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CHAPTER 118: Head Injury 1133

is a commonly used analgesic agent and has a shorter half-life and of herniation. Increases in the respiratory minute volume mediated
less GI side effects (ileus) than morphine. Bolus doses of fentanyl have by increases in tidal volume and/or respiratory rate result in alveolar
been reported to mildly elevate ICP ; however, continuous infusions hyperventilation that decreases the Pa CO 2 causing cerebral vasoconstric-
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of fentanyl and sufentanil may minimize ICP elevations. There is tion, reduced CBF, decreased cerebral blood volume, and decreased
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a lack of studies on the effect of continuous fentanyl or sufentanil ICP. The degree of hyperventilation found within 20 minutes of
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on hemodynamics and ICP, but the changes appear to be minimal. hospital admission in severe TBI patients requiring intubation may
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Remifentanil is an analgesic narcotic with a very short half-life that correlate with survival with 15% in-hospital mortality in normocar-
may facilitate frequent awakening to allow neurological examination. bic (Pa CO 2 35-45 mm Hg) patients versus 77% mortality in hypocarbic
However, in patients with severe TBI, high doses of remifentanil (up to (Pa CO 2 <35 mm Hg) patients reported in a retrospective review. Of
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1.0 mg/kg/min) may be insufficient to lower ICP, and as for most seda- note, the mortality rate for hypercarbic (Pa CO 2 >45 mm Hg) patients was
tives or analgesics, high does lead to more hypotension and the need for also increased (61%). The factors influencing admission Pa CO 2 after TBI
increased vasopressors to maintain cerebral perfusion pressure. The may be related to prehospital treatment or the severity of both neuro-
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effect of any sedative-analgesic agents on the ICP should be determined logical and systemic injuries.
on an individual basis. A small randomized study comparing normal ventilation, hyperven-
Propofol, a sedative-hypnotic anesthetic agent, has the benefits of a tilation, and hyperventilation with tromethamine (THAM) to maintain
short half-life and rapid onset of action and is regularly used in neuro- hyperventilation-induced reduction in CSF acidosis found significantly
critically ill patients, but when administered for prolonged periods (eg, poorer GOS at 3 and 6 months in the prophylactic hyperventilation
>3 days), in obese patients and at high doses, the half-life is significantly without THAM group; however, this difference was not present at
prolonged. Like barbiturates, propofol reduces the cerebral metabolic rate 12 months. Independent of the level of hyperventilation, CBF is often
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and lowers oxygen consumption. While propofol may blunt rises in ICP, markedly reduced after severe TBI with a mean CBF of 27 mL/100 g/min
several studies suggest that the ICP only decreases slightly (eg, 2.1 mm Hg) early after TBI and <18 mL/100 g/min in 31.4% of patients. In this
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after several hours of dosing. 146,149,150 Propofol exerts an overall stabiliz- setting, hyperventilation may further decrease CBF contributing to the
ing effect on control of breathing. Propofol when used for prolonged likelihood of ischemia, particularly if cerebral injury is diffuse. After
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periods or in high doses (>5 mg/kg/h) may rarely lead to propofol TBI, the responsiveness of the cerebral vasculature to hypocarbia is vari-
infusion syndrome (PRIS); this should be considered in any patient on able and may be absent, normal, or in areas adjacent to areas of injury
propofol with unexplained acute renal failure, metabolic acidosis, rhab- such as contusions and subdural hematomas or in patients with severe
domyolysis, hyperkalemia, or myocardial failure. It can be lethal and diffuse injuries, hyperactive resulting in worsening of ischemia to com-
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may be associated with the concomitant use of vasopressors. 153 promised areas of injury. 126,161,162
Dexmedetomidine is a selective central α -agonist that provides Studies relating the effects of hyperventilation on cerebral oxygen-
2
anxiolysis and reduces agitation while allowing the patient to remain ation via Sj O 2 and Pbt O 2 monitoring are inconclusive, 163-165 and this is
arousable, allowing for serial neurological testing without respiratory partly due to the technical limitations of both Sj O 2 and Pbt O 2 monitoring.
