Can We Do Anything Else before Removing a Button Battery from the Esophagus?-Hyaluronic Acid.

OBJECTIVE: This article tests the protective effect of a commercially available mixture of hyaluronic acid, chondroitin sulfate, and poloxamer 407 on the damage caused by the exposure of esophageal mucosa to button batteries in an animal model. METHODS: Experimental study. Sixty porcine esophageal samples were distributed in three groups: control (CG), exposure (EG), and exposure-protection (EPG). In EG and EPG, one CR2032 button battery per sample was inserted, both were subdivided into 2-, 4-, 6-, and 24-hour exposure subgroups, with subsequent battery removal. EPG samples were irrigated with the solution 1 hour after battery exposure. Esophageal pH and final voltage of the battery were measured. RESULTS: pH in CG remained stable. No significant differences in pH at 1 hour were found between EG and EPG. In EPG, the pH of the mucosa exposed to the anode was lower than in GE at 2 hours (12.44 vs. 11.89, p = 0.203) and 4 hours (13.78 vs. 11.77, p < 0.0001). In the cathode pH was significantly higher in EG at 2 hours (2.5 vs. 4.11, p < 0.0001), 4 hours (2.33 vs. 4.78, p < 0.0001), and 6 hours (2.17 vs. 2.91, p < 0.0001). Significant voltage reduction at 1 hour was found in EG compared to EPG (0.48 vs. 1.08 V, p = 0.004). CONCLUSION: Exposure to hyaluronic acid solution buffers the acidification on the side exposed to the cathode and basification on the anode. This effect can be maintained up to 3 to 5 hours, even after stopping its application. Our results suggest that a solution containing hyaluronic acid could be used as an esophageal protector after accidental ingestion of button batteries.

[Atrophy of the cervical spinal cord as a consequence of a prenatal ischemic infarct]. / Atrofia de la medula espinal cervical tras infarto isquemico de origen prenatal.

INTRODUCTION: Spinal cord injuries in newborn infants following a traumatic delivery are well known, but occasionally cord damage is appreciated in children whose birth did not involve any complications; in some of them there has been proof of an ischemic process that originated inside the uterus. CASE REPORT: We describe the case of a newborn female with atrophy of the cervical spinal cord compatible with an intrauterine ischemic infarct. It extended to the C4-C6 territory of the anterior spinal artery, with greater participation on the left side. Clinical symptoms were apparent from the moment of birth and took the form of an asymmetric pseudoarthrogryposis in the upper limbs. The left arm was held in abduction at the height of the shoulder, with complete flexion of the elbow and the hand at the height of the chin was hypotonic, inactive and hypotrophic; the right arm was extended and in adduction. The patient presented episodes of hyperthermia that remitted on cooling the body. CONCLUSIONS: When faced with a newborn infant with symptoms that are compatible with chronic cervical spinal cord damage and in the absence of any perinatal traumatic injury, other causes, including prenatal ischemic infarct, must be taken into account.