Dexmedetomidine in Traumatic Brain Injury, Why Not?-Juniper Publishers
Juniper Publishers-Journal of Anesthesia
Editorial
Dexmedetomidine is an alpha-2 adrenoreceptor agonist
with sedative, analgesic and anxiolytic properties. Since its release in
the US market in late 1999, it has gained remarkable attention in the
adult, pediatric and geriatric populations, predominantly because of its
minimal respiratory depression. However, beyond its well-known
properties, dexmedetomidine has recently been investigated for its
potential in many other clinical scenarios, including neuroprotection,
cardioprotection and renoprotection, with promising results [1].
Traumatic brain injuries, intracranial hemorrhage,
intracranial malignancies, stroke, subarachnoid hemorrhage, and other
conditions can precipitate the development of Cerebral edema and
intracranial hypertension. Management options for intracranial
hypertension include elevating the head of bed, normoventilation,
eunatremia, pain control, reduction of noxious stimuli, and prevention
of fever, hypoxemia, and hypotension. Sedation and analgesia with
continuous infusions are considered first-line therapies to control
intracranial hypertension in comatose patients who are intubated. The
theoretical mechanism of continuous IV sedatives for ICP control is a
safe reduction in cerebral blood flow and hence blood volume by reducing
cerebral metabolic demand. Dexmedetomidine acts as a potent and
specific alpha-2 adrenergic receptor agonist; it is unique in providing
sedative-analgesic and anxiolytic effects without causing respiratory
depression [2].
It has been hypothesized that global and focal
cerebral ischemic events can be attenuated by the use of alpha-2
adrenoreceptor agonists. Catecholamine release is likely a factor
contributing to injury. Catecholamines can potentially exacerbate
neuronal injury by multiple mechanisms (catecholamines mediated
increases in sensitivity to neurotransmitters such as glutamate;
increased neuronal activity leading to expression of catabolic enzymes
and possibly cell death due to excessive excitation; direct toxic effect
of catecholamines on neurons; free radical formation) [3].
However, there is a significant and unresolved issue
with respect to the safety and suitability of dexmedetomidine for use in
patients who have or who are at risk for neurologic injuries. That
issue is the matter of the uncertainty as to the effect of
dexmedetomidine on the ratio of cerebral oxygen supply to cerebral
oxygen demand (the ratio of cerebral blood flow CBF to cerebral
metabolic rate CMR). The concern arises because the limited existing
body of information suggests that dexmedetomidine might result in a
reduction of the CBF/CMR ratio. The available information indicates that
dexmedetomidine causes a reduction of CBF in humans. The effect of
dexmedetomidine on CMR is less well documented [4].
Kendra J [5]
and his colleagues suggested that Dexmedetomidine may avoid increases
in the need for rescue therapy when used as an adjunctive treatment of
refractory intracranial hypertension without compromising hemodynamics.
He did his study on 23 patients undergo refractory intracranial
hypertension. The primary objective of this review was to determine the
change in quantified need for rescue therapy (hyperosmolar boluses and
extraventricular drain [EVD] drainages). He used a dose of infusion 0.2 -
0.7 mcg/ kg/hours [5].
Ji-shen LUO [6]
and his colleagues found that Dexmedetomidine could alleviate the
stress as result of moderate and severe traumatic brain injury, and its
anti-stress, and sedative effect was similar to those of propofol, but
it's necessary to monitor the blood pressure. He did his study on 90
patients. He used a dose of bolus 0.5 - 1 mcg/kg on 30 minutes then
infusion 0.2 - 0.6 mcg/kg/hours for 24 hrs [6].
Pajoumand M [7]
and his colleagues cautioned that Dexmedetomidine was found to be
associated with significantly more hypotension. He did his study on 198
patients. On the other hand, Hao J [8]
and his colleagues results coincide with The sedation efficacy of DEX
was superior to propofol in moderate and severe TBI, and was able to
control excessive stress response after TBI better, and with more effect
on blood pressure. He used the same protocol used by Ji-shen LUO [6].
Nakano T [9]
and his colleagues suggested that Hypertension following the
administration of high-dose dexmedetomidine is associated with cerebral
hypoperfusion and the exacerbation of ischemic brain injury, possibly
through alpha-2-induced cerebral vasoconstriction. He did his research
on rat model. However Manhe Zhang [10]
and his colleagues found that the mechanism by which dexmedetomidine
reduces TBI is related to inhibition of autophagy in the hippocampal
neurons of rats.
From all the above, I agreed with authors that
Dexmedetomidine have a leading effect on reducing stress related
secondary brain injury. However, Other beneficial effects in reducing
apoptosis, and CBF/CMR ratio have limited existing evidences.
Conclusion
In Conclusion, Dexmedetomidine has a promising role
in traumatic brain injury management, however hypotension must be
avoided. Therefore, larger studies are needed to identify the role of
Dexmedetomidine in traumatic brain injury and the effect on cerebral
metabolic rate
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