of manuscript, article type, name(s) of all authors, including graduate degrees of authors, name of institution or affiliation where work was done. 2. Structured Abstract. An abstract of 250 words or less should be submitted in English and Spanish. Abstracts are needed for original scientific articles only. Short summaries or introductions in English and Spanish should be submitted for all other articles. Format for the abstract is: 1. Background. 2. Study Design. 3. Results. 4. Conclusions. 3. Text. Original scientific articles are divided into four sections: Introduction, Methods, Results, and Discussion. Use generic names for drugs and in parentheses provide the trade name, and company. Do not use patient names, initials, or hospital numbers. 4. References. References should be listed in consecutive numerical order as they are cited in the text. Once a reference is cited, all subsequent citations should be to the original number. All references must be cited in the text or tables. References to journal articles should include: authors, title, journal name as abbreviated in Index Medicus, year, volume number, and inclusive page numbers in that order. References to books should include: authors, chapter title, if any; editor in any; title of book; year; city and publisher. Volume and edition numbers, specific pages, and name of translator should be included when appropriate. The author is responsible for the accuracy and completeness of the references and for their correct text citation. 5. Originality. Manuscripts and illustrations submitted for consideration should not have been published elsewhere except for such preliminary material presented to the Panamerican Trauma Society. 1. Título. Debe ser la primera página del manuscrito. El título debe ser corto, claro y específico. No puede exceder de 45 carácteres por línea y está limitado a dos líneas. La página del título incluye el nombre completo y la posición académica de los autores. En la parte inferior se debe indicar dónde se llevó a cabo el trabajo. 2. Resumen estructurado. Un resumen de 250 palabras o menos debe ser enviado en Inglés y Español. El resumen se requiere solamente para los artículos científicos originales. Para todos los demás artículos se debe enviar un resumen corto o introducción en Inglés y Español. El formato del Resumen es: 1. Antecedentes, 2. Diseño del estudio, 3. Resultados, 4. Conclusiones. 3. Texto. Los artículos científicos originales se dividen en cuatro secciones: Introducción, Métodos, Resultados y Discusión. Para los medicamentos utilice nombres genéricos y entre paréntesis coloque el nombre comercial y la compañía. No utilice nombres de pacientes, iniciales o números del hospital. 4. Referencias. Las referencias se citan en orden numérico consecutivo, tal como aparecen en el texto. Una vez se cita una referencia, las siguientes deben seguir a continuación. Todas las referencias deben estar citadas en el texto o en las tablas. Las referencias de revistas deben incluir: autores, título en el idioma original, nombre de la revista en su forma abreviada según el Index Medicus, año de publicación, volumen de la revista y páginas iniciales y finales. Las citas de libros incluyen: autores o editor y así se debe identificar (ed.), título del libro, edición, ciudad de publicación, la empresa editorial y año. Las referencias deben ser verificadas por los autores y ésta es una de sus responsabilidades. 5. Originalidad. Los manuscritos deben ser inéditos y no haber sido publicados en otra parte, excepto como material presentado a la Sociedad Panamericana de Trauma. PANAMERICAN JOURNAL OF TRAUMA Editors: RICARDO FERRADA, M.D., Cali, Colombia RAO IVATURY M.D., Richmond, Virginia DARIO BIROLINI, M.D., Sao Paulo, Brasil Assistant Editors: SAMIR RASSLAN M.D., Sao Paulo, Brasil ANDREW PEITZMAN M.D., Pittsburgh, Pennsylvania JORGE NEIRA, M.D., Buenos Aires, Argentina RAFAEL ANDRADE, M.D. Panamá, Panamá JUAN ASENSIO, M.D. Los Ángeles, California CARLOS BARBA, M.D. Hartford, Connecticut LUIS BÁEZ, M.D. Caracas, Venezuela MARY BEACHLEY, R.N. Baltimore, Maryland RICARDO ESPINOZA M.D. Santiago, Chile EUGENE FAIST, M.D. Münich, Germany DAVID FELICIANO, M.D. Atlanta, Georgia ALBERTO GARCÍA, M.D. Cali, Colombia LUIS GRANJA MENA, M.D. Quito, Ecuador GERARDO GÓMEZ, M.D. Indianapolis, Indiana FRANCISCO HOLGUÍN, M.D. Cartagena, Colombia LENWORTH M. JACOBS, M.D. Hartford, Connecticut TEÓFILO LAMA PICO, M.D. Guayaquil, Ecuador CHARLES LUCAS, M.D. Detroit, Michigan ROBERT MACKERSIE, M.D. San Francisco, California KATZIUKO MAEKAWA, M.D. Kitasato, Japan KIMBALL MAULL, M.D. Birmingham, Alabama ERNEST E. MOORE, M.D. Denver, Colorado DAVID MULDER , M.D. Montreal, Canadá DAVID ORTEGA, M.D. Lima, Perú RENATO POGGETTI, M.D. Sao Paulo, Brazil ABRAHAM I RIVKIND, M.D. Jerusalem, Israel AURELIO RODRÍGUEZ, M.D. Pittsburgh, Pennsylvania CLAYTON SHATNEY, M.D. San Jose, California RAÚL COIMBRA M.D. San Diego, California JOSÉ MARIO VEGA, M.D. San Salvador, El Salvador VIVIAN LANE, R.N. Hartford, Connecticut Orthopedic Trauma: BRUCE BROWNER, M.D. Hartford, Connecticut Pediatrics: MARTIN EICHELBERGER, M.D. Washington, D.C. Plastic Surgery: DAVID REATH, M.D. Knoxville, Tennessee Prehospital Care: ALEJANDRO GRIFE, M.D. México, México SECTION EDITORS Critical Care: DAVID HOYT, M.D. San Diego, California Emergengy & Disaster SUSAN BRIGGS, M.D. Boston, Massachusetts Infection: RONALD MAIER, M.D. Seattle, Washington Nursing: ROBBIE HARTSOCK, R.N. Baltimore, Maryland Coordinación Editorial: DISTRIBUNA Editorial y Librería Médica Autopista Norte 123 - 93 Fax: (57) 2132379 Tel: (57) 213-2379 (57) 620-2294 Bogotá - Colombia w w w. l i b re r i a m e d i c a . c o m Impreso por: Gente Nueva editorial PANAMERICAN JOURNAL OF TRAUMA CONTENT 1. CONTENIDO AN INTERNATIONAL NEED FOR THE IMPLEMENTATION OF TRAUMA REGISTRIES AND ONE SUCH EXPERIENCE IN COLOMBIA ............................................................ 4 2. CLEARING THE CERVICAL SPINE .............................................................................. 10 3. COMPLEX HEPATIC TRAUMA: THE ROLE OF ANGIOGRAPHY ................................ 14 4. CHALLENGING ABDOMINAL PENETRATING INJURIES I: THE UPPER ABDOMEN (“THE SURGICAL SOUL”) ............................................................................................. 18 5. CHALLENGING ABDOMINAL PENETRATING INJURIES II: FLANK, BACK AND GLUTEAL WOUNDS ....................................................................................................... 22 6. INTRACRANIAL PRESSURE MONITORING IN TRAUMATIC BRAIN INJURY: TECHNIQUES AND CLINICAL APPLICATIONS ............................................................ 26 7. TRAUMA IN THE OBESE: AN OVERVIEW .................................................................... 33 8. SECUELAS NEUROPSICOLÓGICAS EN PACIENTES CON TRAUMA CRANEOENCEFÁLICO ASOCIADO A LESIÓN AXONAL DIFUSA ................................................... 37 9. BILATERAL TRAUMATIC CHYLOTHORACES WITH TENSION ................................... 43 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 4 - 9 AN INTERNATIONAL NEED FOR THE IMPLEMENTATION OF TRAUMA REGISTRIES AND ONE SUCH EXPERIENCE IN COLOMBIA Colin Avery Clarkson, MD,1 and Andrés Mariano Rubiano, MD.2 ABSTRACT encia con el desarrollo inicial de un registro de trauma en Colombia. Background - It is recognized with increasing frequency that trauma is a major public health problem in developing countries. The objective of this article is to outline the background and need for trauma registries in developing countries, and provide our experiences with the initial development of one such trauma registry in Colombia. Métodos - El registro de trauma fue desarrollado e implementado en el principal hospital público en la ciudad de Neiva, Colombia, con recolección de datos desde febrero de 2008. Al mismo tiempo que los datos se recolectaban en Colombia, una base electrónica de datos se desarrolló en Canadá. Methods - The trauma registry was developed and implemented in the main public hospital in the city of Neiva, Colombia, with data collection beginning February of 2008. At the same time that data was being collected in Colombia an electronic database was developed in Canada. Results - During the initial one year trial of the registry, we collected data on over 2.300 trauma patients, including Revised Trauma Scores (RTS) and Kampala Trauma Scores (KTS) for future comparison. Conclusions - It is our hope that this article and registry template will serve to encourage others to continue implementing trauma registries in developing countries. Keywords: Colombia Trauma Registry, Developing Country, RESUMEN Introducción - Se reconoce, cada vez con más frecuencia, que el trauma es un problema mayor de salud pública en los países en vías de desarrollo. El objetivo de este artículo es resumir el trasfondo y la necesidad de registros de trauma en países en vías de desarrollo, y mostrar nuestra experi- Resultados - Durante el primer año del registro, recolectamos datos de más de 2.300 pacientes de trauma, incluyendo los Puntajes de Trauma Revisado (RTS) y los Puntajes de Trauma de Kampala (KTS) para una comparación futura. Conclusiones - Es nuestra esperanza que este artículo y el modelo del registro sirvan para animar a otros a seguir implementando registros de trauma en países en vías de desarrollo. Palabras clave: Registro de trauma, países en desarrollo, Colombia. INTRODUCTION It is recognized with increasing frequency that trauma is a major public health problem in developing countries (1-10). The magnitude and extent of injury as a cause of death and disability has been well documented in high-income countries, but has been inadequately studied in developing countries (1, 11-13). The objectives of this article are to outline the background and need for trauma registries in developing countries, and provide our experiences with the initial development of one such trauma registry in Colombia. BACKGROUND AND NEED 1 Memorial University of Newfoundland. Department of Surgery. St. John’s, Newfoundland, Canada. Email colin_clarkson@ yahoo.ca 2 Neiva City University Hospital. Departments of Surgery and Critical Care. Neiva, Huila, Colombia. 4 Although infectious diseases remain the greatest killer of children aged 5 years and younger in many developing countries, injury is a leading cause of disability and death An international need for the implementation of trauma registries and one such experience in Colombia Age (years) / Edad (años): __________ Sex / Sexo: Female (Femenino) 1, Male (Masculino) 2 __________ Date of injury (month/day/year) / Fecha de Evento (mes/día/año): ___/___/___ Day of injury / Día de Evento: Monday (Lunes) 1,…,Sunday (Domingo) 7 __________ Time of injury / Hora de Evento: __________ Time before arrival at hospital (hours) / Tiempo transcurrido antes de llegar al hospital (horas): __________ Method of arrival / Médio de llegada al hospital: Ambulance (ambulancia) 1, Police (policía) 2, Taxi (taxi) 3, Bus (autobús) 4, Family or friends (familia o amigos) 5, Stranger (desconocido) 6, Other specify (otro - especifique) 7 __________ Mechanism of injury / mecanismo de lesión: Gun (arma de fuego) 1, Knife (cuchillo) 2, In bus (en autobús) 3, In taxi (en taxi) 4, On motorcycle (en motocicleta) 5, In other type of vehicle (en otro tipo de vehículo) 6, Driver (conductor) 7, Pedestrian (peatón) 8, Burn (quemadura) 9, Fall (caerse) 10, Bomb (bomba) 11, Other - specify (otro - especifique) 12, (marcar todos los números que apliquen) __________ Location of injury (can give more than one) / área de lesión (se puede presentar más de una): Head (cabeza) 1, Neck (cuello) 2, Spine (columna) 3, Chest (tórax) 4, Abdomen (abdomen) 5, Extremity (extremidades) 6 __________ Type of injury (can give more than one) / Tipo de lesión (se puede marcar más de uno): Superficial laceration (corte superficial) 1, Fracture (fractura) 2, Organ injury (lesion de órgano) 3, Other – specify (otro - especifique) 4 __________ Intervention (can give more than one) / Tratamiento (se puede dar más de uno): Suture or debridement (sutura o debridamiento) 1, Chest tube (tubo torácico) 2, Laparotomy (laparotomía) 3, Thoracotomy (torocotamía) 4, Splint/cast a fracture (ferula/yeso) 5, Orthopedic surgery (cirugía ortopédica) 6, Spine surgery (cirugía de columna) 7, Craniotomy or burr hole (craneotomía o trepanación) 8, Other - specify (otro - especifique) 9 __________ Outcome / Resultado: Died (muerto) 1, Discharged (dado de alta) 2 __________ Time until death / tiempo hasta que fallece: Less than 24 hours (menos de 24 horas) 0, One day (un día) 1, Two days (dos días) 2,..., Fifty days (cincuenta días) 50, etc. _______ Time until discharge / tiempo hasta ser dado de alta : Less than 24 hours (menos que 24 horas) 0, One day (un día) 1, Two days (dos días) 2,..., Fifty days (cincuenta días) 50, etc. __________ 5 Panamerican Journal of Trauma among older children and adults (14). The majority of trauma deaths occur between the ages of 15 and 40, an age where the trauma victims are often maximally contributing to the work force of a given country (15). In addition to death, injury experienced by working age people in developing countries can have devastating impacts on family and community economies because of lost wages and productivity (16-22). Widely quoted projections which were first published in 1997 predicted that without appropriate action, by 2020 road traffic injuries will become the third leading contributor to the global burden of disease worldwide, and the second leading determinant of disability-adjusted life years (DALYs) in developing countries (23). More recently published data from the World Health Organization (WHO) shows that these dire predictions are perhaps not far off target (12). An estimated 5.2 million people worldwide died from injuries in 2002 - a mortality rate of 83 per 100 000 population (24). Injuries accounted for 9% of the world’s deaths in 2002 and 12% of the world’s burden of disease (24). More than 90% of these deaths occurred in low- and middle-income countries (10). In keeping with patterns from recent years, the WHO projects that between 2000 and 2020 road traffic deaths will increase by 83% in low -and middle- income countries while there will be a further 30% decline in road traffic deaths in high-income countries (25). This decline in death and disability rates from injuries seen in high income countries can be partially attributed to the successful deployment of trauma care systems, and the trauma registries which are an inherent part of many of these systems (13). Trauma registries are not new concepts in the developed world. They were being computerized and recognized for their utility as far back as the late 1960’s and early 1970’s in the United States (26, 27). Since that time, trauma registry use has continued to spread, and today they are widely used throughout the United States, Canada, Australia, Europe, and other parts of the developed world (28-31). With the recent wars in Iraq and Afghanistan, registry use has also been further expanded within the military environment (28, 32-35). Trauma registries were initially developed to describe the patterns of trauma and trauma workloads, as well as to provide data for research and to demonstrate changes in patient outcomes (29, 36-39). Trauma registries are widely recognized as an important part of the implementation of trauma care systems, which in turn have led to decreases 6 in death and disability from injuries within high-income countries (13, 28, 32, 34, 40). Along with the evolution of trauma care systems and trauma registries has been the evolution of trauma scoring systems, although to date none has emerged as the gold-standard (1, 13, 29, 41). Recently a newer scoring system, the Kampala Trauma Score (KTS) was developed for use in developing countries (1, 2, 8). Trauma registries specially designed for use in developing countries can allow for the collection of data which can serve as the basis for public health policy, the development of trauma care systems unique to those environments, and ultimately can lead to improved patient care and outcomes (42, 43). At present, there is no comprehensive trauma registry in Colombia, South America, a country in which violence has long been recognized as a very important problem (44). Among the countries of the Americas, Colombia has been said to have the highest level of deaths due to homicides and armed conflicts (45). It is readily apparent to anyone who travels or lives in Colombia that there are also significant numbers of injuries from violence, road traffic crashes, and other trauma, although these statistics are hard to find without a functioning trauma registry system. We present here our experiences with the initial development of a trauma registry in Colombia. An analysis of registry data from the first year as well as an accompanying prospective comparison of the Revised Trauma Score (RTS) and the Kampala Trauma Score (KTS) will be published separately. MATERIALS AND METHODS The trauma registry was developed and implemented in the main public hospital in Neiva, Colombia. Neiva is a city of about 350.000 inhabitants in southern Colombia. The hospital has approximately 500 beds, including 22 Intensive Care Unit (ICU) beds, and is associated with the local university. The registry was first implemented in February of 2008. Once the setting for registry implementation was determined, one of the first steps was to decide upon a minimal data set (MDS), which is the minimal amount of information collected on each trauma patient. At present, no consensus is available in the literature outlining what should be included in a MDS (13). We designed a MDS which was felt to be most appropriate to not only our trauma populaVol. 16 Number 1 2009 An international need for the implementation of trauma registries and one such experience in Colombia tion, but also to trauma populations in other similarly under resourced environments. The type of data collected ranges from basic patient demographics to time and date of injury, length of time prior to arrival in hospital, mechanism and type of injuries sustained, interventions, and outcomes. Given that this registry is designed to be used in environments where only limited funding is available, we did not implement the World Health Organization’s widely used International Classification of Diseases (ICD) coding systems. We felt that this would be far too complex and time consuming for use in an environment with limited resources. However, we also wanted this registry to have the ability to make comparisons among the various variables and data points, and therefore we implemented a simplified coding system to aid with data analysis. A user friendly form including all of the data points and the relevant codes was produced, with a single page capturing all the information in both Spanish and English (Figure 1). In order to meet our future objective of directly comparing the RTS and the KTS, these scores were also collected for each trauma patient. Discussions were held with the appropriate people throughout the hospital who would be involved in the implementation of the trauma registry. This included representative nurses and doctors from the departments of surgery and emergency, as well as the various hospital administrators. All of the involved staff were made aware of the objectives of the project and the need for accurate data collection, and all questions and concerns were addressed. Initial data for each trauma patient was collected by the staff in the emergency department, with the remaining data points being filled in as the information became available. One paramedic was trained specifically as a data collector. He attended the hospital on a daily basis during the study time period, and completed any outstanding elements of the trauma registry forms as the data became available. This was done via review of the patient’s chart, speaking with the staff involved in the patient’s care, or direct interviews with the patient or the patient’s family. At the same time that data was being collected in Colombia, an electronic database was developed in Canada, utilizing the Microsoft ACCESS™ system. RESULTS The development and implementation of a trauma registry applicable to under-resourced environments was successfully undertaken in the main public hospital in the city of Neiva, Colombia. During the initial one year trial of the registry, we collected data on over 2300 trauma patients, including complete RTS and KTS scores for future comparison. In addition, a user-friendly electronic database was designed to assist with data collection and analysis. This database is in both Spanish and English, with the future option of adding additional languages as required. It allows direct input of patient information into an electronic form designed in the same manner as the paper hardcopy form. This includes both the RTS and KTS scores for each patient. The coding system we designed is built into the electronic database by utilizing a series of drop-down menus. The database was also designed in such a manner as to allow for the addition of other hospitals, districts, and countries in the future. The data can be analyzed separately by hospital or in various combinations of different sites. Data analysis can be easily achieved using all the tools readily available in the Microsoft ACCESS™ program, or it can be exported for use elsewhere. DISCUSSION We have outlined here the need for and utility of trauma registries in developing countries, as well as our own experiences in developing and piloting one such trauma registry in Colombia. Our experiences demonstrate that a functional registry can be implemented with minimal resources. This trauma registry is applicable for use in other similarly resourced environments. Our first step in the development was to identify an area of need within the public health context of Colombia. We then obtained consensus among the appropriate hospital personnel as to the importance of the project, and settled on what we feel to be an appropriate minimal data set for each trauma patient given the resource constraints we are faced with. Data was collected on over 2.300 trauma patients in a one year period of time, including complete RTS and KTS scores on each patient. Furthermore, an important electronic database was developed in order to assist with data analysis and future project expansion. Our intention is to utilize the data from this initial registry to identify areas of need and implement results-based trauma reduction strategies, as has been done successfully in several parts of Central and South American in the past (12, 44, 46). Demonstrating these types of successful results to the governing bodies within Colombia’s health care system will potentially convince them of the trauma registry’s selfsustainability and cost-effectiveness, in order that expansion can be undertaken in the future. 