Review of the Evaluation and Treatment of Vasovagal Reactions in Outpatient Procedures.

BACKGROUND: A vasovagal reaction is a commonly encountered event in outpatient procedures. There is a paucity of discussion on vasovagal reactions (VVRs) in the dermatologic surgery literature. However, recent investigations in the physiology, evaluation, and treatment of VVRs have been reported in other specialties. OBJECTIVE: A comprehensive review of the physiology, evaluation, treatment, and prevention of VVRs. MATERIALS AND METHODS: A search as performed using the PubMed/MEDLINE databases. Search terms included "vasovagal," "vasovagal reaction," "syncope," "reflex syncope," "neurocardiogenic syncope," and "fainting." RESULTS: Studies demonstrate greater understanding in the physiology of a vasovagal reaction. Although permanent sequelae are uncommon, it is important to respond in a prompt manner. A variety of treatment and prevention options are presented. CONCLUSION: Vasovagal reactions should be carefully evaluated. Additional studies may provide greater data in understanding and managing vasovagal reactions.

Finer Needles Reduce Pain Associated With Injection of Local Anesthetic Using a Minimal Insertion Injection Technique.

BACKGROUND: The injection of local anesthetic into the skin is often the only memorable event described by the patient after dermatologic procedures. OBJECTIVE: The authors compared the pain felt during injection of local anesthetic using a minimal needle insertion technique with a 30- or 33-gauge needle. MATERIALS AND METHODS: Three hundred eighteen patients with tumors on the head and neck were injected with lidocaine using a previously described technique with either a 30- or 33-gauge needle. After injection, patients were surveyed using the visual assessment scale for pain. RESULTS: Seventy-seven percent of patients felt no pain with injection on the face using a 33-gauge needle compared with 64% with a 30 gauge, whereas 94% of patients felt no pain on the scalp with a 33-gauge needle compared with 54% with a 30 gauge. Visual analog scale scores were also significantly decreased on the face and scalp using the smaller needle. There was no difference in pain between the 2 needles with injection on the neck. CONCLUSION: This study further validates the use of this technique for the injection of lidocaine and the preference of a 33 gauge over a 30-gauge needle for the initial injection on the face and scalp.

Clinical pearl: mastering the flexible scalpel blade with the banana practice model.

This article describes the various applications of the flexible scalpel blade (FSB), the utility of the banana as a convenient and exceptional training instrument, and the intricacies of mastering the technique for students of different training levels.

Large facial basal cell carcinoma treated with multimodal combination therapy.

Large basal cell carcinomas (BCCs) with mixed intratumoral histology can present treatment challenges. Although a single treatment modality may be appropriate for some portions of the tumor, it may prove to be inadequate or overly aggressive for others. We describe a patient with a large facial BCC who was referred to our clinic for Mohs micrographic surgery. Biopsies revealed both noduloinfiltrative and superficial patterns. To excise the tumor completely would have been disfiguring, and topical therapy alone would have been inadequate. A multimodal approach using Mohs micrographic surgery to excise the central nodular portion and topical imiquimod to treat the surrounding superficial portion resulted in an excellent clinical outcome. This approach, which minimizes morbidity by capitalizing on the benefits of various techniques, can be applied to any BCC demonstrating distinct nodular and superficial portions.

Molecular mechanisms of excitatory signaling upon chronic opioid agonist treatment.

