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BACKGROUND AND OBJECTIVES: Thoracic paravertebral blockade is often used as an anesthetic and/or analgesic technique for breast surgery. With ultrasound guidance, the rate of complications is speculated to be lower than when using landmark-based techniques. This investigation aimed to quantify the incidence of pleural puncture and pneumothorax following non-continuous ultrasound-guided thoracic paravertebral blockade for breast surgery. METHODS: Patients who received thoracic paravertebral blockade for breast surgery were identified by retrospective query of our institution's electronic database over a 5-year period. Data collected included patient demographics, level of block, type and volume of local anesthetic, occurrence of pleural puncture, occurrence of pneumothorax, evidence of local anesthetic toxicity, and patient vital signs. The incidence of block complications, including pleural puncture, pneumothorax, and local anesthetic toxicity, were ascertained. RESULTS: 529 patients underwent 2163 thoracic paravertebral injections. Zero pleural punctures were identified during block performance; however, two patients were found to have a pneumothorax on postoperative chest X-ray (3.6 per 1000 surgeries, 95% CI 0.5 to 13.6; 0.9 per 1000 levels blocked, 95% CI 0.1 to 3.3). There were no cases of local anesthetic systemic toxicity or associated lipid emulsion therapy administration. CONCLUSIONS: Pneumothorax following non-continuous ultrasound-guided thoracic paravertebral block using a parasagittal approach is an uncommon occurrence, with a similar rate to pneumothorax following breast surgery alone.

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We describe two patients-both who underwent general anesthesia-in whom we theorize that hydraulic pressure on carotid artery baroreceptors resulted in transient asystolic cardiac arrest (TACA) during diagnostic or therapeutic procedures. Patient #1 was a 58-year-old female who experienced TACA in response to rapid injection of radiocontrast material into the carotid artery during diagnostic cerebral angiography. Her history was remarkable for aneurysmal subarachnoid hemorrhage at least 13 hr prior to angiography, radiographic evidence of intracranial hypertension, and baseline bradycardia, collectively suggestive of increases in baseline vagal tone. Potentially contributing to TACA, the patient had a 90° curve in the internal carotid artery, just distal to the carotid bifurcation and tip of the angiography catheter, that likely diminished runoff of injected contrast solution and, in turn, would have exacerbated any intracarotid pressure increases in response to injection. There was no evidence of increased baseline vagal tone in Patient #2, a 79-year-old female having carotid endarterectomy surgery. She experienced TACA immediately after full release of an occlusive clamp on the common carotid artery proximal to the now closed carotid arteriotomy, but while the internal carotid was still occluded. Of note, the carotid artery baroreceptors were not treated with local anesthetic in these patients, thus they should have retained much of their normal function. We describe the possible pathomechanisms involved in TACA in these patients, measures to diminish the likelihood of the phenomenon occurring in future patients, and methods for treating the asystole.

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The GAS6/TYRO3-AXL-MERTK (TAM) signaling pathway is essential for full and sustained platelet activation, as well as thrombus stabilization. Inhibition of this pathway decreases platelet aggregation, shape change, clot retraction, aggregate formation under flow conditions, and surface expression of activation markers. Transgenic mice deficient in GAS6, or any of the TAM family of receptors that engage this ligand, exhibit in vivo protection against arterial and venous thrombosis but do not demonstrate either spontaneous or prolonged bleeding compared to their wild-type counterparts. Comparable results are observed in wild-type mice treated with pharmacological inhibitors of the GAS6-TAM pathway. Thus, GAS6/TAM inhibition offers an attractive novel therapeutic option that may allow for a moderate reduction in platelet activation and decreased thrombosis while still permitting the primary hemostatic function of platelet plug formation.