Ebony Hilton
CPP in TBI:
*Patients with severe TBI (GCS ≤8) &/or clinical symptoms suggesting
possible impending herniation from elevated ICP (unilateral or bilaterally
fixed and dilated pupil(s), decorticate or decerebrate posturing,
bradycardia, hypertension, and/or respiratory depression) should be
treated urgently, with head elevation, hyperventilation, and osmotic
therapy (mannitol 1 g/kg iv) concurrently with neuroimaging and other
assessments.
*The principle focus of critical care management for severe TBI is to limit
secondary brain injury. In general, treatment efforts are aimed at
intracranial pressure management and maintenance of cerebral perfusion
as well as optimizing oxygenation and blood pressure and managing
temperature, glucose, seizures, and other potential secondary brain
insults.
*Intracranial pressure — Elevated intracranial pressure (ICP) is associated
with increased mortality and worsened outcome
-Simple techniques should be instituted as soon as possible:
*Head of bed elevation to 30 degrees
*Optimization of venous drainage: keeping the neck in neutral
position, loosening neck braces if too tight
*Monitoring central venous pressure and avoiding excessive
hypervolemia
-Indications for ICP monitoring in TBI
*GCS score ≤8
*abnormal CT scan showing evidence of mass effect from lesions such
as hematomas, contusions, or swelling
-ICP monitoring in severe TBI patients with a normal CT scan may
be indicated if two of the following
features are present (age >40 years, motor posturing, SBP<90
mm Hg).
-A ventricular catheter connected to a strain gauge transducer is the most
accurate and cost-effective method of ICP monitoring and has the
therapeutic advantage of allowing for CSF drainage to treat rises in ICP .
-treatment for elevated ICP should be initiated when ICP rises above 20
mmHg
*Ventricular drainage is generally attempted first.
*CSF should be removed at a rate of approximately 1 to 2 mL/minute,
for two to three minutes at a time, with
intervals of two to three minutes in between
-until a satisfactory ICP has been achieved (ICP <20 mmHg) or
until CSF is no longer easily obtained.
*Slow removal can also be accomplished by passive gravitational
drainage through the ventriculostomy.
*If ICP remains elevated, other interventions include osmotic
therapy, hyperventilation, and sedation.
-Osmotic therapy — The intravascular injection of hyperosmolar
agents creates an osmolar gradient,
drawing water across the blood-brain barrier. This leads to a
decrease in interstitial volume and a
decrease in ICP.
*Mannitol is the agent used most consistently to achieve
ICP control in various settings and it has also
been shown to improve cerebral blood flow. Mannitol
is administered in boluses of 0.25 to 1 g/kg
every four to six hours as needed. Monitoring of serum
osmolality (maintained <320 mMol/L), fluid
balance, renal function, and electrolytes is required.
*Hypertonic saline is being used increasingly in this
setting, but with varying volumes and tonicity (3
to 23.4 percent) and either as a bolus or continuous infusion.
-Hyperventilation — PaCO2 decreases thereby leading to
cerebral vasoconstriction, which then results in
decreased cerebral blood volume and ICP.
*hyperventilation-induced vasoconstriction may also cause
secondary ischemia and may thereby
worsen outcomes.
*Hyperventilation can also increase extracellular lactate and
glutamate levels that may contribute to
secondary brain injury
*Mild to moderate hyperventilation can be considered at later
stages, but PaCO2 of less than 30 mmHg
should be avoided
-Sedation — may lower ICP by reducing metabolic demand.
*ameliorate ventilator asynchrony and blunt sympathetic
responses of hypertension and tachycardia.
*can cause hypotension and cerebral vasodilation that in turn
may aggravate cerebral hypoperfusion
and elevate ICP.
*Barbiturate coma has been used traditionally in this setting.
*In refractory cases, barbiturate coma, induced hypothermia,
and decompressive craniectomy may be
considered