Fracture of Proximal Femur Clinical Trial
Official title:
Evaluation Effect of Adding Dexmedetomidine to Bupivacaine for Paravertebral Block in Femoral Fractures
Fracture femur is a common that results in severe pain. Many methods of regional and peripheral analgesia have been described to treat such pain. In this study the investigators consider using paravertebral block to treat post-fracture pain. Additionally, they consider adding dexmedetomidine to the used local anesthetic solution to prolong the duration of this block and hence postoperative analgesia.
Fracture femur is a common injury which is associated with excruciating pain . This pain is
one of the most important causes of postoperative morbidity and mortality when it is
insufficiently treated pain. Pain induces neuroendocrine stress response causing problems
like as reduction in vital capacity, pneumonia, tachycardia, hypertension, myocardial
ischemia and even infarction. These problems can be prevented by successful management of
postoperative pain.
In patients with proximal femoral fracture, the use of paravertebral blockade produces
reliable level of analgesia without need for additional nursing skills or monitoring in the
postoperative period. Paravertebral blockade by injection local anesthetic solution alongside
the vertebral column produces ipsilateral analgesia.
Currently available local anesthetics as bupivacaine may not provide reliable periods of
analgesia resulting in block resolution before the period of worst postoperative pain. The
use of a large volume of local anesthetic is one of methods to overcome this problem that may
lengthen the duration of analgesia but at increased risk of local anesthetic toxicity. Adding
adjuvants is another potential alternative.
Dexmedetomidine, a selective α 2 agonist, has been used to prolong the duration of analgesia
of nerve blocks. Dexmedetomidine has also been reported to enhance central and peripheral
nerve blockade. Alpha adrenoceptors located at the nerve endings have a possible role in the
analgesic mechanisms by preventing norepinephrine release. The spinal mechanism is the
principle mechanism for the analgesic action of dexmedetomidine.
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