Opioid receptor agonists mediate their analgesic effects by interacting with Gi/o protein-coupled opioid receptors. Acute treatment with opioid agonists is thought to mediate analgesia by hyperpolarization of presynatic neurons, leading to the inhibition of excitatory (pain) neurotransmitters release. After chronic treatment however, the opioid receptors gradually become less responsive to agonists, and increased drug doses become necessary to maintain the therapeutic effect (tolerance). Analgesic tolerance is the result of two, partially overlapping processes: a gradual loss of inhibitory opioid function is accompanied by an increase in excitatory signaling. Recent data indicate that chronic opioid agonist treatment simultaneously desensitizes the inhibitory-, and augments the stimulatory effects of the opioids. In the present paper we review the molecular mechanisms that may have a role in the augmentation of the excitatory signaling upon chronic opioid agonist treatment. We also briefly review our recent experimental data on the molecular mechanism of chronic opioid agonist-mediated functional sensitization of forskolin-stimulated cAMP formation, in a recombinant Chinese hamster ovary cell line stably expressing the human delta-opioid receptor (hDOR/CHO). To interpret the experimental data, we propose that chronic hDOR activaton leads to activation of multiple redundant signaling pathways that converge to activate the protein kinase, Raf-1. Raf-1 in turn phosphorylates and sensitizes the native adenylyl cyclase VI isoenzyme in hDOR/CHO cells, causing a rebound increase in forskolin-stimulated cAMP formation upon agonist withdrawal.

Converging protein kinase pathways mediate adenylyl cyclase superactivation upon chronic delta-opioid agonist treatment.

Adenylyl cyclase (AC) superactivation is thought to play an important role in opioid tolerance, dependence, and withdrawal. In the present study, we investigated the involvement of protein kinases in chronic delta-opioid agonist-mediated AC superactivation in Chinese hamster ovary (CHO) cells stably expressing the human delta-opioid receptor (hDOR/CHO). Maximal forskolin-stimulated cAMP formation in hDOR/CHO cells increased by 472 +/- 91, 399 +/- 2, and 433 +/- 73% after chronic treatment with the delta-opioid agonists (+)-4-[(alphaR)-alpha-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxy-benzyl]-N,N-diethyl benzamide (SNC 80), [d-Pen2,d-Pen5]-enkephalin, and deltorphin II, respectively. Concurrently, chronic SNC 80 (1 micro M, 4-h) treatment augmented 32P incorporation into a 200-kDa protein immunoreactive with the ACV/VI antibody by 300 +/- 60% in hDOR/CHO cell lysates. The calmodulin antagonist calmidazolium significantly attenuated chronic deltorphin II-mediated AC superactivation. Tyrosine kinase (genistein) and protein kinase C (chelerythrine) inhibitors individually had minimal effect on chronic delta-opioid agonist-mediated AC superactivation. Conversely, simultaneous treatment with both genistein and chelerythrine significantly attenuated AC superactivation. Because we showed previously that the Raf-1 inhibitor 3-(3,5-dibromo-4-hydroxybenzylidene-5-iodo-1,3-dihydro-indol-2-one (GW5074) attenuates AC superactivation, we hypothesize that parallel calmidazolium-, chelerythrine-, and genistein-sensitive pathways converge at Raf-1 to mediate AC superactivation by phosphorylating AC VI in hDOR/CHO cells.

Involvement of Raf-1 in chronic delta-opioid receptor agonist-mediated adenylyl cyclase superactivation.

Chronic delta-opioid receptor agonist treatment of Chinese hamster ovary (CHO) cells stably expressing the human delta-opioid receptor (hDOR/CHO) leads to increased cAMP formation after the removal of the agonist (adenylyl cyclase superactivation). We have previously found that at the same time, chronic delta-opioid receptor agonist treatment augments phosphorylation of the adenylyl cyclase VI isoenzyme. Since phosphorylation of adenylyl cyclase VI by Raf-1 protein kinase was recently shown, we tested the role of Raf-1 in adenylyl cyclase superactivation in hDOR/CHO cells. We found that pretreatment of the cells with the selective Raf-1 inhibitor GW5074 (3-(3,5-dibromo-4-hydroxybenzylidene-5-iodo-1,3-dihydro-indol-2-one) (10 microM, 30 min) attenuates chronic deltorphin II-mediated increase in forskolin-stimulated cAMP formation by 40% (n = 6, P < 0.05). Better understanding of the molecular mechanism of adenylyl cyclase superactivation should aid in the development of analgesics that act longer and have fewer side effects.