Transnasal Sphenopalatine Ganglion Block

Ever been stumped by the patient with a stubborn headache which nothing seems to be helping?  An intractable migraine or relentless post-LP headache? Consider performing an SPG block.

How it works

In migraines and cluster headaches, the SPG is involved in mediating parasympathetic outflow causing vasodilation of cranial vasculature. This vasodilation results in the activation of nociceptors in the meninges inflammatory mediators, resulting in classic migraine-type pain. An SPG block is theorized to mitigate headaches arising from this pathway.

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How it's done

Steps:

1.   Place patient on monitor. Although you are using below-toxic dose of local anesthetic, the nasal mucosa is highly vascularized. Have patient lie supine in the sniffing position.

2.   Cut off red cap from Qtip from used for swab culture; the Qtip is hollow. Using a blunt 18 gauge needle, draw up 1-2mL of bupivicaine without epithat is well below the toxic dose (ex: 2mL of 0.25% bupivicaine for 70 kg patient) into a syringe.

3.    Thread the blunt needle onto the Qtip.

4.    Dip the cotton end of the Qtip into 2% viscous lidocaine.

5.    While patient supine and in sniffing position, GENTLY insert the Qtip straight into one nare until resistance is met. GENTLY adjust the angle slightly superiorly. Do not push against resistance.

6.   Inject the bupivicaine through the Qtip.

7.   Remove the syringe along with the blunt needle while keeping the Qtip in place. Instruct patient to remain supine for 10-15 minutes.

8.   After 10-15 minutes, remove Qtip. If patient experiences hemifacial pain relief, offer to repeat the block via the other nare. 

*note there are other variations, please see links 

Note that procedure must be done with patient supine

Note that procedure must be done with patient supine

Side effects:

  • Bitter taste from the anesthetic

  • Nausea

  • Local trauma causing epistaxis

  • Light-headedness

  • Numbness in the posterior pharynx

Data

 No large trials available, but small studies and case reports are promising.

https://www.acepnow.com/article/migraine-care-why-and-how-to-block-the-sphenopalatine-ganglion-nerve/?singlepage=1

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Gastrointestinal Bleeding: The Next Frontier (for TXA)

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TXA has been shown to improve outcomes in cases of bleeding including postpartum hemorrhage (WOMAN trial), trauma (CRASH-2 trial), epistaxis, oral bleeding and even inhaled TXA for hemoptysis (shout out to Dr Bogach for a recent case of this).  It’s low rate of complications (remember its antifibrinolytic, NOT prothrombotic) makes it a great choice for controlling bleeding.  

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Given its success in controlling hemorrhage from these sources, there has been investigation into the use of TXA in other kinds of bleeding including ICH (TICH-2 trial showed promising but inconclusive results, needs to be streamlined) and TBI (CRASH-3 trial, ongoing). Gastrointestinal bleeding (GIB) is a 

A Cochrane review on the use of TXA I'm GiB was conducted in 2012, which showed no change in transfusion needs, surgery or bleeding.  Another systematic review was conducted in 2014 that showed a reduction in mortality but noted that several of the studies used had some design flaws.  Additionally, the number of subjects in the combined studies was below the number needed to reliably find a significant result. 

Currently, the Hemorrhage ALleviation with Transexamic acid - InTestinal system Trial or HALT-IT Trial in Great Britain (I would have gone with Patient Oriented Outcomes in GiB or Stop Hemorrhage In Intestinal Tract but it is what it is) is currently enrolling patients with a goal of 8000+ subjects by summer 2019.  Treatment arm will consist of 1g IV bolus dose and then 3g IV over 24hrs (compared with CRASH-2 which gave 1g IV bolus with another 1g IV over the next 8hrs) with the control receiving NS.  Currently, TXA is not included in current recommendations in the management of nonvariceal GIB. However, given its utility in other types of bleeding and it's low risk of complications, it could be considered in severe cases. 


Summary: No evidence to support TXA in GIB but hopefully there will be some data coming out within the next year. Consider it in cases that are refractory to standard of care. 

Would live to hear from anyone with experience with using TXA for GiBs. 

The TRs

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More pressure more problems

High Pressure Injection Injury Occurs when fluid is expelled at least 100 pounds per square inch.  The fluid punctures skin and can dissect up along facial plains, neurovascular bundles, and tendons.   This can easily cause compartment syndrome, deep infections, and debilitating fibrosis.  Extremity necrosis can develop within 12 hours.  Even with expeditious OR debridement and washout there is a 38% risk of amputation and with caustics or higher pressure the risk is up to 80%.  Those that keep their limb lose a great deal of functionality.

Demographic:

  • Young adult typically male injured non-dominant hand

  • Inexperienced operator of equipment

  • exposure material is paint, grease, water, oil, diesel, paint thinner,

Acute phase

  • onset within 4-6 hours

  • paresthesias, pain, swelling,

  • vascular compromise

  • compartment syndrome

  • injury site may have no skin perforation or small subtle pinhole

ED steps:

  1. Recognize this minuscule puncture site is a huge life changing problem

  2. Broad spectrum antibiotics

  3. Tetanus

  4. Hand consultation for OR wash out/debridement

  5. X-ray--> lead base paint is radio opaque but may appear like calcifications. Other paints will show sub-cutaneous emphysema. Grease will appear as a lucency.

  6. analgesia

  7. council patient of detriment to extremity function

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