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Spinal epidural hematomas (SEHs) are rare but potentially devastating injuries and are the most common cause of neuraxial injury leading to litigation. Although the incidence of SEHs is low, it is likely underestimated. An emerging risk factor for SEHs is the use of anticoagulants, and knowledge of guidelines can help limit this risk. Prompt diagnosis is necessary to restrict neurological deterioration and improve chances for recovery, with magnetic resonance imaging (MRI) as the gold standard. Computerized tomography (CT) should be considered if MRI is not immediately available in order to avoid delaying diagnosis. Treatment of clinically significant SEHs typically involves decompressive laminectomy with evacuation of the hematoma. Outcomes are best in patients who undergo surgical decompression within 8 hours of the onset of symptoms, but full recovery is not guaranteed.

Spinal cord ischemia (SCI) after thoracic endovascular aortic repair (TEVAR) can cause permanent neurologic deficits and poor long-term survival. Targeted treatment of new SCI symptoms after TEVAR (rescue therapy [RT]) might improve/resolve neurologic symptoms but few data characterize the association of specific interventions with SCI outcomes. We evaluated the effectiveness of post-TEVAR RT at our tertiary aortic center.Our institutional TEVAR database was reviewed for SCI incidence and details of RT. This included cerebrospinal fluid drainage (CSFD), medical therapy, and optimization of spinal cord oxygen delivery. SCI outcomes were categorized at discharge as paralysis/paraparesis and temporary/permanent.Nine hundred forty-three TEVAR procedures were performed in 869 patients from 2011 to 2020. Post-TEVAR SCI occurred in 7.8% (n = 74) with permanent paraplegia in 1.5%. Older patient age, chronic obstructive pulmonary disease, and previous abdominal aortic surgery were predictive of SCI. Half (n = 37) of SCI episodes resulted in only temporary paralysis/paraparesis. Rescue postoperative cerebrospinal fluid drains were implanted in 3.7% (n = 35) of procedures and was predicted by higher American Society of Anesthesiologists class, lower serum hemoglobin level, elevated international normalized ratio, bilateral iliac artery occlusion, nonelective procedures, and penetrating atherosclerotic ulcer/intramural hematoma indication. The most commonly used RTs were emergent placement of or increased drainage from an existing cerebrospinal fluid drain (87.8%), induced/permissive hypertension (77.0%), corticosteroid bolus (36.5%), and naloxone infusion (33.8%). Neurologic improvement occurred in 68.9% (n = 51/74). New/increased drainage was associated with improved SCI outcome.Permanent paraplegia from post-TEVAR SCI is rare (1.5%). Older patients with comorbidities carry greater post-TEVAR SCI risk. SCI symptoms improved/resolved with CSFD and multimodal RT in 68.9% of patients, but no intervention was independently associated with improvement. TEVAR centers should have robust protocols for timely and safe CSFD placement to augment RT strategies for SCI.

Background and objectivesWe assume that intrafascicular spread of a solution can only occur if a large enough portion of the distal needle orifice is placed inside the fascicle. Our aim is to present and evaluate a mathematical model that can calculate the theoretical vulnerability of fascicles, analyzing the degree of occupancy of the needle orifice in fascicular tissue by performing simulations of multiple positions that a needle orifice can take inside a cross-sectional nerve area.MethodsWe superimposed microscopic images of two routinely used nerve block needles (22-gauge, 15° needle and 22-gauge, 30° needle) over the microscopic images of cross-sections of four nerve types photographed at the same magnification. Fascicular tissue that was overlapped between 80% and 100% by a needle orifice was considered at risk to possible intrafascicular injection. The effect of three angular approaches was evaluated.ResultsThere were statistical differences between the vulnerability of fascicular tissue depending on nerve type, the bevel angle of the needle and the angle approach. Fascicular vulnerability was greater in nerve roots of the brachial plexus after using a 22-gauge 30° needle, as was choosing a 45° angle approach to the longitudinal axis of the nerve.ConclusionsOur results suggest that clinicians may want to consider needle insertion angle and bevel type as they perform peripheral nerve blocks. Furthermore, researchers may want to consider this mathematical model when estimating vulnerabilities of various nerves, needle types and angles of approach of needles to nerves.

Placement of an epidural blood patch is the gold standard treatment for a postdural puncture headache when conservative measures have failed. If unsuccessful in relieving the symptoms, a second epidural blood patch may be warranted. However, when the accepted gold standard treatment has failed, alternative therapies may be pursued. A pterygopalatine ganglion block has been shown to be effective as an alternative to epidural blood patch placement. This case demonstrates the use of a suprazygomatic pterygopalatine ganglion block as a rescue technique for failed repeated epidural blood patch, with complete and permanent resolution of the headache.