depression. It decreases central nervous system (CNS) sympathetic Therefore, extreme, prolonged, or prophylactic hyperventilation may be
outflow in a dose-dependent manner and has opioid-sparing analgesic deleterious after TBI and level II evidence indicates that prophylactic
effects. The main side effects of dexmedetomidine are sinus bradycardia hyperventilation to Pa CO 2 ≤25 mm Hg may be harmful. Hyperventilation
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and hypotension. It may reduce ICP and increase cerebral perfusion is indicated as part of emergency measures to temporarily avert
pressure, but neurocritically ill (including TBI) patients may need herniation before definite treatment can be delivered; however, in
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higher doses of dexmedetomidine to achieve adequate sedation. 155 general hyperventilation should be avoided after TBI, particularly
Intermittent boluses of haloperidol may also be added to other during the first 24 hours after injury to limit the risk iatrogenic cerebral
sedative agents in severely agitated patients, or be used as a primary ischemia.
agent when the goal is to taper off continuous intravenous sedatives.
Haloperidol may lower the seizure threshold but does not suppress ■ HYPEROSMOLAR THERAPY
respiration. Although dexmedetomidine is used to control agitation and
also does not suppress respiration, it may not provide adequate control Mannitol or hypertonic saline are the two hyperosmolar agents used to
of agitation, or it may be desirable to taper off continuous IV drips and reduce intracranial pressure. They depend on creating an osmotic gradi-
haloperidol may be helpful in these situations as well. Chronic antipsy- ent across the blood brain barrier (BBB) that results in the movement
chotic usage has been noted to impede cognitive recovery after TBI in of water from brain tissue, decreasing brain volume and reducing the
animals, so they should be used with caution. 156 ICP. Relatively normal brain with an intact BBB is required for hyperos-
If sedation is inadequate, paralytic agents can be added in cases molar therapy to be effective. Hyperosmolar agents are beneficial in the
refractory of IH to help reduce ICP. However, the early, routine, and short term when used emergently in patients with signs of transtento-
long-term use of neuromuscular blocking agents may increase ICU stay rial herniation or potential herniation with progressive neurological
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and lead to increased neuromuscular complications. 106 deterioration not of an extracranial etiology, while interventions such
as imaging, ventriculostomy placement, or surgical decompression and
■ CSF DRAINAGE evacuation of hematomas are undertaken. Hyperosmolar agents are
Placement of an EVD allows both ICP monitoring and CSF drainage. also used on a more prolonged basis for the reduction of elevated ICP;
however, there is a lack of studies on the efficacy of repeated, regular
The advantage of CSF drainage is that it can effectively lower the ICP administration over several days. 166
while preserving or improving CPP and CBF. CSF is drained intermit-
tently or continuously to maintain ICP generally <20 mm Hg. Other Mannitol: Mannitol is effective in reducing ICP in the management of
therapies used to control ICP such as hyperosmolar agents, high-dose traumatic IH. In addition to the osmotic effect on ICP reduction with
sedatives (barbiturates), or hyperventilation bear the risk of further increased CBF, other reported mechanisms by which mannitol may
reducing cerebral perfusion by lowering MAP (CPP) or by causing cere- exert beneficial effects include reduction of free radical formation,
bral vasoconstriction (hyperventilation). plasma volume expansion, reduced blood viscosity, increased red blood
■ HYPERVENTILATION cell deformability, and increased cerebral oxygen delivery. 166
The dose of mannitol is 0.25 g/kg to 1 g/kg body weight given as bolus
Hyperventilation is a normal physiological response to traumatic doses as needed. The onset of the osmotic effect of mannitol is about
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injury, including TBI, and may be beneficial (level III evidence) when 15 to 30 minutes after bolus administration and the effects persist for
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induced emergently to lower the ICP in a patient with impending signs a variable time period of 1.5 hours to up to 6 hours or more. Bolus
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