Documentos de Académico
Documentos de Profesional
Documentos de Cultura
Caso Clinico 1 Neuropatologia Robbins 7a Ed. Ortiz C Juan C. 2018
Caso Clinico 1 Neuropatologia Robbins 7a Ed. Ortiz C Juan C. 2018
PROGRAMA: MEDICINA
PROFESOR: Dr. Juan Carlos Ortiz Carrillo MD MSc. Ciencias Básicas Médicas
Programa de Medicina
e-mail: neurosciencejoy.ut@gmail.com
Dirección: calle 42 barrio santa Helena parte alta. Teléfono: (57) 8-2771212 Ext. 9371. Ibagué-
Tolima-Colombia.
INSTRUCCIONES: El siguiente caso clínico es basado en el del CD del texto patología estructural y
funcional de Robbins-7ª edición en Inglés. El estudiante debe trabajarlo en casa como medio de
aprendizaje a medida que lee el texto guía y se complementará con artículos que enviará el
profesor al correo. La resolución del caso clínico se hará en clase de manera oral con la
participación de todos los estudiantes.
Caso 1:
A 29-year-old motocyclist skidded on an icy patch in the road and was thrown onto the pavement. Witnesses
reported that, following impact and a brief period of consciousness, the patient became disoriented and rapidly
lost consciousness. Emergency medical personnel stabilized the victim and transported him to a local hospital.
In the emergency room, the patient was found to have a fracture of the right lateral skull. Ophthalmological
examination revealed a dilated right pupil. An emergent CT scan revealed an accumulation of blood between
the brain and the skull (Image 1). While the patient was being prepared for emergency surgery, his breathing
became labored and gasping, and progressed to respiratory arrest. Resuscitative efforts were
unsuccessful.
Postmortem examination confirmed the presence of a skull fracture involving the squamous portion of the
right temporal bone. Approximately 100 mL of fresh blood was present between the dura mater and the skull
(Image 2). Additional changes included generalized brain edema, right uncal gyral herniation, hemorrhage in
the right medial occipital cortex, cerebellar tonsillar herniation, and flattening of the ventral brainstem.
These computerized tomographic images, taken in the emergency room, reveal evidence of a right lateral
skull fracture and associated hemorrhage in the epidural space.
Epidural hematomas, or accumulations of blood between the external surface of the dura mater and the inner
surface of the skull, are almost always traumatic in origin.
They typically follow a fracture of the lateral skull, associated with laceration of one or more branches of the
middle meningeal artery.
What are the three main types of hemorrhages/hematomas that occur between the brain and skull?
Which types are most often the result of trauma?
Why are lateral skull fractures so often associated with tears of the
This image is of the superior surface of the brain from a patient dying with an acute epidural hematoma.
The dura mater has been removed, and the epidural hematoma is no longer visible.
Marked distortion of the right lateral parieto-occipital area is evident, caused by mass effect of the epidural hematoma.
Acute hematomas of this type can cause a significant elevation in intracranial pressure in a relatively brief period of time,
often necessitating rapid surgical evacuation of the lesion.
This image demonstrates another form of traumatic intracranial hemorrhage, the acute subdural hematoma,
visible here through the dura mater as an area of purple discoloration overlying the left cerebral hemisphere.
As in the case of epidural hematomas, subdural hematomas may cause significant
mass effect, and often require surgical intervention.
What is the other type of hemorrhage that can develop between the surface of the brain and the skull?
5 - Brain, acute subdural hematoma – Gross, autopsy presentation
7 - Brain, right medial temporal (uncal) herniation – Gross, whole brain, ventral surface
This image illustrates the ventral surface of the brain following removal of the cerebellum and brainstem.
The arrow points to a prominent notch in the medial aspect of the right temporal lobe (uncus),
caused by compression of the medial temporal lobe against the free margin of the tentorium cerebelli.
Any expanding hemispheric lesion, e.g., hematomas, tumors, or edema, may cause medial temporal herniation.
This image illustrates another important herniation pattern often encountered in patients with increased intracranial pressure.
Cerebellar tonsillar herniation occurs when the brain is displaced caudally through the foramen magnum.
The notching evident in this example is caused by compression of the cerebellum against the margins of the foramen magnum.
How does its appearance differ from that of a primary brainstem hemorrhage?
This brain is from a 54-year-old woman with a history of alcohol abuse who died shortly after falling during
a withdrawal seizure. Prominent areas of hemorrhage are visible on the ventral surface of the brain,
particularly in the orbital frontal areas, over the inferior surface of the left temporal lobe and, to a lesser extent,
over the cerebellar hemispheres. The hemorrhage in this case is due to contusions, or bruises,
on the surface of the brain, caused by contact between the surface of the brain and the adjacent skull.
This image illustrates the morphology of a typical contusion on the cut surface of the brain.
Note the areas of hemorrhage, most conspicuous in the superficial gyral crests.
Hemorrhagic infarcts, discussed in Case 1, may be difficult to distinguish from contusions in some cases.
However, in contrast to the superficial distribution of the hemorrhage in classic contusions,
hemorrhagic infarcts show relative sparing of the gyral crests and tend to involve the depths of sulci to a greater degree.
REFERENCIAS:
Burns EK, Biggio EH. Neurophatology. In: Kumar V, Schneider NR, Hagler HK (editors). Phatologic Basis of
Disease-Interactive case study companion. 7th edition. Elsevier; 2004. Disponible en:
www.robbinspathology.com.