7 Panamerican Journal of Trauma An inherent problem with hospital-based trauma registries is that many injured patients in developing countries either do not survive to reach a hospital or do not seek formal hospital treatment, and are therefore not captured in the database (2, 13, 43, 47). This of course limits a hospital-based trauma registry’s use as a tool for public health surveillance (13). With this in mind, some investigators looking at public health surveillance have used hospital-based trauma registries in conjunction with community-based studies or national death registries in order to gather valuable data (48, 49). 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Lesiones de causa externa en menores y mayores de 18 años en un hospital colombiano. Rev Panam Salud Pública 2009; 25(3): 234-41. 51. Garfield R, Llanten M, Claudia P. The public health context of violence in Colombia. Panam J Pub Health 2004; 16(4): 266-271. 52. Frazier RR. A study in trauma and recovery. PITTMED. Spring 2007; 18-22. 53. Kaufman JS, Asuzu MC, Rotimi CN, et al. The absence of adult mortality data for sub-Saharan Africa: a practical solution. Bulletin of the World Health Organization 1997; 75(5): 389-395. 54. Kobusingye O, Guwatudde D, Lett R. Injury patterns in rural and urban Uganda. Inj Prev 2001; 7: 46-50. 55. Posada J, Ben-Michael E, Herman A, et al. Death and injury from motor vehicle crashes in Colombia. Rev Panam Salud Pública 2000; 7(2): 88-91. 9 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 10 - 13 CLEARING THE CERVICAL SPINE Therese M. Duane, MD, FACS.1 SUMMARY Cervical spine clearance after blunt trauma can be challenging. The purpose of this manuscript is to review the current literature on the available options for c-spine evaluation. Current studies demonstrate the importance of clinical examination along with computed tomography to rule out these injuries. MRI also has a select role particularly for ligamentous injuries but should not be used routinely. RESUMEN La revisión cervical de la columna después de un trauma cerrado puede ser un desafío. El propósito de este manuscrito es revisar la literatura actual con las opciones disponibles para la evaluación de la columna cervical. Los estudios actuales demuestran la importancia del examen clínico junto con la tomografía computada para descartar estas lesiones. La Resonancia Nuclear Magnética (RNM) también tiene un papel, particularmente en las lesiones ligamentosas, aunque no se debe utilizar de rutina. INTRODUCTION With advanced technology the evaluation of the cervical spine (c-spine) has gone through a transition. Basic history and physical exam has been used to identify those patients who may be at risk of cervical spine injury. In the past the clinical exam has been complemented by adding radiographs, either the 3-view or 5-view films. When these have not fully answered the question and there continues to be pain, flexion/extension films have been taken. New technology has developed that includes dynamic flexion/ extension, and helical computed tomography (CT) with 1 Associate Professor of Surgery Director of Infection Control, STICU Division of Trauma, Critical Care and Emergency Surgery Virginia Commonwealth University Medical Center Richmond, Virginia 10 reconstructions. In many institutions these technologies have supplanted many of the old methods of identifying cervical spine injuries. Finally the MRI continues to be suggested for use in identifying ligamentous injuries. Clear guidelines for the clearance of the c-spine are valuable since a significant proportion of blunt trauma victims may have cervical spine injury. Previously it has been suggested 1 to 3%, however more recent studies suggest upwards of 10% of patients have cervical spine injuries. Direct mortality associated with this injury is 6.7% and the morbidity can range from 10 to 39%. Missed injury can be from 15 to 30% resulting in the possible sequelae of paralysis. More recent concerns include the associated morbidity with prolonged collar use, the development of decubiti, its interference with nursing care and central line access. Other real concerns include the medical/ legal implications of missed injuries countered by the increased cost of newer technology. It is important to identify when appropriate evaluation tools are indicated to streamline diagnosis and optimize identification of these injuries. The purpose of this manuscript is to review the literature in an effort to establish guidelines for the clearance of the c-spine after blunt trauma. VALUE OF CLINICAL EXAM The National Emergency X-Radiography Utilization Study Group in 2000 (1) brought to light the value of the clinical exam in identifying cervical spine injuries. This was a prospective observational study at 21 centers They evaluated five criteria, a patient with a non-tender neck, no deficits, who was alert, not intoxicated with no distracting injuries, was felt to have a reliable enough exam that it could adequately be evaluated by clinical exam alone. They enrolled 34,000 patients and identified 818 fractures. All patients underwent subsequent evaluation via 3-view plain films or CT scan to determine whether their criteria were valid. They found that only eight cervical spine fractures were not identified by these criteria and only two of these were Clearing the cervical spine significant. Therefore, they concluded that the vast majority of patients who were evaluable based on the above criteria did not require any kind of x-ray evaluation. The major criticism to this paper is that this included all blunt trauma patients who came into the emergency department. This is not just the sicker cohort of patients who require trauma activation based on initial hemodynamics or mechanism. However, based on these findings and other work, EAST practice guidelines in 2000 (2) subsequently recommended that no radiographic evaluation would be required for the cervical spine in the blunt trauma patients with no complaints of neck pain, no distracting injuries, no neurologic deficits, no mental status changes, or an awake and alert patient and a non-tender cervical spine to palpation. We performed a study to challenge this in which we looked at 534 patients, 52 of whom had fractures, 482 did not have fractures. We broke down the subsets into all initial trauma patients, those with a GCS of 15 and those with a GCS of 15 who were not intoxicated with no distracting injuries. Overall we identified 12 negative clinical exams for patients with CT findings of fracture. In those patients with a GCS of 15 there were eight negative clinical exams for a sensitivity of 66.7%. Patients with a GCS of 15 who were not intoxicated with no distracting injuries, we still had seven negative clinical exams giving a sensitivity of under 60%. Of those seven patients three did not require any further treatment but four required further evaluation for arterial injury as well as prolonged collar placement. Based on this study (3) we concluded that patients who are compromised enough to require trauma team activation require cervical spine CT. Furthermore, the majority of patients require CT for other reasons making it the diagnostic tool of choice to be done much more quickly with potential cost savings. VALUE OF THE PLAIN FILM EAST practice management guidelines (2) published in 2000 recommend 3-view plain films to include the lateral c-spine, AP view and open-mouth odontoid for trauma patients with any signs or symptoms of cervical spine injury. They quote a rate of 0.1% false negative if studies are technically adequate and properly interpreted. The problem with this supposition is that it is very difficult to obtain these films adequately. For example, an open-mouth odontoid must visualize the entire dens and lateral masses to C1. The AP view must reveal the spinous processes to C2-C7 and the lateral c-spine must be of good quality and adequately visualize the base of the occiput to the upper part of the first thoracic vertebra. Again we preformed a study (4) in which we evaluated the value of the lateral C-spine in the initial workup of the blunt trauma patient. We found 84 patients with fractures and 920 did not have fractures, of the 84 fractures 68 had either a negative or an incomplete lateral C-spine and seven of the 920 had a false positive lateral C-spine, giving us a sensitivity of less than 20% and a negative predicted value of 93%. The charge of each lateral c-spine is $264.00 including interpretation; hence elimination of the 1,000 films obtained in our study could have saved the institution over $265,000. Other trials have demonstrated the poor quality of plain films in this group of patients. Griffin et al (5) did a retrospective review of almost 1200 symptomatic patients of which 116 had a c-spine fracture and 41 of these were missed by plain films. All of the 41 that were not diagnosed by plain films required treatment. Gail et al (6) did a study retrospectively hypothesizing not only that plain films are inadequate but they are also very inefficient. They performed 640 plain films including a lateral c-spine and AP view, 462 with these two combined modalities were inadequate, thereby requiring CT scan. There were 19 fractures identified by CT scan and only six of these also had positive plain films. This gave the plain film a sensitivity of 31.6%. Based on these studies the majority of lateral c-spine films are inadequate and inaccurate in identifying fractures. THE VALUE OF FLEXION/EXTENSION FILMS With the use of flexion/extension films it is important to understand the proper technique. For the voluntary flexion/ extension films the patient must be able to perform painless excursion that exceeds 30 degrees. If they are unable to do that the collar has to be replaced and the films repeated. Insko et al (7) reviewed 106 patients who had static flexion/ extension views. They found that 74 (70%) were adequate and that 5 of the 74 had c-spine injuries. However, of the 32 that were inadequate four had ligamentous injuries, suggesting that when these films are adequate they have a false-negative rate of zero but 30% are limited in the acute setting secondary to pain. Pollock et al (8), using the NEXUS database, evaluated 86 patients who had flexion/extension of the 818 with fractures. They found only two stable bony injuries, four had subluxation detected in patients with other injuries. They concluded that the flexion/extension added little to the evaluation of these patients. Bolinger et al (9) reviewed 56 comatose patients with a dynamic or fluoroscopic examination of flexion/extension and only 4% had adequate visualization. Padayachee et al (10) evaluated traumatic brain injury patients who underwent c-spine clearing using dynamic fluoroscopy. Their algorithm initially included 3-view supplemented by CT but CT soon became the standard 11 Panamerican Journal of Trauma evaluation for c-spine injury. The dynamic fluoroscopy did not add anything to their findings, and they found that many were also inconclusive. Based on these findings there is minimal literature to support its routine use. VALUE OF CT In addition to the two previously described studies supporting CT, Barba et al (11) did a prospective trial where they evaluated 158 patients with lateral c-spine and CT. Only 66 patients were evaluated with 3-view or clinical exams. There were 15 injuries detected at a rate of 4.6%, seven injuries were detected by the lateral cervical spine and CT where six were missed by lateral c-spine alone. The CT was found to increase the accuracy of plain films from 54 to 100%. A further study by McCullough et al (12) did a prospective comparison of 58 fractures by CT and 3-view plain films with blinded radiologist in both studies. They found that plain films were inadequate in 52% of the patients giving a sensitivity of 45% and a negative predicted value of 91%. However, the CT sensitivity was 98% with a negative predicted value of 99%. Concern for the cost involved with routine performance of CT of the c-spine becomes an issue as we utilize newer technologies. Mirvis et al (13) studied the cost benefit effect of routine lateral cervical radiography and CT for only the asymptomatic patients. They looked at 138 patients of whom 132 required a CT to adequately visualize the lower C-spine. They found only one nondisplaced transverse process fracture, suggesting that a cost of over $60,000 to identify this one fracture was not cost effective. However, in a cost minimization study by Grogan et al (14), they predicted the cost of c-spine evaluation estimating conservatively a fracture rate of 0.9% with a paralysis of 1.7%. They found that screening plain films would cost over $2,000 because of the missed injury rate, screening CT scans however would cost just over $500 and the settlement cost would average about $58,000. By eliminating missed injuries this would minimize litigation fees and the consequence to the patient. VALUE OF MRI The patients that continue to cause much consternation for the trauma surgeon are those who have either persistent pain or the obtunded patient whose neck cannot be adequately evaluated. Sanchez et al (15) did a prospective data collection of over 1,400 patients who suffered blunt trauma and had associated head injuries. A hundred patients have cervical spine and spinal cord injuries. Patients with significant closed-head injury but who were moving all extremi12 ties had their collar removed if their CT scan was negative, and none of these patients developed subsequent neurologic deficits, suggesting that no further workup for ligamentous injury was needed. Diaz et al (16) did a prospective study of which only 85 patients qualified for MRI secondary to a number of factors including a CT without fracture but malalignment, neurologic deficit, cervical pain or tenderness, or an obtunded patient. In their study only ten of the patients were obtunded. They had 21 of 85 that had ligamentous injuries diagnosed by MRI, seven of whom had an abnormal CT, only three of whom had an abnormal x-ray. Their argument was that MRI was superior for patients with ligamentous injury. In the largest study done so far by Hogan et al (17) they looked at over 300 patients who were obtunded with normal CT scans. All these patients underwent MRIs and for unstable injury CT had a negative predicted value of 100%. There were a limited number of injuries identified by MRI, none of which were unstable and so they argued that MRI did not add anything to CT. Como et al (18) prospectively evaluated 115 obtunded patient with MRI after negative CT scan. Only six of these MRIs had identified a total of eight acute injuries, three of them were micro trabecular injuries, two were intraspinous ligamentous injuries, one was a minimal capsular injury, one was a questionable cord signal abnormality and one was a cervical epidural hematoma. The epidural hematoma was an extension for the thoracic spine injury. None of these injuries required continued cervical collar usage, and in fact they had a 5.6% complication rate from the collar, all of which were severe decubitus ulcers. The cost of MRI in their study was over $250,000. MRI is clearly costly and resource depleting and is often done in the remote areas of the hospital on very sick patients. It clearly has no benefit over CTs diagnosing bony injuries and its benefit may be limited to patients with neurologic deficits. To date there is no direct comparison between MRI and flexion/extension in the literature and routine use seems to be unnecessary for the obtunded patient. CONCLUSIONS Clearance of the cervical spine continues to be a dilemma when one considers the risk of missing an injury to the additional resource utilization in expensive radiologic technology. The updated EAST guidelines (19) due to come out this year continue to recommend that the asymptomatic patient with a reliable examination be cleared clinically based on NEXUS as well as the Canadian c-spine trial (20). We believe that clinical clearance may be appropriate but only in patients who have a very minor mechanism as suggested by the Canadian-c-spine rule. All other patients Vol. 16 Number 1 2009 Clearing the cervical spine deserve a CT of the c-spine. The updated EAST guidelines also make these recommendations doing away with plain films altogether. Additional flexion and extension films should not be routine and for the most part should be replaced by MRI in the select group of patients with continued symptoms and negative CT’s. REFERENCES 1. 2. 3. 4. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National emergency X-radiography utilization study group. N Engl J Med 2000; 13: 94-99. Eastern Association for the Surgery of Trauma (EAST) Guidelines. Determination of Cervical Spine Stability in Trauma. Available at http.www.east.org (Accessed March 2006). Duane TM, Dechert T, Wolfe, LG, Aboutanos MB, Malhotra AK, Ivatury RR. Clinical examination and its reliability in identifying cervical spine fractures. Accepted to the Journal of Trauma. Duane et al. Dechert T, Wolfe, LG, Aboutanos MB, Malhotra AK, Ivatury RR. The Lateral Cervical Spine Film: Is it obsolete? J of Surgical Research 2008; 147: 267-269. 5. Griffen MM, Frykberg ER, Kerwin AJ, et al. Radiographic clearance of blunt cervical spine injury: plain radiograph or computed tomography scan? J Trauma 2003; 55: 222-227. 6. Gale SC, Gracias VH, Reilly PM, Schwab CW. The inefficiency of plain radiography to evaluate the cervical spine after blunt trauma. J Trauma 2005; 59: 1121-1125. 7. Insko EK, Gracias VH, Gupta R, Goettle CE, Gaieski DF, Dalink MA. Utility of flexion and extension radiographs of the cervical spine in the acute evaluation of blunt trauma. J Trauma 2002; 53: 426-429. 8. 9. Pollack CV, Hendey GW, Martin DR, Hoffman JR, Mower WR, et al. Use of flexion-extension radiographs of the cervical spine in blunt trauma. Ann Emerg Med 2001; 38: 8-11. Bolinger B, Shartz M, Marion D. Bedside fluoroscopic flexion and extension cervical spine radiographs for clearance of the cervical spine in comatose trauma patients. J Trauma 2004; 56: 132-136. flexion-extension fluoroscopy versus computed tomography with three-dimensional reconstruction. J Trauma 2006; 60: 341-345. 11. Barba CA, Taggert J, Morgan AS, et al. A new cervical spine clearance protocol using computed tomography. J Trauma 2001; 51: 652-657. 12. McCulloch PT, France J, Jones DL, et al. Helical computed tomography alone compared with plain radiographs with adjunct computed tomography to evaluate the cervical spine after high-energy trauma. J Bone Joint Surg Am 2005; 87: 2388-2394. 13. Mirvis SE, Diaconis JN, Chirico PA, Reiner BI, Joslyn JN, Militello P. Protocol-driven radiographic evaluation of suspected cervical spine injury:efficacy study. Radiology 1989; 170: 831-834. 14. Grogan EL, Morris JA, Dittus RS, et al. Cervical spine evaluation in urban trauma centers: lowering institutional costs and complications through helical CT scan. J Am Coll Surg 2005; 200: 160-165. 15. Sanchez B, Waxman K, Jones T, Conner S, Chung R, Becerra S. Cervical spine clearance in blunt trauma: evaluation of a computed tomography-based protocol. J Trauma 2005; 59: 179-187. 16. Diaz JJ, Aulino JM, Collier B, et al. The early work-up for isolated ligamentous injury of the cervical spine: Does computed tomography scan have a role? J Trauma 2005; 59: 897-904. 17. Hogan GJ, Mirvis SE, Shanmuganathan K, Scalea TM. Exclusion of unstable cervical spine injury in obtunded patients with blunt trauma: is MR imaging needed when multi-detector row CT findings are normal? Radiology 2005; 237: 106-113. 18. Como JJ, Thompson MA, Anderson JS, et al. Is magnetic resonance imaging essential in clearing the cervical spine in obtunded blunt trauma patients? J Trauma 2007; 63: 544-549. 19. Como JJ, Diaz JJ, Dunham M, et al. Practice management guidelines for the identification of cervical spine injuries following trauma-2008 update. Accepted J Trauma. 20. Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-Spine Rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med 2003; 349: 2510-2518. 