To the Editor It was with great interest that we read the informative and groundbreaking report by Wahal et al .[1][1] in which they describe the pathway of hypertension following tourniquet application. This is an important paper, because the pathway and mechanism they describe is in principle

The mechanism of ipsilateral shoulder pain (ISP) after thoracic surgery remains unexplained definitively in the literature. Regional techniques targeting specific nerves more precisely will provide practitioners with a better understanding of the pain source. We report the case of a 51-year-old woman who underwent robotic-assisted plication of the right hemidiaphragm. ISP was adequately managed using a low-volume infusion through a continuous phrenic nerve block in addition to a thoracic epidural for her chest pain. ISP after thoracic surgery likely originates from diaphragm manipulation. Phrenic nerve blockade is a successful strategy that does not worsen subjective dyspnea in this setting.

Somatic and visceral nociceptive signals travel via different pathways to reach the spinal cord. Additionally, signals regulating visceral blood flow and gastrointestinal tract (GIT) motility travel via efferent sympathetic nerves. To offer optimal pain relief and increase GIT motility and blood flow, we should interfere with all these pathways. These include the afferent nerves that travel with the sympathetic trunks, the somatic fibers that innervate the abdominal wall and part of the parietal peritoneum, and the sympathetic efferent fibers. All somatic and visceral afferent neural and sympathetic efferent pathways are effectively blocked by appropriately placed segmental thoracic epidural blocks (TEBs), whereas well-placed truncal fascial plane blocks evidently do not consistently block the afferent visceral neural pathways nor the sympathetic efferent nerves. It is generally accepted that it would be beneficial to counter the effects of the stress response on the GIT, therefore most enhanced recovery after surgery protocols involve TEB. The TEB failure rate, however, can be high, enticing practitioners to resort to truncal fascial plane blocks. In this educational article, we discuss the differences between visceral and somatic pain, their management and the clinical implications of these differences.

Background and aims Intrafascicular injection of a local anesthetic, its toxicity, and direct needle trauma to nerve tissue are generally considered the primary reasons for nerve injury after intraneural injection. We hypothesize that the only way that the local anesthetic can enter the fascicle is if at least 80% of the distal needle orifice is inside the fascicle. the aim of this study was to calculate the theoretical vulnerability of nerve fascicles given their actual sizes and that of different needle openings. Methods We superimposed microscopic images of two routinely used nerve block needles (a 22-G, 15 ‘StimuplexOD’ needleand a 22-G, 30 ‘StimuplexOUltra 360O’ needle) over microscopic images of four nerve types taken at the same magnification. We calculated the chances of distal needle orifice overlap of the fascicles and assigned 80%, 90%, and 99% overlap as significant for fascicle vulnerability to intrafascicular injection. We assigned a color for the amount of overlap (vulnerability) to demonstrate this graphically. Results Figures 1 and 2 demonstrate the overlap vulnerability. table 1 summarizes the sizes of the fascicles and the chances of overlap of the needles and the fascicles. None of the fascicles accommodated 99% of the distal needle orifices. Conclusions The analysis of partial to full occupation of the distal needle orifices inside the nerve fascicles allowed us to document and visually demonstrate how the different microanatomic architecture of each nerve type affects its vulnerability to intrafascicular injection.

