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Sickle cell trait (SCT), the heterozygous form of sickle cell disease, is generally thought of as a benign condition. However, it is possible for those with SCT to have serious complications, especially when they are exposed to high altitudes where oxygen levels are low. We present a case of a 41-year-old man with a history of SCT who developed severe epigastric pain and nearly lost consciousness while traveling on a commercial airplane. His twin brother, who also has SCT, had a similar episode in the past and required a splenectomy. A splenic subcapsular hematoma was found in a computed tomography scan of the abdomen and pelvis with intravenous contrast. He was admitted and managed conservatively until his symptoms resolved. Though SCT is prevalent in our population, the complications that can arise, such as altitude-associated splenic syndrome, have likely not been thoroughly investigated. Physicians should add this condition to their differential if they practice at locations near airports or in areas of higher altitude and if their patients have a past medical history of SCT. [ABSTRACT FROM AUTHOR]

Objectives: Most cases of irresolvable hoarseness are due to deficiencies in the pliability and volume of the superficial lamina propria of the phonatory mucosa. By using a US Food and Drug Administration-approved polymer, polyethylene glycol (PEG), we created a novel hydrogel (PEG30) and investigated its effects on multiple vocal fold structural and functional parameters. Methods: We injected PEG30 unilaterally into 16 normal canine vocal folds with survival times of 1 to 4 months. Highspeed videos of vocal fold vibration, induced by intratracheal airflow, and phonation threshold pressures were recorded at 4 time points per subject. Three-dimensional reconstruction analysis of 11.7 T magnetic resonance images and histologie analysis identified 3 cases wherein PEG30 injections were the most superficial, so as to maximally impact vibratory function. These cases were subjected to in-depth analyses. Results: High-speed video analysis of the 3 selected cases showed minimal to no reduction in the maximum vibratory amplitudes of vocal folds injected with PEG30 compared to the non-injected, contralateral vocal fold. All PEG30-inject- ed vocal folds displayed mucosal wave activity with low average phonation threshold pressures. No significant inflammation was observed on microlaryngoscopic examination. Magnetic resonance imaging and histologie analyses revealed time-dependent résorption of the PEG30 hydrogel by phagocytosis with minimal tissue reaction or fibrosis. Conclusions: The PEG30 hydrogel is a promising biocompatible candidate biomaterial to restore form and function to deficient phonatory mucosa, while not mechanically impeding residual endogenous superficial lamina propria. [ABSTRACT FROM AUTHOR]

Acute exposure to hydrogen sulfide (H2S) causes 4 dose-dependent responses: hyperpnea, unconsciousness or knockdown, apnea, and death. At present, scientific mechanisms for these effects are unknown, but inhibition of cytochrome oxidase in the central nervous system (CNS) by sulfide has been suggested. In this study, the premise of brain as target is examined by comparing peripheral with direct delivery of sulfide to brain. NaHS was administered to anesthetized Sprague-Dawley male rats, by femoral intravenous, or carotid intra-arterial injection. With apnea as the test, ED100 values of 0.6 and 3.0 mg kg1 were found for peripheral and direct delivery to brain, respectively. Peripheral delivery is 5 times as effective as direct delivery to the brain, and greater if the relative dilution factors are considered. Lidocaine, applied to the vagus, prevented apnea, so lung-brain transmission was essential. It was therefore concluded that the lung is the peripheral site of action. Hyperpnea increased in duration with dose. The carotid body, located distal to the arterial catheter, sensed the high doses of NaHS but did not trigger apnea. Intravenous infusion or intraperitoneal injection with NaHCO3 prevented hyperpnea, apnea, and death. The following conclusions are drawn: the carotid body is not implicated in NaHS-induced apnea, the lung and not brain harbors the primary site of action of H2S, and an afferent neural signal from the lung via the vagus induces the apnea. Finally, NaHCO3 appears to prevent toxicity from sulfide, and therefore H2S, by some unexplained mechanism. Practical emergency treatment for acute toxicity In the field may be possible. [ABSTRACT FROM PUBLISHER]