10. Padayachee L, Cooper DJ, Irons S, et al. Cervical spine clearance in unconscious traumatic brain injury patients: dynamic 13 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 14 - 17 COMPLEX HEPATIC TRAUMA: THE ROLE OF ANGIOGRAPHY Rao R. Ivatury, MD; AK Malhotra, MD; MB Aboutanos, MD; TM Duane, MD; J Whelan, MD; J Mayglothling, MD. SUMMARY Current evidence supports the role of angiography and embolization techniques in the treatment of complex, highgrade hepatic trauma as an adjuvant in the preoperative, post-operative phases or non-operative phases. Careful selection of patients, even those with hemodynamic instability, may provide optimal outcomes. Trauma centers must equip themselves with appropriate logistics, personnel and protocols to realize the benefits of such a multi-modal therapy for these lethal injuries. RESUMEN Los avances recientes han llevado a una estabilización de la mortalidad por trauma hepático alrededor de un 10% aproximadamente. La mayoría de estas muertes se producen por hemorragia no controlada. Para optimizar la sobrevida de estos pacientes se considera crucial un enfoque multidisciplinario, con la madurez suficiente para evitar la agresividad quirúrgica en los pacientes inestables, y que incluya los principios de control de daños y la aplicación oportuna de la hemostasia mediante el uso de la angiografía y la embolización. INTRODUCTION The evolution of our current treatment of hepatic trauma, elegantly summarized by Richardson (1) and associates with a 25-year perspective, is a tale of many milestones. These include non-operative management for the majority, damage-control principles and the increasing emphasis on multidisciplinary approach to these lesions. One of the major components of this multi-disciplinary group is the interventional radiologists with their ability to map the vasculature of the liver and identify and control life threatDivision of Trauma, Critical Care & Emergency Surgery Virginia Commonwealth University Medical Center Richmond, Virginia. 14 ening lesions both in the acute as well as delayed phases of hepatic trauma. This review will summarize the current role of angiography for complex hepatic trauma. Indications for angiography and embolization: Patients with severe blunt trauma and high grade (Grades III-V) liver injuries are potential candidates for angiography, depending upon the initial CT scan findings (pseudoaneurysms, A-V fistulas between the hepatic artery and the portal vein, and biliovenous fistulas). Hemodynamic stability is an important pre-requisite for hepatic angiography after trauma. On occasion, patients who are marginally normal in hemodynamic parameters may benefit from angiography after initial exploratory laparotomy and damage-control procedures with or without peri-hepatic packing. Another role for interventional radiology is in the late post-operative or post-trauma phase for delayed complications (pseudoaneurysms, aretriovenous fistulas or bilio-venous fistulas causing hemobilia etc.). IR as an aid in the non-operative management of blunt hepatic injuries: Mirvis et al (2) developed a CT classification of liver injury to predict successful outcome of nonoperative management. This is based on the AAST organ injury scale (3) and is summarized in Table 1. Polletti et al (4) and Hagiwara et al (5) used the Mirvis classification to predict the need for hepatic arteriography in blunt hepatic injury. Both these studies demonstrated that highgrade (grade III to V) hepatic injuries are at a higher risk of ongoing or delayed bleeding and may benefit from early hepatic arteriography to improve the success rate of nonoperative management. In a pioneering work done more than two decades ago, Sclafani et al (6) reported the results of interventional radiology in 17 patients with 20 procedures. These included controlling hepatic hemorrhage by embolizing hepatic branches of the artery (5 patients), arteriovenous fistulas (3 patients) and pseudoaneurysms (2 patients), as well as drainage of intra-abdominal collections. Hagiwara et al (5) analyzed 54 patients with hepatic injuries who did not need exploratory laparotomy. 28 were classi- Complex hepatic trauma: the role of angiography fied as having high-grade hepatic injury (Mirvis classification of 3 or 4). They had arteriography, and angiographic embolization (AE) was performed in single or multiple hepatic arterial branches when extravasation was seen in 15 patients. The authors concluded that IR is an effective alternative to surgery for patients with high-grade liver injury. In 2002 (7), these authors reported on 51 patients with Grades 3-5 liver injury. Of the 37 patients with a grade 3 injury, 18 underwent AE. Of 13 patients with a grade 4 injury AE was successful in 11 patients and unsuccessful in 2. One patient with a grade 5 injury underwent immediate laparotomy after AE. The authors concluded that the combination of the presence of a CT scan grade 4 or 5 lesion and the fluid requirements of more than 2,000 mL/h to maintain normotension indicated the absolute necessity of surgery. who had AE early compared with those whi did not have AE (OR only) or late. (0% vs. 50% and 35%). Early AE did decrease blood use and the number of liver-related operations and arrested hemorrhage in 83% of cases. In another series (10), 37 patients underwent hepatic angiography and 26 patients had hepatic embolization performed. Eleven patients underwent early-AE, immediately after CT and 15 underwent late-AE, after liver-related operations or later in their hospital course. There was a 27% mortality rate overall. There were 11 liver-related complications in the 26 embolizations. Those patients that underwent early-AE received significantly fewer blood transfusions and more commonly had sterile hepatic collections. Only 26% of patients required liver-related surgery after AE.. AE, therefore, may be superior, if performed early. The significance of “blush” or “pooling of contrast” on CT: Blush or pooling of contrast may have a special significance as a point of major hemorrhage. In a series of 105 children (ages 1 to 16) with blunt liver injury the authors (8) analyzed 75 patients with severe liver injuries (grades III-V). Those patients with a blush (n = 22) on CT had a significantly higher ISS, larger transfusion requirement and mortality rate (23% v 4%; P =.02), compared to patients without a blush (n = 53), suggesting that these patients may benefit from AE. Fang JF et al (9) noted pooling of contrast material in 15 of 276 patients with blunt hepatic injuries. Six patients showed extravasation and pooling of contrast material in the peritoneal cavity and became hemodynamically unstable soon after CT and required emergent laparotomy. Six other patients showed simultaneous presence of hemoperitoneum and intraparenchymal contrast material pooling. Four of these patients required laparotomy for hemostasis. Three patients had intraparenchymal contrast material pooling without hemoperitoneum and remained hemodynamically stable. The authors concluded that it is possible to predict the necessity of operative management or angiography for patients with blunt hepatic injury before deterioration of hemodynamic status by the presence of pooling of contrast material within the peritoneal cavity. Impact of the type of AE on subsequent complications: Hagiwara et al (11) investigated the method of AE and its impact on delayed complications. In 75 patients who underwent angiography and cholescintigraphy. Follow-up angiography revealed pseudoaneurysms in 7 of these 11 patients. All six patients in whom only gelatin sponge pledget injection was used to embolize had pseudoaneurysms. In contrast, only one of five patients who received the combination of gelatin sponge pledget injection and stainless steel coils to permanently embolize injured arteries had a pseudoaneurysm. These pseudoaneurysms had to be coiled with AE, suggesting that this is the optimal technique for AE. The significance of timing of AE: Wahl et al (10) focused on the timing of AE and its impact on non-operative treatment. They stratified patients with blunt hepatic injury into four groups: those who received AE as an early intervention (six patients), those who underwent AE after liver-related operation or later in the hospital course (six patients) those treated with operation only (20 patients). Ninety four of 126 patients did not go to the O.R. nor had AE and did well. There was a trend toward lower mortality for those Should AE be restricted to hemodynamically normal patients?: It is generally agreed that hemodynamic stability is an essential requirement for transporting patients for AE. It is inevitable, however, that the enthusiasm for this nonsurgical approach is expanded to the unstable patient with high grade liver injury. There have been occasional case reports (12) that recommend in the unstable patient aggressive resuscitation and AE rather than laparotomy. A recent series seemed to support this concept (13) Fourteen patients who had high-grade injuries (grade III [n = 2], grade IV [n = 9], grade V [n = 3]) underwent AE. Four patients in unresponsive shock had laparotomy with packing and, then, AE for persistent bleeding. Ten patients who were hemodynamically stable or even unstable underwent AE first, based on CT findings. AE was successful in all cases. The mortality rate was 7% (1/14). This study is significant in that even unstable patients received AE as the initial treatment. This can lead to catastrophic results, however, and cannot be recommended for general use. 15 Panamerican Journal of Trauma Table 1. CT injury severity grade for blunt hepatic trauma (after Mirvis et al , 1989) Grade 1 Capsular avulsion, superficial lacerations < 1 cm deep, Subcapsular hematoma < 1cm , periportal blood tracking Grade 2 Laceration(s) 1-3 cm deep,central/subcapsular hematomas(s) 1-3 cm diameter Grade 3 Laceration(s) >3 cm deep,central/subcapsular hematomas(s) >3 cm diameter Grade 4 Massive central/subcapsular hematoma >10 cm, lobar destruction Grade 5 Grade 5 : Bilobar tissue destruction or devascullarization were statistically comparable, both with a mean ISS of 31. Patients selected for non-surgical management increased from 28 (51%) to 45 (76%) (p<0.05), without increasing failure rate, liver-related complications, mortality or transfusion rate. Angiography was performed in 26 patients in the protocol group (44%). Only nine patients underwent embolization (35%). These data confirm the efficacy of the interventional radiology as an important adjuvant in the management of hepatic trauma. The roles of surgery and radiology should be complimentary and the treatment of hepatic trauma should involve a multimodal approach to ensure optimal success. REFERENCES AE as an integral component of a multi-disciplinary treatment for complex hepatic injuries: Along with timely surgical intervention, hemostatic technics for hepatic hemorrhage, peri-hepatic packing and damage-control techniques, AE has established itself in this role. From USC, Asensio and colleagues (14) have documented this in a prospective study of complex hepatic injuries. In a 54-month study of 75 patients, the benefit of angiography and angioembolization was vindicated: 12% mortality (2/17) among those that received it versus a 36% mortality (21/58) among those that did not (p = 0.074). From the University of Pennsylvania, Johnson et al (15) emphasized the role of AE in the damage-control population who had initial laparotomy. Nineteen patients had hepatic trauma and underwent perihepatic packing as a part of DC laparotomy. Eleven had sustained penetrating injury and 8 had blunt injury with 13 AAST Grades 3-4 injuries. Eight patients in the study population underwent hepatic angiography. One hepatic angiogram was obtained before operation and seven were obtained in the immediate postoperative period. Six underwent embolization of bleeding hepatic vessels, for a therapeutic liver angiography rate of 75%, without complications. Similar results were noted by the group from Thailand (16) and in a few series alluded to earlier. Our current practice is to supplement damage-control surgery and peri-hepatic packing with angiography in high grade hepatic injuries causing hemodynamic instability. A series from Norway (17) supports the concept that a formal treatment protocol for liver injuries including angiography would increase the non-operative management rate and also would be efficient as an adjunct to damage control surgery. In a prospective study of 138 adult patients with liver injuries, 55 belonged to the period of the study without a formal protocol for AE and 59 were admitted after the institution of such a protocol. The groups 16 1. Richardson JD, Franklin GA, Lukan JK, et al. Evolution in the management of hepatic trauma: a 25-year perspective. Transactions of the American Surgical Association 2000; CXVIII: 38-44. 2. SE. Mirvis, NO. Whitley, JR. Vainwright et al. Blunt hepatic trauma in adults: CT-based classification and correlation with prognosis and treatment. Radiology 1989; 171: p. 27-32. 3. EE. Moore, TH. Cogbill, GJ. Jurkovich, et al. Organ injury scaling: spleen and liver. J Trauma 1995; 38: p. 323-324 (1994 revision). 4. PA. Poletti, SE. Mirvis, K. Shanmuganathan et al. CT criteria for management of blunt liver trauma: correlation with angiographic and surgical findings. Radiology 2000; 216: p. 418-427. 5. Hagiwara A, Yukioka T, Ohta S, et al. Surgical management of patients with blunt hepatic injury: efficacy of transcatheter arterial embolizationAJR Am J Roentgenol 1997; 169(4): 1151-6. 6. Sclafani SJA, Shaft GW, McCauley J, et al. Interventional radiology in the management of hepatic trauma. J Trauma 1984; 24: 256-262. 7. Hagiwara A, Murata A, Matsuda T, et al. Efficacy and limitations of transarterial embolization for severe hepatic injury. J Trauma 2002; 52(6): 1091-6. 8. Eubanks JW 3rd, Meier DE, et al. Significance of ‘blush’ on computed tomography scan in children with liver injury. J Pediatr Surg 2003; 38(3): 363-6. 9. Fang JF, Chen RJ, Wong YC, et al. Classification and treatment of pooling of contrast material on computed tomographic scan of blunt hepatic trauma. J Trauma 2000; 49(6): 1083-8. 10. Wahl WL, Ahrns KS, Brandt MM, et al. The need for early angiographic embolization in blunt liver injuries. J Trauma 2002; 52(6): 1097-101. Vol. 16 Number 1 2009 Complex hepatic trauma: the role of angiography 11. Hagiwara A, Tarui T, Murata A, et al. Relationship between pseudoaneurysm formation and biloma after successful transarterial embolization for severe hepatic injury: permanent embolization using stainless steel coils prevents pseudoaneurysm formation. J Trauma 2005; 59(1): 49-53. 12 Nijhof HW, Willemssen FE, Jukema GN. Transcatheter arterial embolization in a hemodynamically unstable patient with grade IV blunt liver injury: is nonsurgical management an option? Eerg Radiol 2006; 12(3): 111-5. 13. Monnin V, Sengel C, Thony F. Place of arterial embolization in severe blunt hepatic trauma: a multidisciplinary approach. Cardiovasc Intervent Radiol 2008; 31(5): 875-82. AAST-OIS grades IV-V: a prospective study. Scand J Surg. 2007; 96(3): 214-20. 15. Johnson JW, Gracias VH, Gupta R, et al. Hepatic angiography in patients undergoing damage control laparotomy. J Trauma 2002; 52(6): 1102-6. 16. Sriussadaporn S, Pak-art R, Tharavej C et al. A multidisciplinary approach in the management of hepatic injuries. Injury 2002; 33(4): 309-15. 17. Gaarder C, Naess PA, Eken T, et al. Liver injuries--improved results with a formal protocol including angiography. Injury 2007; 38(9): 1075-83. 14. Asensio JA, Petrone P, García-Núñez L, et al. Multidisciplinary approach for the management of complex hepatic injuries 17 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 18 - 21 CHALLENGING ABDOMINAL PENETRATING INJURIES I: THE UPPER ABDOMEN (“THE SURGICAL SOUL”) Rao R. Ivatury, MD.1 SUMMARY Penetrating injuries to the upper abdomen are one of the most difficult and challenging injuries to manage. The surgeon, who keeps his cool, does not panic and leads his operative and ICU teams, choosing wisely the best options based on the patient’s physiologic stability will be successful in dealing with these lesions (15). The area around the middle of the upper abdomen was aptly called the “surgical soul” by Mattox (1). It is packed densely with vital structures that create unique challenges for management. The best approach for this difficult area is to be well prepared in advance with a good knowledge of surgical anatomy and the available operative options. RESUMEN Las heridas penetrantes del abdomen superior son unas de las lesiones más difíciles de manejar y representan el mayor desafío al cirujano. El éxito depende de mantener la tranquilidad, sin entrar en pánico y dirigir el equipo quirúrgico y de cuidado intensivo, eligiendo las mejores opciones con base en la estabilidad fisiológica del paciente. El área medial del abdomen superior fue acertadamente llamada “alma quirúrgica” por Mattox (1). Se encuentra densamente rodeada de estructuras vitales, que crean un desafío único. El mejor enfoque para esta difícil área es estar bien preparado con anticipación, con un buen conocimiento de la anatomía y de las opciones quirúrgicas disponibles. INTRODUCTION Surgical anatomy of this area should focus on the pancreas, duodenum and the major vessels of the abdomen. The pan1 Virginia Commonwealth University Richmond Virginia USA 18 creas lays almost transversely across the upper abdomen with a flattened head that is intimately attached to the duodenum, with the tail reaching the splenic hilum. The uncinate process projects posteriorly. The neck of the organ is traversed by the superior mesenteric vessels. Posterior to the pancreas is the aorta. The major blood supply to the pancreas comes from the gastroduodenal artery which divides at the superior edge of the pancreas becoming the right gastroepiploic artery and the paired anterior and posterior superior pancreatico-duodenal arteries. These vessels anastomose with the inferior pancreaticoduodenal arteries from the SMA. The splenic artery runs along the superior border of the pancreas, giving off the great pancreatic artery. The major venous drainage of the organ follows the arterial supply. The splenic vein courses in the middle of the posterior surface of the pancreas draining the body and joining the SMV under the pancreas to form the portal vein. The IVC courses upwards along the lumbar vertebral bodies, receiving numerous tributaries including the lumbar, right gonadal, renal, right adrenal, hepatic and phrenic veins. The perirenal area of the IVC lies posterior to the pancreas and the duodenum and receives the renal veins of both sides, a high flow system. The suprarenal IVC is short and a difficult area to control when injured. The retro-hepatic vena cava is even harder to expose and repair. OPERATIVE APPROACHES Patients who are in extremis from a GSW of the midupper abdomen should have an attempt at resuscitation by emergency department thoracotomy (EDT) to restore the cardiac rhythm and clamping of descending thoracic aorta (2-7). Patients who are stable or can be stabilized by EDT are rapidly transported to the operating room. In hypotensive patients who can be swiftly transported to the operating room a preliminary lateral thoracotomy may be indicated in order to prevent extensive blood loss when the distended abdomen is decompressed. Laparotomy is performed through a long midline incision from the xiphoid to the pubis. Challenging abdominal penetrating injuries I: the upper abdomen (“the surgical soul”) Step 1: Suspecting vascular injury: Major vascular injury may be suspected by the presence of a large amount of blood in the abdomen or the presence of a central hematoma. (Zone I supramesocolic and inframesocolic). Step 2: Is to evacuate intraperitoneal blood rapidly and pack the abdomen with laparotomy pads. The point of hematoma or bleeding is compressed manually or with laparotomy packs. The frequent presence of multiple injuries to other abdominal vessels and organs and the severe associated hypotension may make it necessary to compress the aorta under the diaphragm. This may be performed initially by a sponge stick or the assistant’s fingers or aortic compressor against the spine. Longer periods of compression may need enlargement of the aortic isthmas in the diaphragm, mobilization of the aorta and the application of a Satinsky clamp. One useful technique is to divide the left crus of the diaphragm at two o-clock position, widen the aortic isthmus, bluntly dissect the distal portion of the thoracic aorta and then apply a clamp on the suprarenal aorta. A left anterolateral thoracotomy and descending aortic occlusion may be faster and easier, if not done already. Step 3: Volume replacement and attempts at restoration of physiologic stability are the next goals by communicating with the operating room team for initiation of the massive blood transfusion protocol. Recent data support aggressive component therapy with low ratios of packed RBC to FFP (1:1 to 1:3). Step 4: and beyond vary with the injured structure. Abdominal aorta: Proximal control of the aorta at the aortic hiatus in the diaphragm is first accomplished by medial mobilization of all the left sided intraabdominal viscera including the kidney (Mattox manuever). This will allow exposure of the celiac axis, the SMA as well as the origin of the renal arteries. An alternative approach for the supra-renal, infra SMA abdominal aorta is by an extensive Kocherization of the duodenum medially and by incision of the retroperitoneal tissue to the left of IVC. Once proximal control is achieved, the aorta is dissected distally exposing the perforation (s). Bleeding is controlled by manual compression either by sponge sticks or hand Lumbar arteries may cause troublesome bleeding and may need to be ligated. Renal vessels, may have to be controlled with vessel loops. In the majority of patients injuries to the suprarenal aorta are small defects in the wall that can be closed after debridement with a continuous suture of 3 or 4-0 polypropylene More