There may be a direct relationship between size of the dural puncture hole and resulting cerebrospinal fluid (CSF) leak and between external diameter of needle and incidence of PDPH. a larger size dura-arachnoid puncture produces more CSF leakage so that incidence of hypotension and postdural puncture headache (PDPH) is probably higher. Our findings oppose the classical notion that dura mater1 composed of longitudinal fibers running parallel to each other and oriented in the same axis as the spinal cord. the concept is that several needle tips allow separation rather than cutting of dural fibers and a smaller dural lesions. We, under transmission and scanning electron microscopy, studied the human spinal dura mater, arachnoid layer and the lesion caused by 25G and 27G Whitacre needles and 22G, 25G, and 29G Quincke needles with the bevel oriented vertically and horizontally in relation to the spinal axis, performing standard punctures on the fresh cadavers.2–9 The results of dural and arachnoid lesions are shown in table 1. the lesion in the arachnoid layer was found partially open in some instances, while in others the edges were better approximated and appear almost closed. In samples with the arachnoid lesion partially open, we would often observe through the opening of the arachnoid layer, the dural laminae to be partially or fully closed. the lesions always consisted of a dural structural lesion underpinning the arachnoid lesion. In this context, ‘closed’ applies to lesion edge approximation rather than physical sealing of the hole flaps. Quincke spinal needles caused a precise and controlled cut, while Pencil (Whitacre) point tips caused greater tearing of tissue margins and folding at the edges of the lesion. the edges of dural and arachnoid lesions caused by pencil point needles were ragged and irregular. There were no significant differences between parallel and perpendicular bevel approach using the same needle type. For the arachnoid injury, which may contribute primarily to PDPH, pencil-point needle injury wounds are ‘avulsion’ lesions not ‘splitting’ lesions. The etiology and pathogenesis of PDPH cannot be solely explained by the type and size of needle used, the effect of cerebral vasodilatation also should be considered.10 References Franksson C, Gordh T. Headache after spinal anesthesia and a technique for lessoning its frequency. Acta Chirurgica Scand 1946;94:443–445. Reina MA, Lopez A, Dittmann M, De Andres JA. Structural analysis of the thickness of human dura mater with scanning electron microscopy. Rev Esp Anestesiol Reanim 1996;43:135–137. Reina MA, Lopez A, Dittmann M, De Andres JA. Analysis of the external and internal surface of human dura mater with scanning electron microscopy. Rev Esp Anestesiol Reanim 1996;43:130–134. Reina MA, Dittmann M, Lopez A, van Zundert A. New perspectives in the microscopic structure of human dura mater in the dorso lumbar region. Reg Anesth 1997;22:161–166. Reina MA, Prats-Galino A, Sola RG, Puigdellivol-Sanchez A, Arriazu Navarro R, De Andres JA. Structure of the arachnoid layer of the human spinal meninges: a barrier that regulates dural sac permeability. Rev Esp Anestesiol Reanim 2010;57:486–492. Reina MA, Lopez A, Dittmann M, De Andres JA. Ultrastructure of spinal dura mater. In: Reina MA, Ed. Atlas of Functional Anatomy of Regional Anesthesia and Pain Medicine. New York: Springer; 2015, pp.411–434. Reina MA, Pulido P, Garcia De Sola R. Ultrastructure of spinal arachnoid layer. In: Reina MA, Ed. Atlas of Functional Anatomy of Regional Anesthesia and Pain Medicine. New York: Springer; 2015, pp. 435–454. Reina MA, De Leon Casasola OA, Lopez A, De Andres JA, Martin S, Mora M. An in vitro study of dural lesions produced by 25 Gauge Quincke and Whitacre needles evaluated by scanning electron microscopy. Reg Anesth Pain Med. 2000;25:393–402. Reina MA, Lopez A, Badorrey V, De Andres JA, Martin S. Dura-arachnoids lesions produced by 22G Quincke spinal needles during a lumbar puncture. J Neurol Neurosurg Psychiatry 2004;75:893–897. https://player.vimeo.com/external/292039987.hd.mp4?s=6363d2ea7cc617dd69a7589123a25003814d2e8a&profile_id=175 revised May 19, 2019.

It has generally been accepted that intrafascicular spread of local anesthetic solution is the major cause of severe and devastating neurological complications after intraneural local anesthetic injection.1 Furthermore, the validity of the human extrapolation of animal experiment conclusions has been recently disputed.2 After performing deliberate intraneural injections using StimuPlex D, 22-guage (15° bevel) needles with a new marker (heparinized erythrocytes)3 under ultrasound guidance mimicking clinical practice, and creating the worst possible conditions for regional block, we microscopically analyzed the longitudinal and circumferential spread in the extrafascicular and intrafascicular compartments in human sciatic and median nerves. This was also done in sciatic nerves of dogs, pigs and sheep. Swelling of the nerves confirmed intraneural injection. Extrafascicular spread was seen in all human and animal samples outside the perineurium, intermingled between the interfascicular adipocytes except in extrafascicular compartments where adipocytes were absent. Intrafascicular spread was absent in almost all samples. the marker was also observed filling the entire thickness of perineurium between the perineurium cellular layers. Erythrocytes were not found inside the endoneurium of most of the fascicles examined. Intrafascicular intraneural injection has been entertained as possible option in a few cases, but we were surprises to find no evidence of intrafascicular spreading in the vast majority of fascicles. the compact endoneural structure and the absence of endoneural spaces4–5 probably explain our findings and may help to understand the relatively low number of neurological complications caused by peripheral regional anesthesia considering the high number of blocks that are performed and the high number of intraneural injections that may be done intentionally or unintentionally. References Brull R, Hadzic A, Reina MA, Barrington MJ: Pathophysiology and etiology of nerve injury following peripheral nerve blockade. Reg Anesth Pain Med 2015;40:479–90. Server A, Reina MA, Boezaart AP, Prats-Galino A, Esteves Coelho M, Sala-Blanch X. Microanatomical nerve architecture of six mammalian species: Is trans-species translational anatomic extrapolation valid?Reg Anesth Pain Med 2018;43:496–501. Reina MA, Boezaart AP, Sala-Blanch X, Monzo E, Tubbs S, Server A, Bigeleisen P. A novel marker for studying nerves. Clin Anat 2018; In Press. doi:10.1002/ca.23253 Reina MA, Maches F, De Diego-Isasa P, Del Olmo C. Ultrastructure of endoneurium, Atlas of Functional Anatomy of Regional Anesthesia and Pain Medicine. Edited by Reina MA. New York, Springer, 2015, pp 37–58. Reina MA, Sala Blanch X, Arriazu R, Maches F. Microscopic morphology and ultrastructure of human peripheral nerves, Nerves and Nerve Injuries, Vol. 1: History, Embryology, Anatomy, Imaging, and Diagnostics. Edited by Tubbs RS, Rizk E, Shoja M, Loukas M. Cambridge, MA, Elsevier, 2015, pp. 91–106.

