METHODS: Both patients had features of difficult airway, American Society of Anesthesiologists (ASA) physical status class III and central venous occlusive disease. The common approach, i.e., ultrasound-guided supraclavicular brachial plexus block was technically difficult with inherent risk of vascular puncture due to dilated venous collaterals at the supraclavicular area possibly compromising block quality. The risk of general anesthesia (GA) was significant as patients were morbidly obese with possible risk of obstructive sleep apnea postoperatively. As an alternative, we performed the ultrasound-guided costoclavicular approach infraclavicular brachial plexus block with 20 mL local anesthetic (LA) ropivacaine 0.5% delivered at the identified costoclavicular space using in-plane needling technique. Another 10 mL of LA was infiltrated along the subcutaneous fascia of the proximal medial aspect of arm.
RESULTS: Both surgeries of >2 hours' duration were successful, without the need of further local infiltration at surgical site or conversion to GA.
CONCLUSIONS: Ultrasound-guided costoclavicular approach can be an alternative way of providing effective analgesia and safe anesthesia for vascular access surgery of the upper limb.
OBJECTIVE: To study the neuroprotective effect of minocycline via different routes in adult Sprague Dawley rats with brachial plexus injury.
METHODS: The C7 nerve roots of the animals were avulsed via an anterior extravertebral approach. Traction force was used to transect the ventral motor nerve roots at the preganglionic level. Intraperitoneal and intrathecal minocycline (50 mg/kg for the first week and 25 mg/kg for the second week) were administered to promote motor healing. The spinal cord was harvested six weeks after the injury, and structural changes following the avulsion injury and pharmacological intervention were analysed.
RESULTS: Motor neuron death and microglial proliferation were observed after the administration of minocycline via two different routes (intraperitoneal and intrathecal) following traumatic avulsion injury of the ventral nerve root. The administration of intraperitoneal minocycline reduced the microglia count but increased the motor neuron count. Intrathecal minocycline also reduced the microglial count, with a greater reduction than in the intraperitoneal group, but it decreased the motor neuron count.
CONCLUSIONS: Intraperitoneal minocycline increased motor neuron survival by inhibiting microglial proliferation following traumatic avulsion injury of the nerve root. The inhibitory effect was augmented by the use of intrathecal minocycline, in which the targeted drug delivery method increased the bioavailability of the therapeutic agent. However, motor neuron survival was impaired at a higher concentration of minocycline via the intrathecal route due to the more efficient method of drug delivery. Microglial suppression via minocycline can have both beneficial and damaging effects, with a moderate dose being beneficial as regards motor neuron survival but a higher dose proving neurotoxic due to impairment of the glial response and Wallerian degeneration, which is a pre-requisite for regeneration.