extensive loss in the aortic wall needs resection of a part of the aorta and insertion of an interposition graft, usually of 12 to 14 mm of Dacron or PTFE. Infrarenal injuries are easier to expose and manage. Celiac axis and SM vessels Injury to the celiac axis is usually treated with ligation because of the lack of any short term morbidity. Operative exposure of the SMA is very difficult because of its high location and a dense celiac plexus and lymphatics around the origin of the artery. Active bleeding from the region behind the pancreas may be an indication of SMA injury in zone I. This zone is best approached by medial visceral rotation by incising the avascular line of Toldt of the left colon, dividing the lienosplenic ligament and rotating the left colon, spleen, the tail and body of the pancreas and stomach towards the midline, along with the left kidney (“Mattox maneuver”) to gain access to the proximal infradiaphragmatic aorta and its first two branches, (celiac axis and the SMA). Transection of the dense celiac and peripancreatic venous plexus is also required. Potential pitfalls are: damage to spleen, kidney and renal pedicle during the maneuver. In addition, the resulting altered anatomy may prove confusing to the inexperienced operator. Further exposure is facilitated by dividing the pancreas at its neck anterior to the mesenteric vessels. Injuries presenting with hematoma below the transverse mesocolon can be approached by several methods. Dividing the mesocolon and doing an extended Kocher maneuver with extension along the third portion of the duodenum allows one to palpate the SM vessels. A Cattell-Braasch manever (dissecting the root of the small bowel mesentery in a diagonal line to the junction of the third and fourth portions of the duodenum and reflecting it cephalad) also exposes the SMA pulsations for dissection and isolation of the vessels. Once exposure is achieved, small lateral injuries are treated with 5.0 or 6.0 polypropylene suture. Extensive injuries require a synthetic graft. In unstable patients, damage-control principles and a temporary arterial shunt is a valuable option (8, 9). It is usual to plan a second look operation after repair of SMA to detect bowel ischemia early. Injuries to the superior mesenteric vein also may require division of the neck of the pancreas to expose the confluence of splenic and portal veins. These injuries have a high mortality because of the difficulty in exposure and they are best treated by rapid ligation and a second look operation (2-6). Infrahepatic vena cava: Injuries to the IVC will present as a large hematoma next to the duodenum or with active bleeding from this site. This is best exposed by mobilization of the cecum, ascending colon and hepatic flexure medially. The C-loop of the duodenum is mobilized medially by Kocherizing the duodenum. Proximal and distal compression by spongesticks may facilitate the exposure of the caval rent. Usually a large amount of bleeding will ensue, requiring manual compression of the bleeding IVC. One 19 Panamerican Journal of Trauma useful technique is to apply pressure with sponge to control the bleeding, slow withdrawal of the pack to expose small segments of the caval injury which can be sutured sequentially. Other options: control the perforation (s) with rapid application of a Satinsky clamp on the vessel or grasping the edges of the laceration with multiple Allis clamps. The laceration is then rapidly closed with 5-0 polypropylene sutures. A wound in the suprarenal IVC is best approached by obtaining proximal control above the renal veins by retracting the liver superiorly and applying compression on the IVC against the spine. A rapid exposure of both renal veins and IVC will facilitate control of the entire IVC and exposure of the injury. The presence of a posterior laceration must be suspected in through and through injuries, identified and repaired. The best approach for this is to repair the posterior laceration through the anterior laceration by direct visualization. The IVC may also be rotated to look at the posterior aspect. Ligation of the lumbar veins may facilitate this rotation and exposure and repair of the posterior perforation. In the profoundly hypotensive patient who is coagulopathic, or with near total destruction of the IVC, ligation is an option with potential survival. Portal venous injuries, hepatic artery injuries: Massive bleeding from the hepatoduodenal ligament or from behind the liver are indicative of these injuries. Exposure of the first two is obtained by dissection in the free edge of the lesser sac and identification of the portal vein in its posterior plane. More proximal portal venous injuries at the confluence of splenic and superior mesenteric veins require transection of the neck of the pancreas. Lateral venorrhaphy is the preferred mode of repair of the portal vein. Occasionally an end-to-end anastomosis may be necessary. More complex repairs are not needed since ligation of the portal vein is a viable option, provided the hepatic artery is intact. If the portal vein or the SMV is ligated, the entire small bowel may begin to dilate from venous hypertension. The best treatment for this in these desperate patients is to resuscitate with large quantities of fluids. Injured hepatic artery may be ligated and this is usually well tolerated. Step 4: Once even temporary control of bleeding is achieved, quick control of bowel perforations to prevent continued contamination is very important. Step 5: Look for retroperitoneal injuries especially the pancreatic-duodenal complex. Kocherization and the CattellBraasch maneuver described above facilitate inspection 20 of DI, DII, DIII, pancreatic head, periampullary area and distal CBD. DIV may be evaluated by mobilizing the ligament of Treitz (10-13). Injuries to the body and tail with ductal involvement (Grade III) are best treated by distal pancreatectomy. Those in the head of the pancreas (to the right of superior mesenteric vessels, Grade IV) are the most difficult to treat and pose the most problems. Sub-total resection is indicated for a totally disrupted gland but is avoided if the body and tail are uninjured, since 85% to 90% resection will result in pancreatic exocrine or endocrine insufficiency. In the hemodynamically compromised patient with multiple vascular injuries, the best option is to establish wide drainage in the region of the injury, accepting the formation of a fistula. In such patients, the addition of pyloric exclusion is recommended, especially in the presence of associated injuries to the duodenum. The goal of duodenal exclusion is to divert gastric secretions away from the duodenal repair and allow time for adequate healing of repair. It consists of primary repair of the duodenal wound, closure with nonabsorbable sutures of the pylorus through a gastrotomy or a staple line across the pylorus and a gastrojejunostomy at the gastrotomy site. Pancreatic-duodenectomy is the ultimate option for extensive injuries causing uncontrollable peripancreatic hemorrhage, distal bile duct and proximal pancreatic duct or ampullary injuries with extensive tissue destruction, and combined devascularizing injuries to the duodenum and head of the pancreas (Grade V). It is usually done as a staged procedure. Recent paradigms emphasize a highly conservative approach that avoids major resections and pancreato-enteric anastomosis in pancreato-duodenal injuries and relies on duodenal repair, resection, pyloric exclusion and wide drainage of the pancreatic head. Frequently, patients with major abdominal vascular injuries will have extensive blood loss and hemodynamic instability. The onset of the critical “triad of death”, namely hypothermia, acidosis and coagulopathy is often the rule rather than the exception, precipitated by associated abdominal injuries, multiple transfusions, the need for aortic compression and dilutional coagulopathy. In these circumstances, it is prudent to institute “damage-control” principles (8), Figure 1. Rapid termination of the laparotomy is the goal. Since the patient may not tolerate a prolonged vascular replacement at this time of physiologic exhaustion, placement of a temporary arterial shunt between the ends of the divided arteries is the preferred approach (9). Vol. 16 Number 1 2009 Challenging abdominal penetrating injuries I: the upper abdomen (“the surgical soul”) GSW to “ The Surgical Soul” Relative hemodynamic stability Hemodynamic instability Damage Control Hemorrhage control Aortic Compression Proximal and distal control Repair if possible of arteries Rapid closure of GI Peforations for intra-abdominal pressure. It is our practice to perform decompressive laparotomy if the bladder pressure is greater than 20 mmHg with organ dysfunction (14). REFERENCES 1. Mattox KL. GSW to the Surgical Soul. Trauma, Critical Care & Acute Care Surgery, Las Vegas 2008. 2. Asensio JA, Chahwan S, Hanpeter D, et al. Operative management and outcome of 302 abdominal vascular injuries. Am J Surg 2000; 180: 528-33. 3. Asensio JA, et al. Vascular trauma: Complex and Challenging Injuries. Surg Clin North Am. December 2001. 4. Feliciano DV. Abdominal vessels. In Ivatury RR, Cayten CG: The Textbook of penetrating trauma. Williams & Wilkins, Baltimore 1996; 209: 698-705. 5. Feliciano DV: Injury to abdominal aorta and visceral arteries. In Vascular trauma, 2nd Ed Rich NM, Mattox KL, Hirshberg A (eds). Elsevier Science, Philadelphia 2004. p. 219-314. 6. Davis TP, Feliciano DV, Rozycki GS, et al. Results with abdominal vascular trauma in the modern era. Am Surg 2001; 67: 565-570. 7. Coimbra R. Prelaparotomy thoracotomy: Is there a role in abdominal trauma? Panamerican Journal of Trauma 2008; 15(2): 91-93. 8. Rotondo MF, Schwab CW, McGonigal MD, et al. “Damage control”: An approach for improved survival in exsanguinating penetrating abdominal injury. J. Trauma 1993; 35: 375- 1993. 9. Reilly PM, Rotondo MF, Carpenter JP, et al. Temporary vascular continuity during Damage control: Intraluminal shunting for proximal superior mesenteric artery injury. J Trauma 1995; 39: 757-760. Shunts for arterial injury Ligation of all veins ICU resuscitation Definitive reconstruction at repeat laparotomy B. Combined pancreatoduodenal injuries Grade III duodenal and pancreatic injuries: Duodenal repai r or resection and EEA, distal pancreatectomy, pyloric exclusion Grades IV duodenal and pancreatic injuries: Duodenal repair/ resection and EEA, pyloric exclusion, drainage Grade V pancreatico-duodenal injuries: Two-stage pancreatoduodenectomy Figure 1. Algorithm for potential injuries and their management. Javed shunts or any vascular shunt available in the operating room will serve the purpose. If none is immediately available, intravenous infusion tubing will be a good substitute. This will maintain flow distally and avoid mesenteric ischemia. These shunts are well tolerated for at least 24 hours. Heparin bonded shunts, if available, is another option. Control of contamination is achieved by rapid closure of bowel perforations. In these patients the abdomen is usually left “open” by the placement of “vac-pac” dressing. The patient is transferred to the intensive care unit for resuscitation. This ICU phase of “damage-control” will focus on the correction of hypothermia, acidosis and coagulopathy. Acidosis is reversed by aggressive blood and fluid resuscitation. Intra-abdominal hypertension and the abdominal compartment syndrome are common complications in these circumstances and must be carefully watched for by frequent measurement of bladder pressure as a surrogate 10. Ivatury RR, Malhotra AK, Aboutanos MB, et al. Duodenal injuries; a review. Eur J Trauma Emerg Surg 2007; 33: 231-237. 11. Ivatury RR. Duodenal injuries: are complex repairs indicated? Panamerican Journal of Trauma 2008; 15(2): 72-76. 12. Subramanian A, Dente CJ, Feliciano DV. The management of pancreatic trauma in the modern era. Surg Clin North Am 2007; 87: 1515-32. 13. Stawicki SP, Schwab CW. Pancreatic trauma: demographics, diagnosis and management. Amer Surg 2008; 74: 11331145. 14. Ivatury RR, Cheatham M, Malbrain M, Sugrue M. Abdominal Compartment Syndrome Landes Bioscience, 2007, Houston, Texas. 15. Tyburski JG, Wilson RF, Dente C, et al. Factors affecting mortality rates in patients with abdominal vascular injuries. J Trauma 2001; 50: 1020-1026. 21 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 22 - 25 CHALLENGING ABDOMINAL PENETRATING INJURIES II: FLANK, BACK AND GLUTEAL WOUNDS Rao R. Ivatury, MD.1 SUMMARY Penetrating wounds of the posterior abdomen, including the gluteal region need a careful consideration of the organs at risk and the hemodynamic status of the patient. With the advent of CT scanning, an organized approach in stable patients will select patients for a therapeutic laparotomy and minimize missed injuries. RESUMEN Las heridas penetrantes del abdomen posterior, incluyendo la región glútea, necesitan una consideración cuidadosa de los órganos en riesgo así como del estatus hemodinámico del paciente. Con el advenimiento de la tomografía computarizada y un enfoque organizado, los pacientes estables se pueden seleccionar para evitar las laparotomías innecesarias y, al tiempo, reducir las lesiones inadvertidas. INTRODUCTION Injuries to the posterior aspect of the abdomen present many challenges in diagnosis and management. In hemodynamically normal patients, judiciously applied non-operative treatment may suffice, even with penetrating wounds. On the other hand, occult injuries with life-threatening consequences may result from an innocuous appearing wound (1-6). This review will summarize current concepts in the management of flank, back and gluteal regions to emphasize a rational approach to these wounds for optimal outcomes. The duration of selective observation was investigated by Mcleod and colleagues (19). 93 patients undergoing observation for a penetrating flank/back wound subsequently required a therapeutic laparotomy. The time from admission 1 Virginia Commonwealth University Richmond Virginia USA 22 to operation was less than 3 hours for 84 per cent of the patients requiring therapeutic intervention. A further 10 per cent presented with symptoms between 4 to 6 hours, and 6 per cent between 7 to 18 hours. All the injuries caused symptoms within 18 hours of the injury event. The authors concluded that the majority of patients (94%) who require a laparotomy after a period of observation for a penetrating flank/back wound will develop signs and symptoms within 6 hours of admission. After 18 hours no further injuries were detected. A 24-hour period of observation, therefore, should suffice with penetrating injuries to the back. Controversies in the operative treatment of renal injuries: In patients with flank and back wounds taken to the operating room, the treatment of a retroperitoneal hematoma that is not expanding and not pulsatile at the time of emergency laparotomy is controversial (6-12). Immediate exploration of all patients with penetrating renal injuries has been recommended by some. In a prospective study over a two-year period (20), 50 patients (43 GSW and 7 SW) underwent laparotomy for 53 renal injuries. Excluding three O.R deaths, routine renal exploration lead to simple drainage in 13 (26.5%), renal repair in 17 (35%), partial nephrectomy in 6 (12%), and nephrectomy in 13 (26.5%). The authors recommended routine renal exploration. Armenakas et al (11), analyzed a 20 year experience with 199 patients with 200 renal injuries from stab wounds. Non-operative treatment was selected in 108 patients (54%). The other 92 renal injuries were explored. Seventy four were reconstructed (80.4%) and 11 required nephrectomy (12%) for an overall renal salvage rate of 94.5%. These authors suggested that meticulous attention to reconstructive techniques in renal exploration can ensure an excellent renal salvage rate. Several studies (6-12), however, have shown that in patients with penetrating renal injury, a selective approach can be safely implemented in hemodynamically stable patients. Several prerequisites are important for this practice. First, one must ascertain that the hematoma is truly a Zone II (lateral) hematoma that is perinephric, in contrast to Zone Challenging Abdominal penetrating injuries II: Flank, Back and Gluteal wounds I (mid-line) hematomas. All Zone I hematomas need to be explored to rule out major abdominal vascular injuries (1-3, 19). Second, the perinephric retroperitoneal hematoma must be non-expanding and stable on continued observation. There must be no suspicion of a renal pedicle injury which may be suggested by continued hemorrhage or a large hematoma in the midline, or urinary extravasation. If there is any suspicion of a pedicle or hilar injury, these structures can be explored without violating the integrity of the Gerota’s capsule and preserving the tamponade effect of the intact capsule. If the exploration is negative and the hematoma is stable, the perinephric hematoma may be left unexplored (13-18). Gunshot wounds to the kidney, especially from highvelocity missiles or close-range shotguns, may have an increased risk of delayed complications because of extensive tissue damage. Low velocity GSW and knife or stab injuries, according to current opinion, may have a selective exploration of the hematoma, as long as the conditions described above are met. In one series (20) 52 consecutive patients with renal GSW renal injuries were explored only if they involved the hilum or were accompanied by signs of continued bleeding. Thirty-two patients underwent renal exploration and 17 of them required nephrectomy for major renovascular or high grade parenchymal injuries. Renal exploration was successfully avoided in the remaining 20 patients. The authors concluded that mandatory exploration of all gunshot wounds to the kidney was not necessary. Even in the presence of multi-organ injuries in the abdomen, selective exploration of the kidneys may be successful. In one series (21), in the absence of an expanding hematoma and/or hemodynamic instability, associated injuries by themselves did not increase the risk of nephrectomy. Despite multiorgan penetrating injuries, 54% of kidneys were salvaged. The role for early vascular control: The transperitoneal approach to early vascular control has the advantage of avoiding catastrophic bleeding that may ensue when the Gerota’s fascia is opened and its tamponading effect is lost. Preliminary control of the pedicle will facilitate a more elective assessment of injury and salvage of the kidney by repair or partial resection. Nephrectomy rates have been reduced by such a maneuver from 56% to 18% in one series (22). Since the need for vascular control cannot always be identified before entering the perinephric hematoma, some authors recommend it for all patients. However, this is not universally accepted. One Level 1 study randomized patients managed surgically for penetrating renal injuries to early vascular control or direct exploration of the kidney (23) and noted a lack of difference in nephrectomy rates. Renal reconstruction: Renal salvage can be accomplished by a variety of techniques. The first step is a complete exposure of the kidney by entering the fascia and compressing the organ to staunch bleeding. If vascular isolation had not been done previously, the pedicle may be controlled by atraumatic vascular clamps at this time to reduce bleeding and facilitate an assessment of the injury. All nonviable tissue is debrided, and bleeding vessels are ligated under vision. If the collecting system is lacerated, these defects are closed with non-absorbable sutures in a watertight repair. The parenchyma of the kidney is then repaired by buttressing with omentum or renal capsule (6-11). Absorbable meshes made of polyglycolic acid (Dexon® or Vicryl®) are useful alternatives. We have used a “wrap” technique with mesh either as a “cap” at one pole after a partial nephrectomy or around the entire kidney when there are multiple lacerations (24). Nephrectomy: The nephrectomy rate for immediate exploration of major renal lacerations varies depending on the type and severity of the trauma and hemodynamic instability. Penetrating mechanism, high-velocity weapons and multiple injuries are associated with a higher nephrectomy rate. In one series (25), 69 of 87 renal injuries were surgically explored (79.3%), and 12 patients underwent nephrectomy (13.8%). Forty-six (66.6%) renal units were reconstructed by various methods, including renorrhaphy, omental pedicle flaps, mesh or peritoneal patch grafts, partial nephrectomy, and vascular repair. The overall renal salvage was 86.2%. Early renal vascular control was achieved in all patients who underwent renal exploration. These findings suggest early vascular control and careful selection of reconstructive techniques can ensure a high renal salvage rate in patients with high grade renal gunshot injuries. Renovascular and Renal pedicle injury: Avulsed or lacerated vessels usually mandate renal exploration to control hemorrhage with either ligation of the artery, with or without nephrectomy, or repair of the vessel (26, 27). The success of arterial reconstruction is related to the duration and degree of ischemia and presence or absence of accessory renal arteries providing collateral flow. With a warm renal ischemia time of > 2 h irreversible damage ensues (6-11). Nephrectomy may be required in 67-86% of patients with main renal artery injuries and in 25%-56% of those with main renal vein injuries. The kidney may be spared in segmental vessel injuries alone. Injuries to the left renal vein near the vena cava can be managed with ligation, as adequate venous drainage will be provided by the gonadal and adrenal veins. Injuries to the main renal vein on the right must be repaired and this is usually achieved with a lateral venorrhaphy. Auto-grafting with the inferior 23 Panamerican Journal of Trauma mesenteric, hypogastric or splenic artery has occasionally been reported with limited success. Autotransplantation or removal of the kidney and bench surgery before reimplantation, on occasion, may be necessary in the treatment of an injury to a solitary kidney (6-11). A multi-center study from the Western Trauma Association documented the poor outcomes from renovascular injuries (26). Arterial repairs had significantly worse outcomes than venous repairs. Neither the time to definitive surgery nor the operating surgeon’s specialty significantly affected outcome. In this series, 15 had immediate nephrectomy. (21%), genitourinary (14%), pulmonary (11%), sphincter (9%)]. Overall, 76% required surgical management, with 14% developing postoperative complications. Independent predictors of a need for stoma placement were gunshot wounds (odds ratio = 10, p < 0.05) and injury severity score greater than 20 (odds ratio = 27, p < 0.01). These data support the potential morbidity of gluteal injuries and emphasize a careful evaluation of these wounds. REFERENCES 1. Asensio JA, Chahwan S, Hanpeter D, et al. Operative management and outcome of 302 abdominal vascular injuries. Am J Surg 2000; 180: 528-33. 