reserved for patients with brain stem herniation and current evidence, though
severely limited, supports that prophylactic severe hyperventilation to PaCO2
<30 mmHg should be avoided in the initial 48 hours after injury given the
reduction in CBF with resultant ischemia [8]. The clinical diagnosis of herniation
is often hallmarked by the development of nonreactive, dilated pupils and
Cushing’ s triad (abnormal respiration, hypertension, and bradycardia).
Studies have shown that noxious stimuli can increase ICP by increasing
sympathetic tone with resulting hypertension [24,25].^ Sedation and analgesia
should therefore be implemented when clinically possible and safely at the
discretion of the treating physician.^8 Adult studies have shown these
medications to assist in maintaining or decreasing ICP. These medications
must be used with caution as they can also exacerbate hypotension leading to
decreased CBF. In addition to sedation and analgesia, neuromuscular
blockade may be necessary. Importantly, these medications should be
reserved for the patient with increased ICP who are unresponsive to sedation
and analgesia. Overuse of these medications have been associated with
prolonged ICU stays and increased risk of nosocomial infections.
The usage of hyperosmolar treatments for the management of ICP has
been used since the 1960’s [26]. Current recommendations are to begin
therapy in patients with documented intracranial hypertension and/or impending
signs of herniation. Prophylactic use of these solutions is no longer
recommended. Mannitol usage has fallen out of favor due to several side
effects including the rebound effect of secondary cerebral ischemia, serum
marcin
(Marcin)
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