Pediatric emergency medicine trisk 0818 0818
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Brain injury occurs in two phases: primary and secondary. The primary injury
is the mechanical damage sustained at the time of trauma and can be caused by
direct impact of the brain against the internal calvarial structures, by bone or
foreign bodies projected into the brain, and by shear forces delivered to the white
matter tracts. Secondary brain injury is further neuronal damage sustained after
the traumatic event to cells not initially injured. This results from numerous
causes, including hypoxia, hypoperfusion, and metabolic derangements, and may
also result from sequelae of the primary injury (e.g., cerebral edema, expanding
intracranial mass) or be caused by extracranial injuries (e.g., hypotension from
excessive blood loss, hypoxia from pulmonary contusion). The clinician’s goal is
to identify and treat any complications of primary brain injury in order to limit
further neuronal damage by secondary brain injury.
One of the most common causes of secondary brain injury is cerebral ischemia
resulting from impaired perfusion. Cerebral perfusion pressure is the difference
between the mean arterial pressure of blood flowing to the brain and the ICP. In
the healthy child, blood flow to the brain is maintained at a constant rate over a
wide range of systemic blood pressures by means of autoregulatory changes in
the cerebrovascular resistance so that the brain does not suffer ischemia or
excessive blood flow during periods of relative hypotension or hypertension,
respectively. With severe injuries, this autoregulatory control may be lost and the
cerebral blood flow can become directly dependent on the cerebral perfusion
pressure; with low mean arterial pressure or increased ICP, there will be
inadequate blood flow and cerebral ischemia results. In addition to potential for
causing decreased cerebral perfusion, increased ICP, if left unchecked, can lead to
brain herniation and compression. This may be caused by a number of
posttraumatic conditions, including cerebral edema and expanding intracranial
mass.
Clinical symptoms of increased ICP or herniation include headache, vomiting,
irritability, lethargy, visual disturbance, gait abnormalities, and weakness. Signs
include depressed level of consciousness, abnormal vital signs (bradycardia,
hypertension, respiratory irregularity), cranial nerve palsies, hemiparesis, and
decerebrate posturing. The classic findings in transtentorial herniation are
headache, decreasing level of consciousness followed by ipsilateral pupillary
dilatation (cranial nerve III palsy), and contralateral hemiparesis or posturing. If
the process continues unchecked, dilatation of the opposite pupil, alteration in
respirations, and ultimately, bradycardia and arrest ensue (see Chapter 97
Neurologic Emergencies ).
DIFFERENTIAL DIAGNOSIS