2. Asensio JA, et al. Vascular trauma: Complex and Challenging Injuries. Surg Clin North Am. December 2001. 3. Feliciano DV. Management of traumatic retroperitoneal hematoma. Ann Surg. 1990; 211: 109-123. 4. Scalea TM, Bochicchio KM, Lumpkins K, Hess JR, Dutton R, Pyle A, Bochicchio GV. Early aggressive use of fresh frozen plasma does not improve outcome in critically injured trauma patients. Ann Surg 2008; 248(4): 578-84. 5. Zink KA, Sambasivan CN, Holcomb JB, Chisholm G, Schreiber MA. A high ratio of plasma and platelets to packed red blood cells in the first 6 hours of massive transfusion improves outcomes in a large multicenter study. Am J Surg 2009; 197(5): 565-70; discussion 570. 6. Santucci RA, Wessels H, Bartsch G, et al. Evaluation and management of renal injuries: consensus statement of the renal trauma subcommittee. BJU International 2004; 93: 937-954. 7. Wessells H, Suh D, Porter JR, et al. Renal injury and operative management in the United States: results of a population based study. J Trauma 2003; 54: 423-30. 8. Santucci RA, Fisher MB. The Literature Increasingly Supports Expectant (Conservative) Management of Renal Trauma — A Systematic Review. J Trauma 2005; 59: 491-501. 9. Broghammer JA, Fisher MB, Santucci RA. Conservative management of renal trauma: a review. Urology 2007; 70(4): 623-9. GLUTEAL INJURIES Our review of 1982 with 60 patients admitted with penetrating gluteal trauma during a 4-year period supports the concept that these wounds constitute a distinct group of injuries with a potential for serious, or even lethal, damage to a spectrum of organ systems (28). A high index of suspicion, repeated careful evaluation, and aggressive operative management of these injuries are mandatory to achieve a low morbidity and mortality. In a retrospective study (29) of 81 patients with penetrating gluteal wounds (53 gunshot wounds, 28 stab wounds, one impalement), 66% percent of all penetrating gluteal wounds entered the upper zone (above the greater trochanters). Thirty two percent of patients with upper zone penetration had associated vascular or visceral injury. Only one of 27 patients with lower zone penetration sustained major injury. In a series of 27 gluteal stab wounds in 17 patients, 53% were classified as upper zone and 47% as lower zone injuries (30). Sixty six percent of the upper zone injuries had associated neurologic, vascular, or visceral injuries that required invasive procedures or surgery, compared with 12.5% for lower zone injuries (p < 0.05). Therefore, upper zone gluteal stab wounds require prompt multisystem evaluation. Lower zone wounds need observation and repeated evaluations. Proctosigmoidoscopy is essential to rule out injuries to lower rectum and anal canal. Transpelvic gunshot wounds, blood on sigmoidoscopy, retroperitoneal hematoma on CT are some of the urgent indications for laparotomy. Hemodynamic instability mandates immediate operation. In a retrospective analysis of prospectively collected data from the 31st Combat Support Hospital during Operation Iraqi Freedom over a 16 month period, 115 patients (3.3%) suffered penetrating gluteal injuries (31). Mortality was 6% (n = 7). Primary mechanisms of injury were improvised explosive devices (41%) and gunshot wounds (59%). Associated injuries were present in 57% of patients [orthopedic (35%), abdominal (29%), rectal (25%), vascular 24 10. McAninch JW, Carroll PR. Renal trauma: kidney preservation through improved vascular control - a refined approach. J Trauma 1982; 22: 285. 11. Armenakas NA, Duckett CP, McAninch JW. Indications for nonoperative management of renal stab wounds. J Urol. 1999 161(3): 768-71. 12. Wessells H, McAninch JW, Meyer A, et al. Criteria for nonoperative treatment of significant penetrating renal lacerations. J Urol 1997; 157: 24-27. 13. Eastham JA, Wilson TG, Ahlering TE. Urological evalua- Vol. 16 Number 1 2009 Challenging Abdominal penetrating injuries II: Flank, Back and Gluteal wounds tion and management of renalproximity stab wounds. J Urol 1993; 150(6): 1778. 14. Shanmuganathan K, Mirvis SE, Chiu WC, Killeen KL, Scalea TM. Triple contrast helical CT in penetrating torso trauma: a prospective study to determine peritoneal violation and the need for laparotomy. AJR Am J Roentgenol 2001; 177(6): 1247-56. 15. Easter DW, Shackford SR, Mattrey RF. A prospective, randomized comparison of computed tomography with conventional diagnostic methods in the evaluation of penetrating injuries to the back and flank. Arch Surg 1991; 126(9): 1115-9. 16. Burns RK, Sariol HS, Ross SE. Penetrating posterior abdominal trauma. Injury 1994; 25(7): 429-31. 17. Velmahos GC, Demetriades D, Foianini E, Tatevossian R, Cornwell EE 3rd, Asensio J, Belzberg H, Berne TV. A selective approach to the management of gunshot wounds to the back. Am J Surg 1997; 174(3): 342-6. 18. Velmahos GC, Demetriades D, Cornwell EE 3rd. Transpelvic gunshot wounds: routine laparotomy or selective management? World J Surg 1998; 22(10): 1034-8. 19. MacLeod J, Freiberger D, Lewis F, Feliciano D. What is the optimal observation time for a penetrating wound to the flank? Am Surg 2007; 73(1): 25-31. 20. Velmahos GC, Demetriades D, Cornwell EE 3 , et al. Selective management of renal gunshot wounds. Br J Surg 1998; 85(8): 1121-7. rd 21. Nicol AJ, Theunissen D: Renal salvage in penetrating kidney injuries: a prospective analysis. J Trauma 2002; 53(2): 351-3. 22. McAninch JW, Carroll PR. Renal trauma: kidney preservation through improved vascular control - a refined approach. J Trauma 1982; 22: 285. 23. González RP, Falimirski M, Holevar MR, et al. Surgical management of renal trauma: Is vascular control necessary? J Trauma 1999; 47: 1039-42. 24. Delany HM, Ivatury RR, Blau SA, et al. Use of biodegradable (PGA) fabric for repair of solid organ injury: a combined institution experience. Injury 1993; 24(9): 585-9. 25. McAninch JW, Carroll PR, Armenakas NA, et al. Renal gunshot wounds: methods of salvage and reconstruction. J Trauma 1993; 35(2): 279-83. 26. Knudson MM, Harrison PB, Hoyt DB, et al. Outcome after major renovascular injuries: a Western Trauma Association multicenter report. J Trauma 2000; 49: 1116-1122. 27. Ivatury RR, Zubowski R, Stahl WM. Penetrating renovascular trauma. J Trauma 1989; 29: 1620-1623. 28. Ivatury RR, Rao PM, Nallathambi M, Gaudino J, Stahl WM. Penetrating gluteal injuries. J Trauma 1982; 22(8): 706-9. 29. Mercer DW, Buckman RF Jr, Sood R, Kerr TM, Gelman J. Anatomic considerations in penetrating gluteal wounds. Arch Surg 1992; 127(4): 40710. 30. Makrin V, Sorene ED, Soffer D, Weinbroum A, Oron D, Kluger Y. Stab wounds to the gluteal region: a management strategy. J Trauma 2001; 50(4): 70710. 31. Lesperance K, Martin MJ, Beekley AC, Steele SR. The significance of penetrating gluteal injuries: an analysis of the Operation Iraqi Freedom experience. J Surg Educ 2008; 65(1): 6. 25 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 26 - 32 INTRACRANIAL PRESSURE MONITORING IN TRAUMATIC BRAIN INJURY: TECHNIQUES AND CLINICAL APPLICATIONS Almir Ferreira de Andrade, MD, PhD; Wellingson Silva Paiva, MD; Vinicius Paula Guirado, MD; Priscilla Messias Paganelli, MD; Ciro Rhode, MD; Robson Luis Oliveira Amorim, MD; Manoel Jacobsen Teixeira, MD, PhD. SUMMARY Traumatic brain injury is the leading cause of death and disability in children and young adults in industrialized countries. Intracranial hypertension occurs in approximately 50% of all traumas in comatose patients and is more common in those with intracranial hematomas. In this article the authors reviewed the pathophysiological principles and methods of monitoring intracranial pressure in patients who suffer a traumatic brain injury. Keywords: traumatic brain injury, intracranial hypertension, intracranial pressure monitoring RESUMEN La lesión cerebral traumática es la principal causa de muerte e incapacidad en los niños y los adultos jóvenes en los países industrializados. La hipertensión endocraneana ocurre en aproximadamente el 50% de todos los pacientes comatosos traumatizados y es más frecuente en aquellos con hematoma intracraneano. En este artículo, los autores revisan los principios fisiopatológicos y los métodos de monitoría de presión intracraneana en los pacientes que sufren una lesión cerebral traumática. Palabras clave: Lesión cerebral traumática, hipertensión endocraneana, monitoría de presión intracraneala INTRODUCTION Traumatic brain injury (TBI) is the leading cause of death and disability in children and young adults in industrialized countries (1, 2). Permanent brain damage that occurred after TBI is the result of complex pathophysiological Division of Neurosurgery Hospital das Clínicas – University of São Paulo Medical School 26 mechanisms, generating primary lesions as a result of inertial forces and secondary lesions resulting from processes that contribute to cell death after the initial injury. This highlights the role of intracranial hypertension as a major factor of injury to nervous tissue and thus a worse prognosis for functional patients (2, 3). The brain produces energy mainly by the oxidation of glucose. Their high metabolism makes for a consumption under physiological conditions, of about 20% oxygen and 25% of glucose used by the body (1, 2). The oxygen supply to the nerve cells depends on cerebral blood flow (CBF), O2 saturation of hemoglobin in the blood and gas exchange capacity of the capillaries. In physiological situations, the body maintains a constant CBF, between 40 and 60 ml per 100 g per minute within a range of mean arterial pressure (MAP) between 60 and 150 mm Hg. To maintain this constant infusion, the intracranial vessels constrict and dilate according to need. When the MAP is below the limits mentioned above, there may be hypoperfusion. Furthermore, when MAP exceeds these limits is no risk of damage, cerebral lesion of vascular smooth muscle and loss of blood brain barrier. The CBF is then free to vary according to MAP (4). In TBI, the TBI should be evaluated by cerebral perfusion pressure (CPP), which is calculated by MAP minus intracranial pressure (ICP). As the brain is confined in a rigid bony cage and CPP is dependent on the ICP, the control of intracranial hypertension (ICH) assumes the role of maximum importance in TBI (2, 5). The theory of Monro-Kellie, 1783, modified by Burrows in 1846, provides that the adult skull is a non-stretch system and its total volume is constant. It is acknowledged today that eighty percent (80%) of this volume is composed of neural tissue, 10 % blood and 10% of cerebrospinal fluid. Volumetric changes of the components individually lead to reciprocal changes in the other, in order to maintain the intracranial volume (6). Intracranial pressure monitoring in traumatic brain injury: techniques and clinical applications In normal conditions, the cerebrospinal fluid is the first component to move to the spinal cord, followed by the blood to the venous sinuses, the brain remained relatively incompressible. The intracranial pressure remains constant with increases in intracranial volume this does not extinguish the cerebrospinal fluid and blood (6). The elastance is defined as increased ICP (intracranial pressure) per unit of volume added to the intracranial compartment, and compliance is the inverse of elastance and defined as the amount required bringing a unit of ICP, as measured by comparing the different volumes required in many situations to increase ICP in one unit. Defined is therefore a phase of low and high elastance complacency as there are shifts in intracranial volume, and a phase of high elastance and low compliance when such reserves are depleted – pressure / volume Langfitt Curve (Figure 1) (7). In TBI, the presence of elements such as bruises, contusions, edema, accumulation of CSF or increase intravascular volume exceeding the capacity of accommodation increasing ICP (8). dation of the use of continuous measurement of the peak is due to intraventricular Lundberg (10) in 1960 with the publication of his classic study. The ICP values persistent over 20 mm Hg are considered abnormal if the values are between 20 and 40 mm Hg indicates moderate intracranial hypertension. An increase greater than 40 mm Hg in ICP indicate to severe ICH with risk of death (11). The TBI has levels of HIC maintained above 60 mm Hg is almost always fatal, with electrical brain dysfunction and CBF changed when the ICH reaches levels above 40 mm Hg. The limit of 14 to 20 mm Hg is the most widely accepted for the treatment of ICP is started in patients with TBI (12). CLINICAL Intracranial hypertension occurs in approximately 50% of all severe TBI and is more common in those with intracranial mass. HIC was found in 71% of the patients with intracerebral hematoma and 39% of acute subdural hematomas (ASDH) and epidural hematomas (EDH). There is no reliable noninvasive indicator of ICH in patients with severe TBI. Symptoms such as headache and nausea are impossible to be recognized in patients in coma, and papilledema is uncommon in acute ICH. 54% of patients who had ICH, only 3.5% had papilledema (5, 13). Other neurological signs including pupil dilation and posture decerebration may occur in the absence of ICH. Signs of brain swelling on CT, as deviation from the midline structures, tanks of compressed database, are indicative of increased ICP, but the ICH can occur without these findings. If a patient is scheduled for removal of lesion, ICP monitoring is installed during surgery, the ventricular catheter and the device of choice for monitoring ICP can be used also to treat the peak by intermittent drainage of CSF (13, 14). Figure 1. LANGFIT CURVE - graph showing the behavior of complacency Pressure x Volume PRINCIPLES OF ICP MONITORING In 1951, Guillaume and Janny (9) made the first continuous measure of intraventricular CSF pressure. These authors devised a technique for continuous measurement of ICP, through a needle intraventricular and an electromagnetic system that allowed continuous recording. This enabled them to make a series of original observations and show clearly the relationship between neurological signs and symptoms and the changes observed in the ICP. It’s usefulness in clinical practice is well established. The consoli- According to Feldman et al (15), monitoring of ICP was defined by Leyden, Germany, more than one hundred years ago. The interest in monitoring has grown steadily and is currently considered an integral part in the management of patients with TBI in the ICU. The study of the dynamics of the ICP has greatly improved our understanding of the physiology of the brain. TECHNIQUES FOR ICP MONITORING IN TBI PATIENTS Currently, it is stated ICP monitoring in all critically ill patients (3-8 points in Glasgow Coma Scale) followed the guidelines of the Brain Trauma Foundation in 2004 (16, 17). 27 Panamerican Journal of Trauma Methods to quantify the levels of ICP and ICP control have been proposed, but its implementation remains a challenge for most hospitals in Brazil and other developing countries. Costs, feasibility, reliability and risks of complications are important for choosing the method of ICP monitoring. The ventricular catheter procedure was the pioneer (10) and is traditionally regarded as the “gold standard” of reliability of ICP monitoring, serving as a model for comparison, all other proposed methods, is also the only one that allows for drainage of cerebrospinal both for biochemical analysis, cytological and microbiological, and as a measure to control ICP (18-20). The technical difficulties for the puncture of the ventricles, especially those pills, displaced and distorted present in many patients with head trauma and risks of additional lesions of the parenchyma and ventriculitis, led to proposal of other methods of monitoring (15, 18). Among the other available methods stand out systems epidural, subdural, subarachnoid and parenchymal. These other methods despite the ease of deployment and present less risk of infection and less aggression to the parenchyma, may have less trust for the interposition of the dura and the risk of extra pressure on the sensor, caused by improper detachment of the meninges in the case of epidural catheter or by difficulties in CSF drainage (15, 18, 20). increased intracranial pressure severe enough to cause coma. This reasoning was based on ease of monitoring and rapid decompression of the effect of cerebrospinal fluid drainage. The drainage of cerebrospinal still generates two effects: the first is that the ventricular system, when properly open, promotes a way of handling the increased interstitial fluid associated with cerebral edema. This pattern promotes a direct means to dehydrate the brain edema, since the movement of the fluid is influenced by the pressure gradient established with the increase in ICP. Thus, interstitial edema, which communicates with the ventricular fluid, can be drained continuously with ventricular catheter. The second benefit refers to the concentration of pro-inflammatory cytokines, especially leukotriene C4 and interleukin-6 in CSF after severe TBI. The decrease of these proinflammatory mediators by continuous drainage reduce the duration of ICH, which supports the concept that the ventriculostomy promotes several clinical benefits, including the ability to monitor and decompress the intracranial space. The use of ventricular catheters for ICP monitoring allows the measurement and drainage of fluid. The drainage of the ventricular system promotes the ICP decrease and redirection of brain interstitial fluid to the ventricle, which may be increased when associated with intracellular cerebral edema and vasogenic. The ventriculostomy for monitoring of ICP is a simple and rapid procedure that can be performed manually when the lateral ventricles are not very reduced or collapsed alveoli (18) (Figure 2). Andrade et al (19) studied 63 patients with brain swelling by moderate to severe TBI after clinical measures in the ICU who underwent intraventricular monitoring and continuous drainage of CSF. They observed that all patients presented in this study survived. Acidosis in CSF was found in the acute stage of TBI and the improvement corresponded to clinical improvement. Patients without signs of DAI had a better response to treatment. These authors concluded that, despite the small sample, the external ventriculostomy can help in the treatment of brain swelling when associated with clinical measures. Hariri (21) reported the routine use of monitoring ventricular cerebrospinal fluid drainage in all patients who showed 28 Figure 2. ICP system - Ventricular catheter in patient who suffered a TBI. In A - catheter with skeletal fixation. In B - transducer. In C - system of external ventricular. Levy et al (22) treated children with TBI, who had HIC resistant to medical therapy, for ventriculostomy and continuous Vol. 16 Number 1 2009 Intracranial pressure monitoring in traumatic brain injury: techniques and clinical applications drainage of CSF. They concluded that drainage controlled external lumbar subarachnoid space is a useful treatment for children with severe TBI when medical therapy and ventricular drainage of CSF fail to ICP control. QUALITATIVE CHANGES IN INTRACRANIAL PRESSURE With the increase of the peak there is a reduction of the space originally occupied by the brain, and arterial pulses become more pronounced, and the component of venous pulsation tends to disappear. In the evolution to come HIC abnormal waves that can be measured, indicating the need for more aggressive treatment. Waves include pathological patterns termed Lundberg A, B and C. A plateau waves or waves of Lundberg represent elevations in ICP over 50 mmHg lasting 5 to 20 minutes. These waves are accompanied by a simultaneous increase in MAP, but the mechanism is not clearly understood whether the change in MAP is a cause or effect of the increase in ICP. Lundberg B waves of pressure pulses have amplitude of 50 mmHg and occur every 30 seconds to 2 minutes. Lundberg C waves have amplitude of 20 mmHg and a frequency of 4 to 8 minutes; they are viewed under normal conditions, but in pathological conditions C waves of large amplitude can be superimposed to form a plateau wave (10, 23). CONSIDERATIONS CLINICAL MEASURES IN CONTROL OF INTRACRANIAL HYPERTENSION The most important ICH complication is cerebral ischemia with a reduction in CBF