To review the entity "black esophagus" and sequela of a slipped laparoscopic adjustable band. The patient's history, physical examination, imaging, and endoscopic findings were reviewed. Detailed review of pathophysiology, presentation, diagnosis, management, and natural history was conducted. "Black esophagus," also known as acute esophageal necrosis (AEN), is a rare condition resulting in black discoloration of the mid to distal esophagus with less than a hundred reported cases. It has not been previously documented in bariatric surgery or following laparoscopic adjustable gastric banding. The volvulus was reduced at surgery, and the esophageal changes resolved without sequela. "Black esophagus" is an acute, ominous-appearing condition with a spectrum ranging from superficial mucosal disease to transmural involvement with perforation. Fortunately, esophageal resection is rarely required.

The surface epithelial cells of the gastric mucosa transport Na+ from lumen to serosa. The first step in this process is the entry of Na+ through an amiloride-sensitive Na+ channel at the apical membrane. The exact function(s) of this Na+ transport are unknown, but it has been suggested that it might help the stomach to withstand an acid load. The present study was undertaken to examine the effects of low luminal pH and the alkali cations Li+, K+, Rb+, and Cs+ on the amiloride-sensitive Na+ permeability of the apical membrane of Necturus antral cells by measuring the changes in apical membrane voltage (Vmc) using conventional microelectrode techniques. Isosmolar replacement of luminal NaCl (pH 7.25) with LiCl caused a depolarization of the Vmc, a decrease in transepithelial resistance (Rt), and an increase in the transepithelial potential (Vmc), whereas replacement with KCl, RbCl, or CsCl caused a hyperpolarization of the Vmc, an increase in Rt, and a decrease in the Vmc. Luminal acidification from pH 7.25 to pH 3.00 caused very similar changes with all the cation solutions tested, hyperpolarizing the Vmc, increasing Rt, and reducing the Vmc to near 0 mV. Acidification of the luminal NaCl solution from pH 7.25 to pH 2.00 caused a progressive hyperpolarization of the Vmc similar to the effects seen with luminal amiloride (10(-4) M) in pH 7.25 NaCl solutions or luminal Na+-free (N-methyl-D-glucamine) Ringer at pH 7.25. These results demonstrate that 1) of the cations tested only Li+ can substitute for Na+ in maintaining the Vmc, and 2) external H ions (low luminal pH) block cation permeability of the apical membrane.

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The effects of low doses of luminal ethanol on the amiloride-sensitive apical membrane potential of Necturus antral mucosa were studied using conventional microelectrode techniques. Luminal ethanol (0.250-4.0% vol/vol) caused a dose-dependent hyperpolarization of the apical membrane potential (Vmc), an increase in transepithelial resistance (Rt) and resistance ratio (Ra/Rb), and a decrease in transepithelial potential (Vms). Luminal amiloride (100 microM) to 4% ethanol-treated antra did not cause any additional hyperpolarization of Vmc. Compared with luminal 2% ethanol-Ringer, an equivalent osmotic mannitol solution depolarized Vmc and basolateral potential (Vcs), decreased Rt and Ra/Rb, and increased Vms. A single dose of 0.50% ethanol attenuated the effects of a second 2% ethanol exposure on Vmc. No change in periodic acid-Schiff (PAS)-positive mucous granule content could be found between control and 2% ethanol-treated antra. The Ca2+ ionophores A23187 or ionomycin (0.25-5.0 microM) dose dependently hyperpolarized the Vmc and Vcs, increased Rt and Ra/Rb, and decreased Vms. Luminal Ca(2+)-free Ringer had no effect on luminal 2.00% ethanol-induced changes in membrane potentials or resistances. Pretreatment with BAPTA blocked by approximately 70 and 55% the Vmc hyperpolarization of 2 and 4% ethanol, respectively. Pretreatment with ruthenium red (10-50 microM) also dose dependently reduced the 2% ethanol-induced changes in Vmc. The data indicate that 1) low doses of luminal ethanol and Ca2+ ionophores have similar effects on Necturus gastric antral membrane potentials and resistances, 2) ethanol-induced hyperpolarizations of the Vmc are partially mediated through an alteration in intracellular Ca2+, and 3) low doses of luminal ethanol do not cause the release of antral epithelial mucous granules at the time when significant changes are occurring in the Vmc.

HighlightsWe present a case of a 19 year old male with massive hemothorax and refractory, class IV hemorrhagic shock due to proximal left posterior intercostal artery injury with uncontrollable bleeding secondary to a left chest gunshot wound in the 4th intercostal space (ICS).The patient was emergently taken to the operating room for thoracotomy and left chest exploration and found to have massive ongoing massive from his left posterior chest with severe hemodynamic instability and profound levels of hemorrhagic shock. Despite multiple attempts to surgically stop the bleeding intraoperatively as well as using various hemostatic measures, we were unable to control the excessive bleeding.The patient developed refractory class IV hemorrhagic shock with sinus tachycardia to the 170′s and persistent hypotension with systolic blood pressures in the 70′s, which was not amenable to surgical control.Consequently, the patient was taken to the angiography suite in radiology where thoracic aortography was performed and revealed active bleeding from the left 7th posterior intercostal artery < 3 cm from the aorta.The patient underwent thoracic angiography with percutaneous catheter-based embolization of the bleeding intercostal artery. The bleeding arterial segment was controlled with coils and gelfoam along with the vessels immediately above and below the area of extravasation.The patient's hemodynamics significantly stabilized. He was transferred to the surgical ICU for ongoing resuscitation. The patient survived and was ultimately discharged to home in satisfactory condition.This is the first report in the literature of using thoracic angiography with selective catheter based embolization to arrest bleeding of an injured posterior intercostal artery due to penetrating injury or gunshot wound of the chest.