Diving & hyperbaric medicine: Overview

Abstract
Decompression illness is a collective term for two maladies (decompression sickness [DCS] and arterial gas embolism [AGE]) that may arise during or after surfacing from compressed gas diving. Bubbles are the presumed primary vector of injury in both disorders, but the respective sources of bubbles are distinct. In DCS bubbles form primarily from inert gas that becomes dissolved in tissues over the course of a compressed gas dive. During and after ascent ('decompression'), if the pressure of this dissolved gas exceeds ambient pressure small bubbles may form in the extravascular space or in tissue blood vessels, thereafter passing into the venous circulation. In AGE, if compressed gas is trapped in the lungs during ascent, pulmonary barotrauma may introduce bubbles directly into the pulmonary veins and thence to the systemic arterial circulation. In both settings, bubbles may provoke ischaemic, inflammatory, and mechanical injury to tissues and their associated microcirculation. While AGE typically presents with stroke-like manifestations referrable to cerebral involvement, DCS can affect many organs including the brain, spinal cord, inner ear, musculoskeletal tissue, cardiopulmonary system and skin, and potential symptoms are protean in both nature and severity. This comprehensive overview addresses the pathophysiology, manifestations, prevention and treatment of both disorders.

Abstract
Bounce diving with rapid descents to very deep depths may provoke the high-pressure neurological syndrome (HPNS). The strategy of including small fractions of nitrogen in the respired gas to produce an anti-HPNS narcotic effect increases the gas density which may exceed recommended guidelines. In 2020 the 'Wetmules' dive team explored the Pearse Resurgence cave (New Zealand) to 245 m breathing trimix (approximately 4% oxygen, 91% helium and 5% nitrogen). Despite the presence of nitrogen, one diver experienced HPNS tremors beyond 200 m. The use of hydrogen (a light yet slightly narcotic gas) has been suggested as a solution to this problem but there are concerns, including the potential for ignition and explosion of hydrogen-containing gases, and accelerated heat loss. In February 2023 a single dive to 230 m was conducted in the Pearse Resurgence to experience hydrogen as a breathing gas in a deep bounce dive. Using an electronic closed-circuit rebreather, helihydrox (approximately 3% oxygen, 59% helium and 38% hydrogen) was breathed between 200 and 230 m. This was associated with amelioration of HPNS symptoms in the vulnerable diver and no obvious adverse effects. The use of hydrogen is a potential means of progressing deeper with effective HPNS amelioration while maintaining respired gas density within advised guidelines.

Abstract
Introduction: Oxygen toxicity has been defined as acute central nervous system (CNS), acute pulmonary, and chronic pulmonary oxygen toxicity. This study identifies acute and chronic CNS oxygen toxicity under 2.0 atmospheres absolute (ATA) pressure of oxygen. Methods: The authors' medical records from September 29, 1989 to January 20, 2023 and correspondence to the authors (9/1994 to 1/20.2023) from patients with signs and/or symptoms historically identified as acute CNS oxygen toxicity and those with neurological deterioration receiving hyperbaric oxygen for neurological conditions were reviewed. Acute cases were those occurring with ≤5 HBOTs and chronic cases >5 HBOTs. Chronic cases were separated into those at 1.5 ATA, > 1.5 ATA, or < 1.5 ATA oxygen. Cumulative dose of oxygen in atmosphere-hours (AHs) was calculated at symptom onset.

Results: Seven acute cases, average 4.0 ± 2.7 AHs, and 52 chronic cases were identified: 31 at 1.5 ATA (average 116 ± 106 AHs), 12 at >1.5 ATA (103 ± 74 AHs), and 9 at <1.5 ATA (114 ± 116 AHs). Second episodes occurred at 81 ± 55, 67 ± 49, and 22 ± 17 AHs, and three or more episodes at 25 ± 18, 83 ± 7.5, and 5.4 ± 6.0 AHs, respectively. Most cases were reversible. There was no difference between adults and children (p = 0.72). Acute intervention in cases (<3 months) was more sensitive than delayed intervention (21.1 ± 8.8 vs. 123 ± 102 AHs, p = 0.035). Outside sources reported one acute and two chronic exposure deaths and one patient institutionalized due to chronic oxygen toxicity. A withdrawal syndrome was also identified.

Conclusion: Hyperbaric oxygen therapy-generated acute and chronic cases of CNS oxygen toxicity in chronic neurological conditions were identified at <2.0 ATA. Chronic CNS oxygen toxicity is idiosyncratic, unpredictable, and occurred at an average threshold of 103-116 AHs with wide variability. There was no difference between adults and children, but subacute cases were more sensitive than chronic intervention cases. When identified early it was reversible and an important aid in proper dosing of HBOT. If ignored permanent morbidity and mortality resulted with continued HBOT.

Abstract
Background: To explore the therapeutic effect of hyperbaric oxygen combined with subdural drilling and drainage (SDD) on subdural effusion type IV with intracranial infection in infant patients.

Methods: This retrospective controlled study included 328 infant patients with subdural effusion type 4 with intracranial infection between January 2005 and January 2023. 178 patients were treated by hyperbaric oxygen combined with SDD (group A). 142 cases were treated with SDD (group B). 97 infants were only received hyperbaric oxygen (group C). Clinical outcomes, the control time of intracranial infection, complications, and the degree of brain re-expansion after 6 months of treatment were compared among the three groups. According to the comprehensive evaluation of treatment effectiveness and imaging results, it is divided into four levels: cured, significantly effective, improved, and ineffective.

Results: No patient died during follow-up. The three groups were similar regarding age, sex, the general information, and clinical symptoms (p > 0.05). All intracranial infections in the children were effectively controlled. There was no difference in infection control time between group A and group B, and there was no statistical significance. However, the control time of intracranial infection between the two groups was different from that of group C, which was statistically significant. Compared with group B and group C, the degree of brain re-expansion in group A has obvious advantages and significant differences. The effective rates of the three groups were 83.7%, 58.5%, and 56.7%, respectively. There were 28 cases of subcutaneous hydrops in group A and 22 cases of subcutaneous hydrops in group B after operation, and no other serious complications.

Conclusion: The SDD is safe and effective for infant patients with intracranial infections through fluid replacement and intrathecal antibacterial. Hyperbaric oxygen is effective as an adjuvant therapy to promote brain re-expansion.

Abstract
Hyperbaric Oxygen Therapy (HBOT) has garnered significant attention as a therapeutic principle with potential benefits across a variety spectrum of medical conditions, ranging from wound healing and ischemic conditions to neurologic disorders and radiation-induced tissue damage. HBOT involves the administration of 100% oxygen at higher atmospheric pressures, leading to increased oxygen dissolved in bodily fluids and tissues. The elevated oxygen levels are proposed to facilitate tissue repair, reduce inflammation, and promote angiogenesis. This case report presents a compelling instance of the usefulness of HBOT in promoting skin perfusion and healing following peripheral tissue injury resulting from the administration of inotropic and vasopressor agents in septic shock patients.