to levels insufficient to maintain metabolism and brain function and may also result from decreased cerebral perfusion that exceeds the ability of tissue to increase the oxygen uptake of blood. This lead to: (A) inadequate release of O2, (B) inadequate removal of CO2 (C) increased production of intracellular lactic acid, (D) decrease in stock phosphate, (E) decreased ATP, (F) release of excitatory amino acids, (G) break the blood-brain barrier (23). Cerebral ischemia can be global (complete and incomplete) and focal (incomplete). Complete global ischemia affects the entire brain failure in determining the cell membrane, blocking the ion pump. In global ischemia tracked with 15 minute durations followed by reperfusion there is rapid deterioration of cerebral metabolism. There is also a decrease in phosphocreatine concentration, increase in tissue lactate concentration, decreased intracellular pH and gradual increase of free fatty acids (23). Incomplete global ischemia occurs when CPP decreases below the self-regulation, as in profound hypotension. It may be more detrimental than complete ischemia because of inadequate substitutive O2, resulting in anaerobic metabolism (24). The focal cerebral ischemia is restricted to one vascular territory, consisting of two distinct areas: the central, densely ischemic, in which there are metabolic changes similar to complete ischemia and ischemic penumbra perfusion decreased but still detectable, the collateral vessels, partly by metabolism stopped, but where the cells remain viable when there is restoration of the CBF. The opening of collateral blood vessels occurs within minutes after occlusion of a main vessel. In the center of the ischemic area selectively vulnerable neurons are affected, but the glial cells are spared, if the CBF is returned within an hour. At this stage the neuronal necrosis is inevitable (2). Cerebral protection in intracranial hypertension consists of physiological and pharmacological measures that are taken early seeking to minimize secondary brain injury. Cerebral protection can be preventive or be achieved by treatment during or after ischemia, and then a measure to minimize the initial tissue injury or improve secondary injury resulting from ischemia. The increase in regional CBF in the vicinity of the ischemic area can be achieved only with the increase of CPP in the ischemic area. Inotropic agents to maintain or increase systemic blood pressure leading to increased CBF in the ischemic area. The early craniotomy for excision of focal lesion may evolve to reactive hyperemia reversible if surgical decompression for late may experience a state of hypoperfusion after hyperemia or without reperfusion injury that progresses to neuronal death, occlusion of the microvasculature by compression or thrombosis, with death of endothelial cells and glial determining a brain swelling, hemispheric or bi-hemispheric (22). Acute TBI initiates a cascade of inflammatory and metabolic events, which may result in the development of cerebral edema and increased ICP. Under these conditions the brain is particularly susceptible to secondary ischemic lesions, as well as hypoxemia and hypotension are associated with worse neurological outcome (2). Cerebral protection by induced comas can be made in the form of sedation with drugs that reduce neuronal metabolism especially benzodiazepines or barbiturate-induced coma when the HIC does not respond to measures of sedation. The Mannitol reduces ICP decreased the water 29 Panamerican Journal of Trauma content of brain, reducing blood viscosity, which improves cerebral perfusion by decreasing the formation of CSF. It acts also as a reduction of free radicals, which may be involved in the formation of cerebral edema. The Mannitol decreases ICP in 27% and CBF remains unchanged when the self-regulation is intact (22), but when self-regulation is compromised, decrease in ICP occurs in only 4.7% and CBF increases by 18% ( 22). Cerebral protection by mild hypothermia in TBI may be a useful technique for treatment of severe TBI. Clinical measures for treatment of ICP in the ICU begin with preventive measures such as lifting the back of the bed to 30 degrees with the horizontal plane, keeping the patient in neutral alignment, avoiding bending, extension and lateral movements cervical nerves in addition to 15; maintenance of patent airways and ventilated for good diffusion of O2 pressure; DTC diagnosis and treatment of cerebral hemodynamic changes, mild hyperventilation (30 - 35 mm Hg) in controlled situations hyperemia or the physician’s discretion. Producing controlled hyperventilation hypocapnia is effective in the short term to reduce the peak by decreasing CBF and VSC. When PaCO2 decreases, the cerebral vessels constrict to the occurrence of vasoconstriction is achieved with PaCO2 approximately 20 mm Hg. If the PaCO2 decreases below 18-20 mm Hg, may lead to ischemia (22). Hyperventilation could exert a protective effect on focal cerebral ischemia by cerebral vasoconstriction normal diverting blood from normal tissue to the ischemic area. Hyperventilation started before the experimental focal ischemia has been shown to decrease the incidence of cerebral infarction, however, has no effect if started after ischemia. In contrast, it has been argued that increasing the PaCO2 improved CBF in areas of ischemia. In a clinical trial found a worse clinical outcome in patients undergoing hyperventilation should be avoided application of the routine method (25). 20 mm Hg is the most widely accepted for the treatment of ICP is started in patients with TBI (29). The measurement of brain temperature is important because it helps in the intensive management of patients because, hypothermia is part of the therapeutic armamentarium for control of ICP and knowledge of the hypothalamic temperature (center) helps to avoid large variations. The disproportion between the axillary and ventricular temperatutra for example, may indicate failure of the treatment employed which can determine change in treatment planning (18). The criteria for permanent ICP monitoring are not firmly established in the literature. The Brain swelling, edema and progression of hemorrhagic lesions are maximal within 48 to 96 hours of TBI. Monitoring should be maintained until the fifth day since the peak is normal. The intraoperative ICP monitoring is also recommended in patients with moderate to severe TBI (29). Figure 3 and 4. Figure 3. Indications for ICP monitoring in patients with TBI according BRAIN TRAUMA FOUNDATION. Should also keep euvolemia with hydro-electrolyte balance, maintaining the PPC in 70mm Hg or greater; maintaining normothermia (body temperature <37.5 °C) prevent seizures by drug prophylaxis (26). Miller et al (27) demonstrated that patients with ICP above 20 mm Hg, uncontrolled, have mortality above 90%. The intensive control of PIC can reduce by 50% the mortality of severe TBI (28). The ECA has levels of HIC maintained above 60 mm Hg, is always fatal (29), electrical brain dysfunction is common and the FSC is often changed when the HIC reaches levels above 40 mm Hg. The limit of 14 to 30 Figure 4. Systems of Ventricular ICP monitoring applicated in our service. Vol. 16 Number 1 2009 Intracranial pressure monitoring in traumatic brain injury: techniques and clinical applications following traumatic brain injury. Rev Assoc Med Bras 2009; 55(1): 75-81. COMPLICATIONS OF ICP MONITORING The most common complications of ventriculostomy are: injury to the brain parenchyma, hemorrhage and infection. Mayhall et al (30) in a prospective study relate the infection rate in patients with intracerebral hemorrhage in the ventricular and intraventricular monitoring of peak time of catheter. Thus, they report that the infection rate is 6 to 9% when the monitoring is maintained for up to 5 days with high and cumulative, and 18% when maintenance is prolonged. Bekaret al (31) in a study with 631 patients concluded that the duration of monitoring should be dictated by the need to monitor developments in the ICP, and not by concern for infection. They stressed the need for less irrigation and minimal manipulation of the catheter. If there ventriculitis, one must introduce specific antibiotic. The success of monitoring with or without benefit of CSF drainage and to minimize the risks of maintaining such a system also depends on the nursing staff through their daily care. Rebuck et al (32) found in 78% of patients infected with a coincidence between the micro-organism isolated in the CSF and the site of infection. Patients with outbreaks in different places of the CNS, especially pneumonia or urinary tract infection, have shown a predilection to present ventriculitis or meningitis. Feldman and Narayan (15) describe that the second complication of ventricular ICP monitoring is the risk of intracranial hemorrhage of 1-2%, this risk is greater in the presence of coagulopathy, disseminated intravascular coagulation or liver failure. 3. Adekoya N, Majumder R. Fatal traumatic brain injury, West Virginia, 1989-1998. Public Health Rep 2004; 119: 486-492. 4. Bor-Seng-Shu E, Hirsch R, Teixeira MJ, Andrade AF, Marino R, Jr. Cerebral hemodynamic changes gauged by transcranial Doppler ultrasonography in patients with posttraumatic brain swelling treated by surgical decompression. J Neurosurg 2006; 104(1): 93-100. 5. Amorim RL, Paiva WS, Andrade AF, Marino R. Hipertensão Intracraniana. J Bras Med 2006; 90: 30-36. 6. Uzzell BP, Obrist WD, Dolinskas CA, Langfitt TW. Relationship of acute CBF and ICP findings to neuropsychological outcome in severe head injury. J Neurosurg 1986; 65: 630-635. 7. Obrist WD, Langfitt TW, Jaggi JL, Cruz J, Gennarelli TA. Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension. J Neurosurg 1984; 61: 241-253. 8. Chesnut RM, Marshall LF, Klauber MR. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34: 216-222. 9. Guillaume J, Janny P. Continuous intracranial manometry, physiopathologic and clinical significance of the method. Presse Med 1951; 59(45): 953-955. 10. Lundberg N. Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Acta Psychiatr Scand Suppl 1960; 36(149): 1-193. 11. Gopinath S, Robertson CS. Intensive care unit management. In: Marion D. Traumatic Brain Injury. New York: Thieme; 1999. p. 101-18. 12. Ross DA, Olsen WL, Ross AM. Brain shift level of consciousness and restauration of consciousness in patients with acute intracranial hematoma. J Neurosurg 1989; 71: 498-502. CONCLUSIONS 13. Selhorst JB, Gudeman SK, Butterworth JF. Papilledema after acute head injury. Neurosurgery 1985; 16: 357-63. Intracranial hypertension is a condition of great importance in patients with traumatic brain injury, resulting in poor outcome prognosis. Application of ICP monitoring and early interventions to reduce secondary injuries with ICH treatment and cerebral hemodynamic control help in the intensive care of these patients. 14. Maset A, Andrade AF, Brock RS, Barbosa R. Monitoração da pressão intracraniana: avanço técnico no sistema hidrostático. Part I: a simplificação do sistema. Arq Bras Neurocir 2004; 23(1): 28-35. REFERENCES 16. Ghajar J. Essay: the future of traumatic brain injury. Mt Sinai J Med 2009; 76(2): 190-3. 1. McArthur DL, Chute DJ, Villablanca JP. Moderate and severe traumatic brain injury: epidemiologic, imaging and neuropathologic perspectives. Brain Pathol 2004; 14: 185-194. 2. Andrade AF, Paiva WS, Amorim RL, Figueiredo EG, Rusafa Neto E, Teixeira MJ. The pathophysiological mechanisms 15. Feldman Z, Narayan RK. Intracranial Pressure Monitoring: Techniques and Pitfalls. In: Cooper PR. Head Trauma. 3a. ed. Baltimore: Willians & Wilkins; 1993. p. 247-74. 17. Fakhry SM, Trask AL, Waller MA, Watts DD. IRTC Neurotrauma Task Force. Management of brain-injured patients by an evidence-based medicine protocol improves outcomes and decreases hospital charges. J Trauma 2004; 56(3): 492-9. 31 Panamerican Journal of Trauma 18. Andrade AF, Marino Jr R, Ciquini Jr O. Guidelines for neurosurgical trauma in Brazil. World J Surg 2001; 25(9): 1186-1201. 26. Rangel-Castilla L, Gopinath S, Robertson CS. Management of intracranial hypertension. Neurol Clin 2008; 26(2): 521-541. 19. Andrade AF, Marino Jr R, Miura FK. Preliminary experience with decompressive ventriculostomy by continuous ventricular cerebrospinal fluid drainage in postraumatic diffuse brain swelling. J Neurotrauma 2002; 19(10): 1381. 27. Miller JD, Becker DP, Ward JD. Significance of intracranial hypertension in severe head injury. J Neurosurg 1977; 47: 503-516. 20. Dantas Filho VP, Falcão AL, Sardinha LA, Facure JJ, Araújo S, Terzi RG. Technical aspects of intracranial pressure monitoring by subarachnoid method in severe head injury. Arq Neuropsiquiatr 2001; 59(4): 895-900. 21. Hariri RJ. Cerebral Edema. Neurosurg Clin North Amer 1994; 5(4): 687-706. 28. Minardi J, Crocco TJ. Management of traumatic brain injury: first link in chain of survival. Mt Sinai J Med 2009; 76(2): 138-144. 29. Rangel-Castilla L, Gasco J, Nauta HJ, Okonkwo DO, Robertson CS. Cerebral pressure autoregulation in traumatic brain injury. Neurosurg Focus 2008; 25(4): E7. 22. Levy DI, Rekate HL, Cherny WB. Controlled lumbar drainage in pediatric head injury. J Neurosurg. 1995; 83: 453-460. 30. Mayhall CG, Archer NH, Lamb VA. Ventriculostimy-related infectons. A prospective epidemiologic study. N Engl J Med 1984; 310(9): 553-559. 23. Safar P. Ressucitation of the ischemic brain. In: Textbook of Neuroanesthesia wich Neurosurgical and Neurosciece Perspectives. Albin MS, editor. Mc Graw-Hill; 1997. p 557-593. 31. Bekar A, Doğan S, Abaş F, Caner B, Korfali G, Kocaeli H, et al. Risk factors and complications of intracranial pressure monitoring with a fiberoptic device. J Clin Neurosci 2009; 16 (2): 236-240. 24. Stávale MA. Bases teóricas das alterações hemodinâmicas e metabólicas encefálicas pós traumáticas. In: Stávale MA. Bases da terapia intensiva neurológica. São Paulo: Ed Santos; 1996. p. 97-132. 32. Rebuck JA, Murry KR, Rhoney DH, Michael DB, Coplin WM. Infection related to intracranial pressure monitors in adult analysis of risk factors and antibiotic prophylaxis. J Neurol Neurosurg Psychiat 2000; 69: 381-384. 25. Stocchetti N, Maas AI, Chieregato A. Hyperventilation in head injury: a review. Chest 2005; 127: 1812-1827. 32 Vol. 16 Number 1 2009 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 33 - 36 TRAUMA IN THE OBESE: AN OVERVIEW Therèse M. Duane, MD, FACS.1 SUMMARY Obesity is a growing problem in the United States and the impact is being increasingly felt in the setting of trauma and critical care. This manuscript is an overview of the literature related to the topic of obesity and trauma. Current literature suggests that safety devices and hospital resources may be inadequate to address this population’s needs and that without them; these patients are at high risk of worse outcomes. RESUMEN La obesidad es un problema cada vez mayor en los Estados Unidos y el impacto se está sintiendo en el escenario del trauma y del cuidado crítico. Este manuscrito es una descripción de la literatura relacionada con la obesidad y del trauma. La literatura actual sugiere que los dispositivos de seguridad y los recursos del hospital pueden ser inadecuados para tratar las necesidades de esta población, y que sin ellos estos pacientes están en mayor riesgo de peores resultados. INTRODUCTION Over the last twenty years there has been an astounding increase in the rate of obesity in the United States (1). Available data in 1985 showed most states having less than a 10% obesity rate. By 1990 the majority of states had a 10-14% rate of obesity which increased significantly into 2000 in which the majority had over a 20% obesity rate. Presently there is approximately sixty million adults, or over 30% of the adult population that are defined as obese, that is a body mass index (BMI) of greater than 30 kg/m (2), which is a doubling of the rate since 1980. The focus of this paper is to review the current limitations related to 1 Division of Trauma, Critical Care and Emergency Surgery. Virginia Commonwealth University Medical Center Richmond, Virginia 33 caring for the obese and how this translates into outcomes for this group of patients. SAFETY DEVICES Moran et al (3) reviewed the National Automotive Sampling System and compared restrained drivers grouped by height and weight to a crash test dummy. They found that heavier patients had lower head injury rates and abdominal injuries, but that the more obese the population has become the less adequate safety device testing is using these crash test dummies suggesting the need to update testing methods. A study by Arbabi et al (3) evaluated 189 patients to determine the effect of the body mass index on outcomes from motor vehicle crashes. They found that obesity was an independent risk factor with an odds ratio of almost four times the risk with a BMI greater than 30 kg/m2. They also noted that the pattern of injury depended in part on the body mass index, noting a higher likelihood of lower extremity injury. They theorize that current safety measures are designed for the average size person and may not be adequate for the obese, thereby leading to more extremity injuries in the obese patients. There in lies a basic limitation in that the obese patient who gets into a vehicle is already going to be potentially at a higher risk for injury because safety devices presently in place are inadequate. EQUIPMENT Foil et al (4) in 1993 identified the problem with managing the obese patients with the equipment designed for the average size person. They found limitations in their own availability and adequacy of the equipment. Furthermore equipment for the bariatric patient is significantly more costly, as an example when looking at bedside commodes; a 20-inch width commode averages approximately $485.00 versus a 30-inch width commode averaging almost $700.00. This is also apparent in wheelchairs where 450-pound capacity chair is $632.00 based on our hospital’s informa- Panamerican Journal of Trauma tion for our bariatric patients, and an 850-pound capacity chair is almost $1500.00. Not only are these patients at higher risk for injuries from trauma but there is already an increased cost simply to have the equipment available to care for these patients. Another major concern is the staff resources that are involved in managing the bariatric population. Drake et al (5) evaluated the nurses’ perspective in treating the obese patient. They noted that they had increased staffing needs because of physical demands. Nurses were concerned that there was not enough specialized equipment available putting themselves and the patients at risk of injury. They concluded that specialized nursing care was needed to appropriately manage these patients. Since then bariatric centers geared toward caring for the obese patient have begun addressing these concerns. ICU PATIENTS There are a number of studies that evaluated the obese patient in the critical care setting. Akinnusi et al (6) performed a meta- analysis to evaluate outcomes in critically ill obese patients and found that they had longer ventilator and ICU lengths of stay compared to their non-obese counterparts. Goulenok et al (7) did a prospective study in a medical ICU evaluating 813 patients. Although they found similar infection rates they also found by regression analysis that a BMI greater than 27 kg/m2 was an independent predictor of mortality. Bercault et al (8) evaluated both medical and surgical ventilator dependent patients. They noted that obese patients defined by a BMI of greater than 30 kg/m2 had a twofold increase in their chance of dying. An increase in mortality has not been consistently observed. Tremblay and Bandi (9) retrospectively studied 41,000 patients and found no difference in mortality with obese patients. Garrouste-Orgeas et al (10) prospectively evaluated medical surgical patients and found that a lower BMI of less than 18.5 kg/m2 had a higher mortality. However, prolonged ICU care for the obese does seem to be detrimental. Nasraway et al (11) looked at 1,373 patients of whom there were 6.8% who were super-obese defined by a BMI of greater than 40 kg/m2. They evaluated patients who were in the ICU greater than four days and found that the super obese patients had a much higher ICU mortality, 33.3% versus 12.3% and as the body mass index increased there was an exponential increase toward 100% mortality. This study suggests that those patients who are both significantly obese and critically injured requiring more ICU care have a higher likelihood of death. 