The epineurium has been accepted as the outer anatomical barrier of the peripheral nerves. Our objective was to characterize the microanatomy of the layers surrounding nerves using different tissue-specific staining methods. Two hundred forty-two cross sections of human sciatic and median nerves, and brachial plexuses of eight fresh unembalmed cadavers, were examined. The samples were fixed in formaldehyde solution and stained with hematoxylin-eosin, Masson's trichrome, or epithelial membrane antigen under standard conditions. Because epithelial membrane antigen only stains the perineurium, we demonstrated using hematoxylin-eosin and Masson's trichrome that there were different collagen layers inside and outside the nerves. All fascicles had a collagen layer that surrounded the perineurium and were in close contact with it, with no adipose tissue between them. Unlike the perineurium, this layer, an "internal epineurium," contained no cells, and it surrounded one or a small group of fascicles. Bundling these fascicles or small groups of fascicles together was the true epineurium, and between the true and internal epineurium, we consistently found an adipose-containing compartment. More proximal to this, the tibial and common peroneal nerves were bundled together by another collagen layer, the circumneurium, which also had a fat-cell-containing compartment deep to it. There were scattered collagen fibers among the adipocytes. Using tissue-specific staining, we were able to demonstrate a collagen layer, the "internal epineurium." Outside the nerves, we identified several fat-containing concentric compartments. Those compartments were limited by collagen fiber layers that were also similar to the epineurium. Clin. Anat. 33:199-206, 2020. © 2019 Wiley Periodicals, Inc.

Acute pain medicine services influence many different aspects of postoperative recovery and function. Here, we discuss the various stakeholders of an acute pain medicine service, review the direct and indirect impact on said stakeholders, review the shared and competing interests between acute pain medicine programs and various payer systems, and discuss how APM services can help service lines align with the interests of the recent CMS Innovations Comprehensive Care for Joint Replacement Model.

To the Editor, Transmission and scanning electron microscopy have allowed the detailed study of the structure of human peripheral nerves, the non-neural connective tissue layers forming it, and other structures inside the nerve.[1][1] The minimum anatomical structure of a nerve is traditionally

To the editor, Since gastric ultrasound was introduced into point-of-care testing in the past decade, it has been helpful in evaluating patients’ gastric content and helping anesthesiologists to determine a safe anesthetic management plan. Fasting guidelines have been around for over 100 years.[1

The onset, spread, density, and duration of a nerve block are functions of what local anesthetic drug is injected, where it is injected, and for how long the nerve is exposed to it. Over the past 27 or more years, as far back as 1988 [1], researchers and companies, initially with topical tetracaine [1], and later as injectable liposomal bupivacaine [2], have been searching for the “magic bullet” to be injected somewhere near a nerve, or infiltrated into tissue, that will eliminate a patient's acute or perioperative pain for as long as the pain lasts without unwanted side effects. The work of the Williams and colleagues, reported in this edition of Pain Medicine , is a further report on such efforts [3–5]. Although we have no or very little evidence of this, which points to a bigger problem eluded upon below, we instinctively know that most pain, especially surgical pain, outlasts our single-injection blocks, and we also know that we have to offer patients nerve blocks that last at least as long as the pain does without causing discomfort and unwanted side effects. Over the years, the challenge of developing a blocking drug that lasts long enough to outlast pain but that does not have similarly long-lasting unwanted side effects has been addressed by combining different drugs and developing new presentations of drugs. Few adjuvant agents, other than perhaps dexamethasone, have stood the test of time [6]. Another attempt was to add epinephrine to the existing arsenal of drugs [7] to cause vasoconstriction and decreased blood flow, thus slowing down the washout of the drugs and increasing the time that the nerve is exposed to the local anesthetic agent. We now know, that epinephrine does not increase the duration of action of bupivacaine or ropivacaine …