Number 2

[RESPONSE LETTER] DOI: 10.22462/03.04.2021.15

[LETTER] DOI: 10.22462/03.04.2021.14

[RESPONSE  LETTER] DOI: 10.22462/03.04.2021.13

[LETTER] DOI: 10.22462/03.04.2021.12

RATIONALE Decompression sickness (DCS, “bends”) is caused by the formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation) [1]. This may occur when ambient pressure is reduced during: ascent from a dive; rapid ascent to altitude in an unpressurized aircraft or hypobaric chamber; loss of cabin pressure in an aircraft [2]; and during space walks. In diving, compressed-gas breathing is usually necessary, although occasionally DCS has occurred after either repetitive or very deep breath-hold dives [3,4]. DCS can rarely occur in hyperbaric tenders after decompression from standard hyperbaric treatment at 2.2-2.5 atmospheres absolute (ATA) [5]. Although arterial gas embolism due to pulmonary barotrauma can occur after a dive as shallow as 1 meter, the threshold depth for DCS in compressed-gas diving is around 20 feet of seawater (fsw) [6]. DCS after a dive can be provoked by mild altitude exposure, such as a commercial aircraft flight [7,8], but without a preceding dive the threshold altitude for DCS occurrence due to acute altitude exposure is generally 18,000-20,000 feet [9,10]. Most cases of altitude DCS manifest as limb pain [11-13]. More serious manifestations of altitude DCS (e.g., neurological, cardiorespiratory DCS: “chokes”) have ..

Hydrogen peroxide (H2O2) ingestion can cause vascular gas embolism (GE). Hyperbaric oxygen therapy (HBO2) is known to improve neurological abnormalities in patients with arterial gas embolism (AGE). Previously, HBO2 based on the U.S. Navy Table 6 diving protocol has been adopted for treating AGE and preventing the progression of portal venous GE, caused by H2O2 ingestion, to AGE. However, the indication and protocol for HBO2 have not been established for GE related to H2O2 ingestion. Herein, we describe a case in which GE caused by H2O2 ingestion was treated using HBO2 with a short protocol.  A 69-year-old female patient presented with abdominal pain, vomiting, and transient loss of consciousness after ingesting 35% H2O2. Computed tomography revealed gastric wall and portal venous gas. She was administered an HBO2 protocol with 2.8-atmosphere absolute (ATA) compression for 45 minutes. This was followed by a 2.0-ATA treatment for 60 minutes with a five-minute air break, after which all gas bubbles disappeared. After HBO2 treatment, brain magnetic resonance imaging revealed focal cytotoxic edema lesions; however, the patient was discharged without additional symptoms. DOI: 10.22462/03.04.2021.10

A 52-year-old male accidentally ingested approximately 100 mL of 35% hydrogen peroxide (H2O2), resulting in the sudden onset of gastrointestinal and neurologic symptoms. Non-contrast abdominal CT revealed extensive portal venous gas and gastric pneumatosis. The patient was treated with hyperbaric oxygen therapy which resulted in complete resolution of symptoms. The case highlights the therapeutic value of hyperbaric oxygen therapy in the treatment of vascular gas embolism and mitigation of concentrated H2O2 ingestion toxicity. DOI: 10.22462/03.04.2021.9

Background: Carbon monoxide (CO) poisoning and cardiac arrest can cause neurological complications such as mental deterioration and movement disorders through ischemic brain injury. We report a case in which neurological sequelae after cardiac arrest caused by CO poisoning improved after hyperbaric oxygen (HBO2) therapy. Case report: A 43-year-old male visited the hospital with cardiac arrest due to CO poisoning. He developed neurological sequelae including mental deterioration and myoclonus after recovering spontaneous circulation. Anticonvulsant therapy was used after target temperature management but did not have a positive effect on neurological symptoms. However, after HBO2 therapy the patient’s neurological symptoms improved, and he was discharged a month later. Conclusion: HBO2 therapy may be considered when neurological sequelae persist after cardiac arrest due to CO poisoning. DOI: 10.22462/03.04.2021.8

Gas embolism is a potential and often life-threatening complication of central venous catheters. We report a case of air embolism after tearing of the central catheter associated with severe acute respiratory distress syndrome. The severity of the clinical situation meant choices had to be made regarding the order of treatments. This clinical case provided useful eye-openers for patient management regarding the prioritization of treatments as well as the possibilities offered by hyperbaric oxygen therapy. z DOI: 10.22462/03.04.2021.7

Introduction: Safe administration of critical care hyperbaric medicine requires specialized equipment and advanced training. Equipment must be tested in order to evaluate function in the hyperbaric environment. High-frequency percussive ventilation (HFPV) has been used in intensive care settings effectively, but it has never been tested in a hyperbaric chamber. Methods: Following a modified U.S. Navy testing protocol used to evaluate hyperbaric ventilators, we evaluated an HFPV transport ventilator in a multiplace hyperbaric chamber at 1.0, 1.9, and 2.8 atmospheres absolute (ATA). We used a test lung with analytical software for data collection. The ventilator uses simultaneous cyclic pressure-controlled ventilation at a pulsatile flow rate (PFR)/oscillatory continuous positive airway pressure (oCPAP) ratio of 30/10 with a high-frequency oscillation percussive rate of 500 beats per minute. Inspiratory and expiratory times were maintained at two seconds throughout each breathing cycle. Results: During manned studies, the PFR/oCPAP ratios were 26/6, 22/7, and 22.5/8 at an airway resistance of 20cm H2O/L/ second and 18/9, 15.2/8.5, and 13.6/7 at an airway resistance of 50 cm/H2O/L/second at 1, 1.9, and 2.8 ATA. The resulting release volumes were 800, 547, and 513 mL at airway resistance of 20 cm H2O/L/sec and 400, 253, and 180 mL at airway ..