34 TRAUMA The data specific to trauma patients also varies somewhat. At our institution we demonstrated no difference in outcome for the obese patient (12). We performed a retrospective review of 338 non-obese patients compared to 115 obese patients defined by a BMI of greater than 30 kg/ m2. Interestingly there was no difference in co-morbidities between the groups. The patients were also equally injured except that the obese patients had a higher GCS (14.5 ± 1.9 obese versus 13.6 ± 3.5 non-obese, p=0.01) suggesting lower head injury rates. We believe a key finding is that our complications were the same regardless of whether the patient was obese or non-obese, potentially having an effect on our subsequent outcome results. There were essentially no differences in ventilator, ICU, hospital length of stay or mortality. In subset evaluation of patients not requiring ICU care we found no differences between the groups in infection and mortality rates but a slightly higher hospital stay in the obese which did not meet statistical significance (3.2 days ± 2.9 obese vs. 2.7 days ± 2.3 non-obese, p=0.055). We performed multiple subset analysis including those patients who were ventilated, those who were not ventilated, those with an injury severity score greater than 15 and those less than 15. All of these analyses failed to demonstrate differences in any of the outcome measures that we evaluated including percent infections, ventilator, ICU, hospital length of stay and mortality. Based on our study we concluded that there were no differences between the populations and that similar results were seen both in the ICU and non-ICU patients. We suggested that if one recognizes the potential for complications in the obese patients that more aggressive care can reduce their complication rate resulting in lower morbidity and mortality after blunt trauma. Alban et al (13) did a much larger retrospective review with 918 patients but also including patients only admitted to the ICU. They had almost a 15% obese rate, defined as a BMI greater than 30 kg/m2 and they too had similar demographic data and APACHE II scores. They found one difference between the groups in that the obese patients had a longer ICU length of stay of 6.8 days versus 4.8 days for the non-obese with a p-value of 0.04. However, the three most common complications associated with death (pulmonary, neurologic degeneration, and cardiovascular compromise) showed no differences between the groups resulting in similar mortality rates between the obese at 5.9% versus 8.0% in the non-obese with a p-value of 0.48. The majority of the studies do show differences in outcome. Bochicchio et al (14) did a prospective study to evaluate the Vol. 16 Number 1 2009 Trauma in the Obese: An Overview microbiology of pneumonia and noticed that obesity in and of itself was associated with increased ventilator and ICU length of stay. Further poor outcomes were identified by Brown et al (15). They did a retrospective review of 690 closed-head injury patients. They had a 19% obese rate and although the obese patients trended toward more complications they clearly had a higher mortality rate of 36% versus 25% with p-value of 0.02. However, they did not find that obesity was an independent risk factor for morbidity or mortality in their study. Ciesla et al (16) performed a prospective observational trial of only ICU patients. They had 716 patients and defined obesity as a BMI of greater than 30 kg/m2. They specifically wanted to look at multiorgan failure and identified that there was no difference in transfusions between the two groups. However the obese group had almost a twofold increase in multiorgan failure with an odds ratio of 1.8 with a confidence interval of 1.2 to 2.7. They also had a higher ICU and hospital length of stay but no difference in mortality. The non-obese group had 11% mortality versus the obese group which had a 7% mortality with a p-value of 0.14. Further studies seem to suggest even greater disparity between outcome measures in the obese and the non-obese. Choban et al (17) did a retrospective review of 184 patients. They grouped patient’s by BMIs of less than 27-31 kg/ m2 and greater than 31 kg/m2. Although they noted no differences in age, injury severity score, length of stay or ventilator length of stay, they had a significantly higher mortality in the severely obese group. The severely obese group had a mortality rate of 42.1% compared to less than 10% in the other groups. They further identified BMI and ISS to be independent predictors of outcome. A more recent study by Byrnes et al (18) performed a retrospective review on almost 1200 patients. Their obese group, defined as BMI > 35 kg/m2 , had a 10.7% mortality versus 4.1% for the lean, and they also found a significantly higher mortality rate in the more severely injured patients defined by an ISS of greater than 15. Further studies have replicated these poor results of the obese population. Brown et al (19) did a retrospective review focusing only on ICU patients. They had 1153 patients with a 25% rate of patients with a BMI of greater than or equal to 30 kg/m2. Their patients were similar demographically and as was presented in previous studies, the distribution of injuries in the obese group was greater in the lower extremities (53% versus 38%, p <0.001). There were fewer head injuries in the obese population (42% versus 55%, p = 0.0001). This trial also showed that the majority of complications were higher in the obese group. Furthermore, this trial identified obesity as an independent risk factor for mortality with an odds ratio of 1.6. Neville et al (20) performed a case control study of all critically injured patients. They had a 26% obesity rate and found similar complications except for higher multiorgan failure in the obese population. They too found BMI to be an independent risk factor for mortality with an odds ratio of 5.7, (CI 1.9- 19.6). In a prospective study by Bochiccio et al (21) in which they studied 1167 patients, the obese patients had a twofold increase in infectious complications including respiratory, genitourinary, and bacteremias. Further multiple linear regression analysis that evaluated obesity as an independent risk factor with adjustments for age and ISS found that obesity was an independent predictor of hospital length of stay, ICU length of stay, ventilator days, foley catheter days and central venous catheter days. These results emphasize that patients who require more invasive procedures, lines and foley catheters, are at increased risk for infectious complications and worse outcome. In the analysis for in-hospital mortality based on regression analysis, the obese patients had a 7-fold increase in mortality compared to their leaner cohorts. CONCLUSIONS The number of obese trauma patients is on the rise. Current safety devices are not designed for the obese population. In addition, equipment and staffing needs often fall short of what is required. Overall there are mixed results when it comes to ICU outcomes for obese patients although they tend to do worse with longer ICU stays. Trauma patients outcome are not all bad particularly in the non-ICU patient and when complications are minimized, but they deteriorate quickly as complications increase. The solution to this problem is multifactorial although at every level it starts with prevention. First, go back to basics with diet and exercise to deter the rise in obesity. Second, improve safety design for vehicles including self-inflating lap belts to disburse energy to minimize injury. Third, focus on eliminating complications for the hospitalized obese patient and finally, mobilize these patients early with enhanced resources to promote them to the next level of care. REFERENCES 1. The Center for Disease Control and Prevention. National Center for Chronic Disease Prevention and Health Promotion. Obesity Trends. Available at http://www.cdc.gov/nccdphp/ dnpa/obesity/trend/maps/index.htm (Accessed June 10, 2005). 35 Panamerican Journal of Trauma 2. Moran SG, McGwin G, Metzger JS, Windham ST, Reiff DA, Rue LW. Injury rates among restrained drivers in motor vehicle collisions: the role of body habitus. J Trauma 2002; 52: 1116-1120. 3. Arabi S, Wahl W, Hemmila MR, Kohoyda-Inglis C, Taheri P, Wang SC. The cushion effect. J Trauma 2003; 54: 10901093. 4. Foil MB, Collier MS, MacDonald KG, Pories WJ. Availability and adequacy of diagnostic and therapeutic equipment for the morbidly obese patient in an acute care setting. Obes Surg 1993; 3: 153-156. 5. Drake D, Dutton K, Engelke M, McAuliffe M, Rose MA. Challenges that nurses face in caring for morbidly obese patients in the acute care setting. Surg Obes Relat Dis 2005; 1: 462-466. 6. Akinnusi ME, Pineda LA, El Solh AA, Effect of obesity on intensive care morbidity and mortality: A meta-analysis. Crit Care Med 2008; 36: 151-158. 7. Goulenok C, Monchi M, Chiche JD, Mira JP, Dhainaut JF, Cariou A. Influence of overweight on ICU mortality. Chest 2004; 125: 1441-1445. 8. Bercault N, Boulain T, Kuteifan K, et al. Obesity-related excess mortality rate in an adult intensive care unit: a riskadjusted matched cohort study. Crit Care Med 2004; 32: 998-1003. 9. Tremblay A, Bandi V. Impact of body mass index on outcomes following critical care. Chest. 2003; 123: 1202-1207. 10. Garrouste-Orgeas M, Troche G, Azoulay E, et al. Body mass index. An additional prognostic factor in the ICU patients. Int Care Med 2004; 30: 437-443. 11. Nasraway SA, Albert M, Donnelly AM, Ruthazer R, Shikora SA, Saltzman E. Morbid obesity is an independent determinant of death among surgically ill patients. Crit Care Med 2006; 34: 964-969. 36 12. Duane TM, Dechert T, Aboutanos MB, Malhotra AK, Ivatury RR. Obesity and outcomes after blunt trauma. J Trauma 2006; 61: 1218-1221. 13. Alban RF, Lyass S, Marguilies DR, Shabot MM. Obesity does not affect mortality after trauma. Am Surg 2006; 72: 966-969. 14. Bochicchio GV, Joshi M, Bochicchio K, Tracy K, Scalea TM. A time-dependent analysis of intensive care unit pneumonia in trauma patients. J Trauma 2004; 56: 296-303. 15. Brown CV, Rhee P, Neville A, Sangthong B, Salim A, Demetriades D. Obesity and traumatic brain injury. J Trauma 2006; 61: 572-576. 16. Ciesla DJ, Moore EE, Johnson JL, Burch JM, Cothren CC, Sauaia A. Obesity increases the risk of organ failure after severe trauma. J Am Coll Surg 2006; 203: 539-545. 17. Choban PS, Weireter LJ, Maynes C. Obesity and increased mortality in blunt trauma. J Trauma 1991; 31: 1253-1257. 18. Byrnes MC, McDaniel MD, Moore MB, Helmer SD, Smith RS. The effect of obesity on outcomes among injured patients. J Trauma 2005; 58: 232-237. 19. Brown CV, Neville AL, Rhee P, Salim A, Velmahos GC, Demetriades D. The impact of obesity on the outcomes of 1153 critically injured blunt trauma patients. J Trauma 2005; 59: 1048-1051. 20. Neville AL, Brown CV, Weng J, Demetriades D, Velmahos GC. Obesity is an independent risk factor of mortality in severely injured blunt trauma patients. Arch Surg 2004; 139: 983-987. 21. Bochicchio GV, Joshi M, Bochicchio K, Nehman S, Tracy K, Scalea TM. Impact of obesity in the critically ill trauma patient: a prospective study. J Am Coll Surg 2006; 203: 533-538. Vol. 16 Number 1 2009 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 37 - 42 SECUELAS NEUROPSICOLÓGICAS EN PACIENTES CON TRAUMA CRANEOENCEFÁLICO ASOCIADO A LESIÓN AXONAL DIFUSA Javier Orozco Mera,1 Miguel Velásquez Vera,2 Alfredo Pedroza Campo.3 SUMMARY Background: Recent studies reveal that patients after diffuse axonal injury (DAI), have impaired cognitive function. Memory and executive functions are most affected. Objetivo: Realizar seguimiento en el tiempo de aquellos pacientes con diagnóstico de lesión axonal difusa, y evaluar la presencia de alteraciones neuropsicológicas. Objective: To follow up on those patients with diffuse axonal injury, and evaluate the presence of neuropsychological sequelae. Materiales y métodos: A 18 pacientes con diagnóstico de LAD, llevados a la unidad de cuidados intensivos, se les siguió por un período variable entre 3 y 6 meses. A aquellos con buenos resultados, según la escala de Glasgow (GOS 4-5), se les practicó evaluación neuropsicológica. Materials and methods: 18 patients with DAI were taken to the intensive care unit, followed by a period variable between 3 and 6 months. For patients with good results on the Glasgow Coma Scale (GOS 4 to 5) a neuropsychological assessment was carried out. Resultados: El 75% de los pacientes evaluados presentaron alteración en las pruebas utilizadas para valorar atención, concentración y funciones ejecutivas. El mayor componente fue dado por los subtest de semejanzas, cálculo, dígitos en regresión. Results: 75% of patients evaluated presented alteration in the tests used to assess attention, concentration and executive functions. The largest component was given by the similarities subtest, calculation, digit decline. Conclusión: Todos tuvieron algún grado de déficit neurológico posterior, lo más marcado fue déficit de atención y en funciones ejecutivas. Conclusion: All had some degree of subsequent neurological deficit, which was more marked by deficits in attention and executive functions. Key words: axonal injury, neuropsychological sequelae, attention deficit, executive function RESUMEN Antecedentes: Estudios recientes revelan que los pacientes, luego de una lesión axonal difusa (LAD), presentan alteración en su función cognitiva. La memoria y las funciones ejecutivas son las más afectadas. 1 Residente de II año de Neurocirugía, Universidad del Valle, Cali, Colombia. 2 Profesor titular, Sección de Neurocirugía, Escuela de Medicina Universidad del Valle. 3 Profesor titular y Distinguido, Jefe de la Sección de Neurocirugía, Escuela de Medicina Universidad del Valle. Palabras clave: Lesión axonal, secuelas neuropsicológicas, déficit de atención, funciones ejecutivas. INTRODUCCIÓN El trauma craneoencefálico (TCE) es la principal causa de discapacidad entre los adultos jóvenes (1) y las secuelas neuropsicológicas de estos TCE son las que mayor impacto tienen en la calidad de vida del paciente y de su familia ya que afectan su desempeño académico, laboral y social (2). El daño cerebral después de un TCE es el resultado de las lesiones estructurales iniciales y de las complicaciones secundarias. Las contusiones, laceraciones, hemorragias intracraneales y la lesión axonal difusa constituyen lesiones primarias, ya que ocurren en el mismo momento del impacto. Las lesiones secundarias se producen por complicaciones de los procesos que se inician en el momento de la lesión, pero no son directamente atribuibles al impacto. En las últimas décadas, se han producido avances significa- 37 Panamerican Journal of Trauma tivos tanto en el conocimiento de los mecanismos básicos de los traumatismos como en su fisiopatología, lo que ha permitido el abordaje terapéutico de muchos de los TCE graves y con ello la disminución del número de muertes (1). 2008, con diagnóstico de trauma craneoencefálico cerrado moderado - severo y lesión axonal difusa, 18 cumplieron los criterios de inclusión. Sin embargo, junto con el aumento de la supervivencia, también ha aumentado el número de personas con graves secuelas neurológicas que sobreviven al TCE, (Hospital Universitario del Valle, Unidad de Cuidados Intensivos neuroquirúrgica, Cali. Colombia) situando al TCE como uno de los más graves problemas de salud de las sociedades desarrolladas. La mayor incidencia de los TCE se observa en tres picos de edad: primera infancia, final de la adolescencia y en la vejez (3), pero sobre todo en la adolescencia y principio de la edad adulta. El mecanismo por el que se produce el TCE está fuertemente asociado con la forma de vida de los países: accidentes de tránsito, deportes u ocio, caídas y agresiones (3). • • • La resolución de los cambios fisiológicos que causan la disrupción funcional más que estructural, es probablemente la mejor explicación de la emergencia del coma y de la primera y espontánea recuperación física y neuropsicológica después del TCE. Ello significa el retorno en horas, días o semanas de funciones o áreas del cerebro temporalmente suprimidas (4, 5). Procedimientos Varios estudios han relacionado las consecuencias neuropsicológicas con variables de esta fase aguda. Una menor puntuación en la escala de coma de Glasgow y la alteración de los reflejos del tronco encefálico (6), la mayor duración del coma (1), la hipertensión intracraneal (2), se relacionan con un peor funcionamiento cognitivo a largo plazo. Asimismo, la presencia de insultos secundarios (hipoxia sistémica, hipotensión arterial) producidos en las primeras horas después del TCE se encuentra relacionada con las secuelas neuropsicológicas a largo plazo (4). El daño axonal difuso (DAD) en el trauma craneoencefálico (TCE) se produce como consecuencia de daño axonal primario y secundario; es el responsable de la mayoría de las alteraciones de atención, memoria, velocidad de procesamiento y alteraciones ejecutivas en los TCE moderados y graves. Materiales y métodos De los pacientes que ingresaron a la unidad de cuidados intensivos neuroquirúrgica del Hospital Universitario del Valle en el período comprendido entre enero y diciembre de 38 Criterios de inclusión Edad entre los 15 y los 70 años Al ingreso Glasgow <13 Permanecieron en la unidad de trauma del Hospital Universitario máximo 24 horas antes de su ingreso a UCI. Criterios de exclusión • • • Lesiones focales en la TAC que requieran manejo quirúrgico Contusiones frontales en la TAC Pacientes posterior a su egreso con evolución según escala de Glasgow de resultados (GOS) 1-2-3. Estos pacientes fueron trasladados a la unidad de cuidados intensivos. En la escanografía inicial ninguno presentaba lesiones focales susceptibles de manejo quirúrgico. Durante su estancia en la unidad de trauma fueron intubados según indicación, monitorizados con gases arteriales, control glicémico, control de electrolitos, curva térmica, radiografías de tórax, control de tensión arterial. En la unidad de cuidados intensivos fueron sedados para Ramsay 6, relajados, puestos en ventilación mecánica, monitoría continua, con PCO2 entre 32 y 35 mmHg, TAM 90-110, en caso de TAM <90 uso de vasoactivos, curva térmica, control con glucometrías cada 4 horas para tener glicemia menor de 140 mg/ dl, inicio de nutrición parenteral en las primeras 24 horas, transfusión de glóbulos rojos si hematocrito era menor a 30, uso de soluciones hipertónicas de rutina en las primeras 72 horas con control electrolítico cada 6 horas, control de líquidos para mantener un balance positivo-neutro. Pasadas 48 horas con evolución escanográfica y en conjunto con equipo de terapia respiratoria, se inició disminución de sedación y relajación para definir estado neurológico del paciente, plan de extubación vs. traqueostomía temprana. Una vez estos pacientes están sin requerimiento de vasoactivos y con una vía aérea definida se trasladaron a la sala de hospitalización para inicio de equipo interdisciplinario de apoyo y educación a la familia. El control se realizó por la consulta externa en un periodo no mayor de 45 días; en esta consulta se captaron pacientes con Glasgow de resultados (GOS) 4-5 los cuales son evaluados por primera vez por neuropsicología entre 3 y 6 meses posteriores al trauma. Vol. 16 Number 1 2009 Secuelas neuropsicológicas en pacientes con trauma craneoencefálico asociado a lesión axonal difusa EVALUACIÓN NEUROPSICOLÓGICA La NEUROPSI es un instrumento de tamizaje utilizado tanto en la práctica clínica como en la investigación de pacientes hispanohablantes. De acuerdo con los autores, fue diseñado para la evaluación del funcionamiento cognoscitivo en pacientes psiquiátricos y neurológicos y está constituido por ítems sencillos y cortos que permiten la valoración rápida de las funciones cognoscitivas. Contiene reactivos que son sensibles y relevantes para la población hispanohablante y que pueden ser aplicados a población de escolaridad nula. Cuenta con normas obtenidas en una muestra de 1.640 sujetos, considerando cuatro niveles de edad (1-16, 31-50, 51-61 y 66-85 años) y dentro de cada rango de edad cuatro niveles educativos: escolaridad nula, 1-4 años de estudio, 5-9 años y más de 10 años. El sistema aporta datos cualitativos y cuantitativos (tabla 1). No se basa en un método univariado de daño cerebral, sino que con los datos independientes de cada habilidad cognoscitiva se obtiene un perfil individual que señala el desempeño del sujeto en cada una de las áreas evaluadas. Los parámetros de estandarización permiten obtener un grado o nivel de alteración que se clasifica en normal, alteraciones leves, alteraciones moderadas y alteraciones severas. El tiempo de aplicación es de 20-25 minutos. Tabla 1. Componentes de evaluación neuropsicológica NEU-ROPSI. PROCESOS Orientación atención y concentración ÁREAS Tiempo (día, mes y año), lugar (ciudad y lugar específico) y persona (¿Cuántos años tiene?) digitos en regresión Detección visual. Se pide al sujeto que marque en una hoja todas las figuras iguales a la que se le presenta. Se registra el número de aciertos y el número de errores. Veinte menos tres cinco veces consecutivas PUNTUACIÓN 6 27 Memoria verbal Memoria verbal. Se presenta una lista de seis palabras (animales, frutas, y partes del cuerpo) en tres ensayos. Después de cada ensayo se le pide al sujeto que diga todas las palabras que pueda recordar. También se registran las intrusiones, perseveraciones y efectos de primacia y recencia. Evocación de información verbal Evocación espontánea. Se pide al sujeto que diga todas las palabras que recuerde de la lista que se le dijo. Se registra el número de aciertos, perseveraciones e intrusiones. Evocación por claves. Se pide al sujeto que diga que palabras de la lista eran animales, frutas o partes del cuerpo. Se registra el número de aciertos, perseveraciones e intrusiones. Evocación por reconocimiento. Se pide al sujeto que diga las palabras que se le presenten pertenecen o no a las que se le dieron anteriormente. Se registra el numero de aciertos, perseveraciones e intrusiones. 24 Memoria visuoespacial Copia de figura semicompleja. Se pide al sujeto que copie la figura que se presenta. Evocación de la figura semicompleja 24 Lenguaje Denominación. Se presentan ocho figuras correspondientes a animales, instrumentos musicales, partes del cuerpo y objetos y se le pide al sujeto que las nombre. Repetición. Se le pide al sujeto que repita las palabras y frases que se le presentan Comprensión. Se le presenta al sujeto una lámina en la que estan dibujados dos cuadrados (grande y pequeño) y dos círculos (grande y pequeño). Posteriormente se le pide que responda a las instrucciones que se le dan. Fluidez verbal semántica. Se pide al sujeto que mencione en un minuto todos los animales que conozca. Se registra el número de palabras correctas y se codifica en una escala de 0 a 4. También se anotan las intrusiones y perseveraciones. Lectura. Se pide en voz alta que lea en voz alta un párrafo y se le hacen tres preguntas. Escritura. Se pide al sujeto que escriba la oración que se le va a dictar y que copie otra oración. 