panamerican journal of trauma - Sociedad Panamericana de Trauma

Transcription

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: ramirezj@upmc.edu 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
ricardoferrada@yahoo.com
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.
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.
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.
Orthopedic Trauma:
BRUCE BROWNER, M.D.
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
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
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
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).
In conclusion, a trauma registry appropriate to under
resourced environments was successfully developed and
implemented in Colombia. The immediate future of this
project includes analysis of the obtained data, as well as
comparing the RTS and KTS scoring systems (50-55).
Longer term goals include using the information obtained
to develop programs to decrease the level of injury and
death in Colombia, as well as further project expansion. It
is our hope that this article and registry template will serve
to encourage others to continue implementing trauma registries in developing countries.
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9
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
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
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
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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
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Guidelines. Determination of Cervical Spine Stability in
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2006).
Duane TM, Dechert T, Wolfe, LG, Aboutanos MB, Malhotra
AK, Ivatury RR. Clinical examination and its reliability in
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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.
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Griffen MM, Frykberg ER, Kerwin AJ, et al. Radiographic
clearance of blunt cervical spine injury: plain radiograph or
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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.
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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;
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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.
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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
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
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.
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
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
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).
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
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
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.
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Am J Surg 2000; 180: 528-33.
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Asensio JA, et al. Vascular trauma: Complex and Challenging
Injuries. Surg Clin North Am. December 2001.
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Feliciano DV. Management of traumatic retroperitoneal
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Scalea TM, Bochicchio KM, Lumpkins K, Hess JR, Dutton
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Zink KA, Sambasivan CN, Holcomb JB, Chisholm G,
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Santucci RA, Wessels H, Bartsch G, et al. Evaluation and
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A Systematic Review. J Trauma 2005; 59: 491-501.
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Broghammer JA, Fisher MB, Santucci RA. Conservative
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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-
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
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
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
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
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.
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.
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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.
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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):
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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
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503-516.
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Neuropsiquiatr 2001; 59(4): 895-900.
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first link in chain of survival. Mt Sinai J Med 2009; 76(2):
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29. Rangel-Castilla L, Gasco J, Nauta HJ, Okonkwo DO,
Robertson CS. Cerebral pressure autoregulation in traumatic
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22. Levy DI, Rekate HL, Cherny WB. Controlled lumbar drainage
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32
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-
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
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.
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dnpa/obesity/trend/maps/index.htm (Accessed June 10,
2005).
35
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.
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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
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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
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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.
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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:
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21. Bochicchio GV, Joshi M, Bochicchio K, Nehman S, Tracy
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533-538.
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
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.
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
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.
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
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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.
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Gary R. Turner, PhD, Brian Levine, PhD.Augmented neural
activity during executive control processing following diffuse axonal injury. Neurology 2008; 71: 812-818.
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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.
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Mar Ariza González, Roser Pueyo Benito, et al. Secuelas
neuropsicológicas de los traumatismos craneoencefálicos.
Anales de Psicología 2004; 20: 303-316.
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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.
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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
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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.
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Philippe Azouvi. Neuroimaging correlates of cognitive and
functional outcome after traumatic brain injury. Curr Opin
Neurol 2000; 13: 665-669.
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Luis Quintana Rojas, Arturo López, Yuria Solovieva, et al.
Evaluación neuropsicológica de pacientes con diferentes
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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.
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-
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.
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
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.

panamerican journal of trauma - Sociedad Panamericana de Trauma

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