Hydrogen sulfide (H2S) is a toxic gas produced via breakdown of organic matter. Hydrogen sulfide exposure can cause symptoms ranging in severity from mild effects (dizziness, headache, nausea) to severe lactic acidosis, respiratory failure, pulmonary edema, cardiac arrhythmias and death. Treatment modalities include oral countermeasures and 100% FiO2 with supportive therapy. However, case studies utilizing hyperbaric oxygen (HBO2) therapy have been reported with general benefit seen in severe cases of toxicity. In this report, cases of mild to moderate H2S toxicity occurred aboard a U.S. Navy ship, resulting in a mass casualty incident of more than 30 patients. Patient symptoms included dizziness, headaches, nausea, vomiting, and one patient with altered mental status. Most patients’ symptoms resolved after several hours of supportive therapy, but six patients had symptoms refractory to 100% FiO2 at 1 atm. These six patients received HBO2 therapy with a USN Treatment Table 9 after consultation with the local emergency room and hyperbaric assets. Four separate chambers were utilized, including two chambers onboard USN ships and the local explosive ordnance disposal (EOD) chamber. Complete resolution of symptoms in all six patients was achieved within the first breathing period. Patients were monitored after treatment aboard the USN ship ..

Middle ear barotrauma (MEB) is a common complication of hyperbaric oxygen (HBO2) therapy. It has been reported in more than 40% of HBO2 treatments and can interrupt the sequence of HBO2. MEB may lead to pain, tympanic membrane rupture, and even hearing loss. The aim of this study was to determine if pretreatment with intranasal fluticasone and oxymetazoline affected the incidence of MEB. We conducted a retrospective chart review of subjects undergoing HBO2 at our institution between February 1, 2014, and May 31, 2019. Subjects in the fluticasone/ oxymetazoline (FOT) treatment group used intranasal fluticasone 50 mcg two times per day and oxymetazoline 0.05% one spray two times per day beginning 48 hours prior to initial HBO2. Oxymetazoline was discontinued after four days. Fluticasone was continued for the duration of HBO2 therapy. A total of 154 unique subjects underwent 5,683 HBO2 treatments: 39 unique subjects in the FOT group underwent 1,501 HBO2; 115 unique subjects in the nFOT (no oxymetazoline or fluticasone treatment) group underwent 4,182 HBO2 treatments. The incidence of MEB was 15.4% in the FOT group and 16.2% in the nFOT group. This was not a statistically significant difference (OR = 0.77; p = 0.636). Treatment pressure, ..

Multiday hyperbaric exposure has been shown to reduce the incidence of decompression sickness (DCS) of compressed-air workers. This effect, termed acclimatization, has been addressed in a number of studies, but no comprehensive review has been published. This systematic review reports the findings of a literature search. PubMed, Ovid Embase, The Cochrane Library and Rubicon Research Repository were searched for studies reporting DCS incidence, venous gas embolism (VGE) or subjective health reports after multiday hyperbaric exposure in man and experimental animals. Twenty-nine studies fulfilled inclusion criteria. Three epidemiological studies reported statistically significant acclimatization to DCS in compressedair workers after multiday hyperbaric exposure. One experimental study observed less itching after standardized simulated dives. Two human experimental studies reported lower DCS incidence after multiday immersed diving.  Acclimatization to DCS has been observed in six animal species. Multiday diving had less consistent effect on VGE after hyperbaric exposure in man. Four studies observed acclimatization while no statistically significant acclimatization was reported in the remaining eight studies. A questionnaire study did not report any change in self-perceived health after multiday diving. This systematic review has not identified any study suggesting a sensitizing effect of multiday diving, and there is a lack of data supporting benefit ..

Update article published in Vol. 48 #4 (View is linked to updated article) Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver ..

Introduction: Pre-dive altitude exposure may increase respiratory fatigue and subsequently augment exercise ventilation at depth. This study examined pre-dive altitude exposure and the efficacy of resistance respiratory muscle training (RMT) on respiratory fatigue while diving at altitude. Methods: Ten men (26±5 years; V̇ O2peak: 39.8±3.3 mL• kg-1•min-1) performed three dives; one control (ground level) and two simulated altitude dives (3,658 m) to 17 msw, relative to ground level, before and after four weeks of resistance RMT. Subjects performed pulmonary function testing (e.g., inspiratory [PI] and expiratory [PE] pressure testing) pre- and post-RMT and during dive visits. During each dive, subjects exercised for 18 minutes at 55% V̇ O2peak, and ventilation (V̇ E), breathing frequency (ƒb,), tidal volume (VT) and rating of perceived exertion (RPE) were measured. Results: Pre-dive altitude exposure reduced PI before diving (p=0.03), but had no effect on exercise V̇ E, ƒb, or VT at depth. At the end of the dive in the pre-RMT condition, RPE was lower (p=0.01) compared to control. RMT increased PI and PE (p<0.01). PE was reduced from baseline after diving at altitude (p<0.03) and this was abated after RMT. RMT did not improve V̇ E or VT at depth, but decreased ƒb (p=0.01) ..