The effect of compression rate and slope on the incidence of symptomatic Eustachian tube dysfunction leading to middle ear barotrauma: a Phase I prospective study.

Introduction: Symptomatic Eustachian tube dysfunction (ETD) and middle ear barotrauma (MEB) are the most common reported complications during hyperbaric oxygen (HBO2) treatment. There is no standardized rate of compression (ROC) reported to decrease the incidence rates of ETD and MEB during hyperbaric treatments. Few studies actually demonstrate that the ROC decreases the incidence of ETD or MEB. Methods: Our study was designed to determine an optimal hyperbaric chamber compression rate that might reduce the incidence of symptomatic ETD leading to MEB during the compression phase of treatment in a multiplace hyperbaric chamber. Data was collected prospectively over 2,807 elective patient treatments compressed using a U.S. Navy Treatment Table 9 (USN TT9) with a modified ROC. ROC was assigned using two variables, time (10 vs.15 minutes) and slope (linear vs. non-linear compression). Patients were exposed to all four compression schedules in a consecutive daily fashion. We recorded any patient requiring a stop during initial compression due to ear discomfort. Anyone requiring a stop was evaluated post treatment for MEB. Findings were compared to our standard 10-minute linear ROC. Evaluation of the tympanic membrane was accomplished using video otoscopy. Barotrauma when present was classified using both the Teed and O'Neill grading systems. Data was analyzed using basic statistical methods. Results: When comparing four different rates of compression during an elective USN TT9 in a multiplace (Class A) chamber there is a decreased incidence for symptomatic ETD when using a 15-minute linear compression schedule (p-value ⟨0.05). Conclusion: Using a 15-minute linear compression schedule is associated with less symptomatic ETD and less MEB when performing an elective 45 fsw (USN TT9) hyperbaric treatment in a Class A chamber. Asymptomatic ETD and MEB were not considered in this study.

Biochemical and molecular diagnosis of glutaric aciduria type 1 in a black South African male child: case report.

Glutaric aciduria type 1 (GA-1) is an inborn error of metabolism caused by a deficiency of the mitochondrial enzyme glutaryl-Co enzyme A dehydrogenase. GA-1 is not uncommon amongst Caucasians but to the best of our knowledge, it has previously not been reported in black African children. We present a case of GA-1 in a black South African boy who was referred to hospital at the age of five years and ten 10 months with dyskinesia and dystonia accompanied by chorea and athetosis. Radiological examination revealed enlarged basal cisterns with bilateral fluid collection around the sylvian fissures suggestive of GA-1. Analysis of urine showed raised levels of glutaric acid at 520 micromol/mmol creatinine (normal <2.0), 3-hydroxyglutaric acid at 113 micromol/mmol creatinine (normal <3.0) and a low blood carnitine level of 31.5 micromol/l (normal 35-84). A definitive diagnosis was reached through DNA analysis which revealed homozygosity for an A293T mutation in the glutaryl-Co-enzyme A dehydrogenase (GCDH) gene.