31 Funciones ejecutivas Funciones conceptuales. Semejanzas. Se presentan tres pares de palabras y se pide al sujeto que diga en qué se parecen. Cálculo. Se presentan tres problemas aritméticos simples. Secuenciación. Se pide al sujeto que continué con la secuencia de figuras que se le presentan. Funciones motoras Cambio de posición de la mano. Se pide al sujeto que realice con la mano (primero derecha y luego izquierda) los movimientos que se le presentan Reacciones opuestas. Se pide al sujeto que siga las instrucciones: si el examinador le muestra el dedo, el sujeto debe mostrar el puño y viceversa. 18 Total 130 39 Panamerican Journal of Trauma RESULTADOS Del total de los pacientes revisados 18 cumplieron los criterios de inclusión. El 55% de los casos con edades entre 15 y 30 años. El 77% de estos pacientes llegaron al hospital víctimas de accidentes de tránsito. El 72% presentó TCE severo con Glasgow < 8. El hallazgo escanográfico más frecuente fueron las microhemorragias puntiformes presentes en todos los casos (tabla 2) (figuras 1, 2 y 3). Tabla 2. Características demográficas de 18 pacientes con TCE moderado – severo Edad Glasgow al ingreso Comorbilidades Trauma asociado Hallazgos escanográficos 15 - 30 10 (55%) 31 - 50 4 (22%) >50 4(22%) <8 13(72%) 9 - 13. 5(27%) Hipertensión 1(5%) Diabetes mellitus 1(5%) EPOC * Torax 5(27%) Abdomen * Facial 4(22%) Fracturas 4(22%) Raquimedular 1(5%) Normal - Microhemorragias 18(100%) Hemorragia subaracnoidea 9(50%) Hemorragia Intraventricular 2(11%) Lesiones focales no quirúrgicas 2(11%) Uso de vasoactivos ( TAM <90 ) 2(11%) Necesidad de transfusión ( Hto < 30) 2(11%) Hiperglicemia 2(11%) Complicaciones Glasgow al egreso Dias estancia en UCI Neumonía 2(11%) Infección urinaria 3(16%) Sepsis origen desconocido 2(11%) 15 - 14 4(22%) 9 - 13. 12(66%) 8 Prom. (5 – 14) De estos, 12 pacientes presentaron hemorragias corticosubcorticales (66%) (figura 1), 8 presentaron compromiso 40 cuerpo calloso (44%) y 4 compromiso de mesencéfalo (22%), de estos últimos murieron dos y los otros dos se presentaron a la consulta externa en estado vegetativo persistente. Los otros 14 pacientes fueron evaluados en la consulta externa, obtuvieron un GOS 3-4, ninguno tuvo GOS 5 (figura 2). De estos, se tomaron los 8 pacientes que tuvieron GOS 4 y fueron llevados a valoración neuropsicológica (figura 2). Ocho pacientes fueron a la entrevista neuropsicológica, se les realizó test abreviado NEUROPSI, y de estos, el 75% presentó puntajes inferiores al rango normal cuando se les evaluó atención, concentración y funciones ejecutivas. La mitad de ellos mostró alteraciones en la memoria verbal y visuoespacial (figura 4). G0S4 Corticosubcordical Cuerpo calloso G0S3 G0S1-2 Mesencefalo Figura 1. Relación entre hallazgos escanográficos y GOS. DISCUSIÓN Esta serie de pacientes fue sometida a la evaluación según los parámetros del test neuropsicológico abreviado NEUROPSI, una herramienta diseñada para pacientes de habla hispana que discrimina según el nivel educativo. Previo a esto se seleccionaron pacientes con buenos resultados según la escala de Glasgow y se excluyeron desde un principio pacientes con contusiones frontales para evitar la disyuntiva entre síndromes frontales y déficit por daño difuso. Los resultados son similares; se observa, que a pesar de ser personas funcionales e independientes presentan alteraciones en sus funciones ejecutivas lo cual se hace más evidente para las personas que los rodean que para los mismos pacientes. La mayoría de ellos (75%) no son capaces de resolver problemas aritméticos sencillos, y tienen gran dificultad para establecer semejanzas cuando se les pide decir en qué se parecen dos o tres objetos. Vol. 16 Number 1 2009 Secuelas neuropsicológicas en pacientes con trauma craneoencefálico asociado a lesión axonal difusa las veces regresar a sus actividades previas, lo cual se correlaciona con el hecho de que ninguno de la serie tuvo una recuperación completa GOS 5. 1. Muerte 2. Estado vegetativo 3. Incapacidad severa 4. Incapacidad moderada 5. Buena recuperación Figura 2. Escala de coma de Glasgow de resultados de 18 pacientes con TCE moderado - severo 3-6 meses postrauma, lesiones focales como daño axonal difuso. Corticosubcordicales Cuerpo calloso No se encontró asociación clara entre la ubicación de los microsangrados y el tipo de déficit que presentaron. La naturaleza y el sustrato neuroanatómico del déficit de atención son cuestiones aún no resueltas. Desde un abordaje neuropsicológico, diversos autores han tratado de esclarecer la causa principal por la que los pacientes con TCE muestran un rendimiento disminuido en diversos tests. Recientemente, se ha demostrado que la disminución del rendimiento en test neuropsicológicos podría estar explicada casi totalmente por un problema de lentitud en el procesamiento de información por daños en tractos o fibras del sistema nervioso difíciles de evaluar en tomografía o resonancia magnética convencional, más que en lesiones focales de cuerpo calloso o en zonas corticales específicas. CONCLUSIONES Mesencefalo Figura 3. Distribución de las microhemorragias en 18 pacientes con lesión axonal difusa. Orientación Atención y concentración Memoria verbal Memoria visoespacial Lenguaje Funciones ejecutivas Figura 4. Pacientes con alteraciones en la evaluación neuropsicológica NEUROPSI discriminado por áreas. Al realizar el seguimiento de estos pacientes que llegan a la unidad de trauma en los servicios de urgencias se percibe la importancia de evitar la injuria secundaria una vez que el manejo es expectante y no requieren manejo quirúrgico. En repetidas ocasiones, se observa con preocupación que estos pacientes que llegan con Glasgow muy bajo son puestos bajo el rótulo de pobre pronóstico. Sin embargo, en la consulta externa se observa que son pacientes con muy buena recuperación que requieren el apoyo de un equipo interdisciplinario para ellos y sus familias. Por otro lado, sabemos que la TAC no es un medio idóneo para hacer diagnóstico de lesión axonal difusa. Si bien realizar resonancia magnética en agudo no es viable en estos pacientes tan comprometidos, los cambios que se evidencian en proyecciones T2 y gradiente eco persisten por mucho tiempo y podrían correlacionar los hallazgos en resonancia con el déficit cognitivo lo cual proporcionaría un pronóstico más claro. Estudios recientes con tensor de difusión por resonancia magnética han permitido evaluar los tractos, los fascículos y dilucidar que la base del problema es probablemente la velocidad de procesamiento (7-16). BIBLIOGRAFIA De la misma manera, una observación repetida en la evaluación de estos pacientes es su dificultad para mencionar dígitos en regresión (20, 19, 18...) lo que refleja déficit en la atención y concentración para llevar a cabo una tarea. Estas alteraciones hacen que los pacientes, a pesar de ser independientes en sus funciones, no puedan la mayoría de 1. Kostas Paterakis, MD, Apostolos H. Karantanas, MD, PhD, Apostolos Komnos, MD. Outcome of Patients with Diffuse Axonal Injury: The Significance and Prognostic Value of MRI in the Acute Phase. J Trauma 2000; 49: 1071-1075. 41 Panamerican Journal of Trauma 2. Gary R. Turner, PhD, Brian Levine, PhD.Augmented neural activity during executive control processing following diffuse axonal injury. Neurology 2008; 71: 812-818. 3. T. Okamotoa, K. Hashimotob, S. Aokia et al. Cerebral blood flow in patients with diffuse axonal injury – examination of the easy Z-score imaging system utility. European Journal of Neurology 2007; 14: 540-547. 4. Mar Ariza González, Roser Pueyo Benito, et al. Secuelas neuropsicológicas de los traumatismos craneoencefálicos. Anales de Psicología 2004; 20: 303-316. 5. McAllister TW, Flashman LA, Sparling MB, et al. Working memory deficits after traumatic brain injury: catecholaminergic mechanisms and prospects for treatment- a review. Brain Inj 2004; 18: 331-350. 6. Wojciech Marks, MD, PhD, Bogna Brockhuis, MD, Dariusz Wieczorek, MD. Brain Perfusion Imaging (SPECT-Tc-99m HM-PAO) in Diagnosis of Diffuse Axonal Injury. Neurosurg Q 2006; 16: 89-91. 7. Kim L. Felmingham, Ian J. Baguley, Alisa M. Green. Effects of Diffuse Axonal Injury on Speed of Information Processing Following Severe Traumatic Brain Injury Neuropsychology 2004; 18: 564-571. 8. Philippe Azouvi. Neuroimaging correlates of cognitive and functional outcome after traumatic brain injury. Curr Opin Neurol 2000; 13: 665-669. 9. Luis Quintana Rojas, Arturo López, Yuria Solovieva, et al. Evaluación neuropsicológica de pacientes con diferentes 42 niveles educativos. Revista española de neuropsicología 2002; 197: 216. 10. Claus-W. Wallesh, Noreen Curio, Susanne Kutz, et al. Outcome after mild-to moderate blunt head injury: effects of focal lesions and diffuse axonal injury. Brain Injury 2001; 15: 401-412. 11. Maike Fork A; Claudius Bartels A; Anne D, et al. Neuropsychological sequelae of diffuse traumatic brain injury. Brain Injury 2005; 19: 101-108. 12. M Takaoka, H Tabuse, E Kumura, S Nakajima, et al. Semiquantitative analysis of corpus callosum injury using magnetic resonance imaging indicates clinical severity in patients with diffuse axonal injury. J Neurol Neurosurg Psychiatry 2002; 73: 289-293. 13. Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain injury: a brief overview. J Hea Trauma Rehabil 2006; 21: 375-8. 14. Jennett B, McMillan R. The epidemiology of head injury. Br Med J 1981; 282: 101-4. 15. Vazquez-Barquero A, Austin O, Pascual J, Gaite L, et al. The epidemiology of head injury in Cantabria. Eur J Epidem 1992; 8: 832-7. 16. Cappa SF, Benke T, Clarke S, Rossi B, et al. Guidelines on cognitive rehabilitation: report of an EFNS. European Journal of Neurology 2005; 12: 665-80. Vol. 16 Number 1 2009 Panamerican Journal of Trauma Vol. 16 No. 1 2009 Pages 43 - 46 BILATERAL TRAUMATIC CHYLOTHORACES WITH TENSION Tariq Fahmeed Siddiqui, MD,1 Kimball I. Maull MD, FACS.1 SUMMARY A patient with bilateral post-traumatic chylothorax is reported. The right chylothorax produced severe respiratory distress and was released under pressure with resolution of symptoms, confirming the diagnosis of tension chylothorax. The precise mechanism of injury in this case remains unclear. There was direct trauma to the lower back from a fall from height, resulting in posterior rib fractures and spinous process fractures. However, there was no indication of spinal instability or vertebral body fracture in contact with the thoracic duct. Acute hyperextension may have occurred at impact which raises the question of co-existing ductal dilatation. The return of the patient four days after injury is consistent with the time of presentation in most series. However, the profound respiratory distress is atypical and the diagnosis of post-traumatic tension chylothorax is rare. The value of dietary restriction with medium chain triglycerides proved an effective ancillary measure in maintaining nutrition while healing progressed. Chylothorax is the collection of chyle in the chest following disruption of the cisterna chyli or thoracic duct. Chylothorax, an uncommon clinical entity in it own right, is even more uncommon following external blunt force trauma. Herein the authors describe a patient with bilateral chylothoraces who presented in extreme respiratory distress from a right-sided tension chylothorax, requiring emergency chest decompression. RESUMEN Se reporta un paciente con quilotórax postraumático bilateral. El quilotórax derecho producía dificultad respiratoria severa, y se drenó con resolución de los síntomas, 1 Section of Trauma Surgery Department of Surgery Hamad General Hospital Doha, Qatar 43 confirmando así el diagnóstico de quilotórax a tensión. El mecanismo exacto de lesión de este caso no es claro. Hubo trauma directo en el tórax posterior bajo, por una caída que resultó en fracturas costales posteriores y fracturas de los procesos espinosos. Sin embargo, no había indicación de inestabilidad de la columna o fractura de cuerpos vertebrales en contacto con el ducto torácico. Pudo ocurrir hiperextensión aguda durante el impacto, con la posible coexistencia de una dilatación ductal. El regreso del paciente, cuatro días después de la lesión, es consistente con el tiempo de presentación de la mayoría de las series. Sin embargo, la dificultad respiratoria severa es atípica y el diagnóstico de quilotórax postraumático a tensión es raro. La restricción dietética con el uso de los triglicéridos de cadena media probó ser una medida auxiliar de valor para mantener la nutrición mientras progresaba la cicatrización. El quilotórax es la colección de quilo en el tórax por ruptura de la cisterna del quilo o del ducto torácico. El quilotórax es una entidad poco común, que es aún menos común después de un trauma externo. En este reporte, los autores presentan un paciente con quilotórax bilateral, quien presentaba dificultad respiratoria extrema debido al quilotórax a tensión del lado derecho, que requirió descompresión de urgencia. CASE HISTORY A 40 year old male laborer fell from three meters height and presented to the Emergency Department complaining of back pain. Examination showed lower dorsal abrasion and localized tenderness. Initial chest x-ay was normal. The patient was treated with analgesics and released. Four days later, the patient returned with severe dyspnea, tachypnea, tachycardia, and peripheral cyanosis. There was decreased air entry bilaterally, and absent breath sounds on the right side. Initial clinical impression was right-sided tension pneumothorax, but bedside ultrasound suggested fluid in the right hemithorax. Chest x-ray demonstrated total opacification of the right hemithorax with blunting of the costo-phrenic angle on the left side (Figure 1). Needle aspi- Panamerican Journal of Trauma ration done in the course of placing the tube thoracostomy yielded pink-tinged white fluid, suspicious for empyema. However, following placement of chest tube, 2500 ccs of similar fluid was recovered, initially under pressure (Figure 2). The patient’s respiratory distress subsided immediately, his oxygen saturation improved, and follow-up chest x-ray showed lung re-expansion on the right side with residual changes on the left. Abdominal and chest computed tomography (CT) was done which confirmed non-displaced posterior fractures of the 10th and 11th ribs on the left side and fracture of the spinous process of the 12th thoracic vertebra (Figure 3). Fluid was also present in the retroperitoneum extending to the right pararenal fossa. A left pleural effusion was noted and treated by left tube thoracostomy, returning 600 ccs of similar fluid. Fluid analysis showed protein content of 34 gram/liter, a pleural triglyceride to serum triglyceride ratio >11 and profuse leukocytes on gram stain (96% lymphocytes). He was kept on chest tube drainage, dietary intake restricted to medium-chain triglycerides, and studied by TC-99 lymphoscintigraphy and magnetic resonance imaging (MRI). The former was non-revealing but the MRI lymphography showed dilatation of the cisterna chyli and abdominal lymphatics with collapse of the thoracic duct, suggesting injury to the lower end of the thoracic duct (Figure 4). Daily chest drain output dropped rapidly (first post admission day left chest drainage = 190cc) but chest drains remained until output was nil and were removed on hospital day 10. He was discharged two days later on a regular diet and remained asymptomatic on follow-up. Figure 1. Repeat chest x-ray showing bilateral chylothoraces with total opacification of right chest. 44 Figure 2. Suction bottle displaying initial volume of right chest effluent. Figure 3. CT reconstruction showing posterior rib fractures and spinous process fracture of T-12. Vol. 16 Number 1 2009 Bilateral Traumatic Chylothoraces with Tension ascent in the left chest along the esophagus posterior to the aortic arch. It passes back over the subclavian artery in the superior mediastinum to enter the venous system between the internal jugular and subclavian veins, in total - a course of approximately 40 cms. However, in some patients, there may be bilateral venous entry sites in the neck or duplicated thoracic ducts, one on either side. The location of injury and the anatomic course of the thoracic duct determine on which side the chylothorax develops. Chylothorax following blunt vertebral trauma to the lower thorax should produce a right-sided chylothorax; penetrating trauma to the neck a left-sided chylothorax. However, these associations are not always constant. CLINICAL PRESENTATION Figure 4. MRI lymphography. DISCUSSION Etiology Chylothorax may be traumatic or non-traumatic. Of the non-traumatic causes, neoplasm is by far the most common (1). Chylothorax caused by trauma is most frequently related to operative trauma following esophageal or pulmonary surgery (2). Penetrating injuries to the neck or lower chest account for the majority of chylothorax from external trauma, leaving blunt external trauma as an uncommon causative mechanism. Associated vertebral fractures, usually involving the lower thoracic vertebrae, and/or hyperextension injuries have been implicated (3). Some authors suggest that the thoracic duct is more vulnerable to injury when distended after eating, which may explain reports of chylothorax appearing after relatively minor injuries or exercise (4). Although the thoracic duct is likely disrupted at the time of the traumatic incident, it is hypothesized that in some patients a “chyloma” forms at the point of injury, enlarges, and ultimately ruptures into the pleural space. This process may happen rapidly or may take several days to occur. A posterior mediastinal mass may be detected during this period of evolution. Chylothorax occurs most commonly on the right side but can occur bilaterally or only on the left side. Because there is wide variation in the anatomy of the thoracic duct, the side of chylothorax is not always predictable. The usual course of the thoracic duct begins at the cisterna chyli, passes through the aortic hiatus, ascends between the esophagus and azygos vein in the right chest to about the fifth thoracic vertebral level where it crosses the vertebral column, and continues its Patients with traumatic chylothorax usually become symptomatic 2-10 days following injury. Presenting signs and symptoms are typical of pleural effusion from any cause, including fatigue, reduced exercise tolerance and a heavy feeling in the chest. Because chyle is non-irritating and bacteriostatic, chest pain and fever are not commonly seen. Physical findings, including decreased breath sounds and a dull percussion note, suggest effusion. Plain chest radiographs verify intra-pleural fluid and lead to thoracentesis in most cases. Acute respiratory distress is unusual and indicates potential tension chylothorax (5, 6). DIAGNOSIS The diagnosis is suggested by the nature of the effluent, usually milky in character, and is confirmed by laboratory examination. Pleural fluid triglyceride/serum triglyceride ratio >1 substantiates the diagnosis. If the etiology remains unclear, the presence of chylomicrons clinches the diagnosis. CT is important in demonstrating the anatomy of the injury, and the site of thoracic ductal injury can be determined by lymphoscintigraphy or MRI in most instances (7). TREATMENT Treatment options are cited in Table 1. Non-operative management is successful in most cases, depending on etiology, but does involve some risk. The body produces from 1-2 liters of chyle per day. This fluid is nutrient rich and contains important elements of the immune system, including an overabundance of t-lymphocytes. Long term drainage of chyle in anticipation of eventual sealing of the injury places the patient at risk for nutritional depletion and 45 Panamerican Journal of Trauma infection. Therefore, early operation should be considered for patients with sustained chyle output > 500 cc/day. Patients undergoing definitive operation for chylothorax, either open or via video-assisted thoracoscopy, should receive a fat load per nasogastric tube at the commencement of the operation to aid in duct identification. Ligation, clipping and application of sealant have all been touted as effective. It is important to interrupt the duct both distal and proximal to the injury. Table 1. Treatment principles for post-traumatic chylothorax. Maintain nutrition Reduce chyle circulation Prevent re-accumulation of chyle Avoid long-term high volume chyle loss Early definitive operation for sustained chyle outputs > 500 cc/24 hours Pleuroperitoneal shunt Pleurodesis Thoracic duct embolization Ligation or clipping of thoracic duct Application of sealants 46 REFERENCES 1. Platis IE, Nwogu CE. Chylothorax. Thor Surg Clinics 2006; 16: 209-214. 2. Nair SK, Petko M, Hayward MP. Aetiology and management of chylothorax in adults. Europ J Cardiothor Surg 2007; 32: 362-369. 3. Dulchavsky S, Ledgerwood, AM, Lucas, CE. Management of chylothorax after blunt chest trauma. J Trauma 1988; 28: 1400-1401. 4. McCormick J, Henderson SO. Blunt trauma-induced bilateral chylothorax. Am J Emerg Med 1999; 17: 302-304. 5. Jenkins JL, Dillard F, Shesser R. Tension chylothorax caused by occult trauma. Am J Emerg Med 2004; 22: 321-323. 6. Ammori JB, Pickens A, Chang AC, and Orringer MB. Tension chylothorax. Ann Thor Surg 2006; 82: 729-730. 7. Porziella V, Cesario A, Margaritora S and Granone P. Role of pre-operative lymphangiogram and lymphangioscintigraphy in the surgical management of spontaneous chylothorax. Europ J Cardiothor Surg 2006; 30: 813-814. Vol. 16 Number 1 2009