Acute oxygen toxicity in the central nervous system primarily exhibits through generic symptoms such as nausea, vomiting, or sensory nerve alterations, up to generalized tonic–clonic seizure IN its most severe form (Paganini and Camporesi, 2019). The underlying pathophysiology takes into account the increased generation of reactive oxygen species (ROS) and nitric oxide (NO) metabolites, along with metabolic changes, altogether causing membrane damages, regional cerebral blood flow alterations, and neurotransmitter derangements (Jain, 2017a, pp. 84–89). Incidence depends on pressure, concentration of inhaled oxygen, and duration of exposure: the higher the factors, the greater the risk. Current data suggest that this is a rare event during treatments performed below 3 ATA for less than 1 h (Paganini and Camporesi, 2019).

There is no specific guideline on the acute treatment of hyperoxic seizures, but the most reasonable action is the fastest reduction of PaO2 back to physiological values. Therefore, oxygen masks should be removed (when used), and room air should be restored in the pressurized chamber. Then, first aid maneuvers should be enacted to preserve the unconscious patient from falling or striking objects as in generalized seizures, while avoiding the routine use of anticonvulsant drugs. Decompression should be started only after the cessation of seizures to avoid the risk of lung barotrauma. In fact, during convulsions, the glottis is usually closed, and an early or abrupt ascent could lead to gas expansion inside the lungs and potential damages (see next section: Pneumothorax). Please see Supplementary Material 1 for the detailed case log.

At pressure, the lungs are particularly vulnerable due to the fragility of the alveoli. Patients undergoing HBOT should be educated not to hold their breath or close the glottis during decompression since, in that phase, gases in the lungs expand and the amount in excess should escape freely. A spontaneous pneumothorax (PNX) due to air trapping can, however, develop typically during the ascent in predisposed subjects, such as those suffering from acute respiratory distress syndrome (Kot et al., 2008), obstructive pulmonary diseases (e.g., asthma, chronic obstructive pulmonary disease), or asymptomatic carriers of bullae. Overall, the incidence of PNX during HBOT is not clearly established (Cakmak et al., 2015). Symptoms and clinical features of PNX vary based on the severity of the manifestation, ranging from sudden-onset pleuritic chest pain to mild or moderate dyspnea. Signs of small PNX can be subtle, but, when clinically relevant, include diminished breath sounds and subcutaneous emphysema. In the hyperbaric chamber, few instruments can help the diagnosis, and the environmental noise further decreases an already low accuracy of physical examination. Point-of-care, chest ultrasound is a useful tool to diagnose PNX (Soldati et al., 2008) early, but the machine should be approved for the use inside the chamber. If a PNX is suspected, any pressure variation should be halted, the patient should be evaluated, and slow decompression of the chamber should be performed. Once outside, a thorough evaluation at the nearest emergency department (ED) is mandatory after the end of the hyperbaric session for several reasons: (a) patients undergoing HBOT usually have multiple comorbidities, (b) chest pain and dyspnea have a broad differential, and (c) imaging is needed to diagnose the size of PNX and determine further management.

Tension PNX is a life-threatening complication, with an unreliable physical exam (Roberts et al., 2015). Emergent needle chest decompression should be performed without delay in the multiplace chamber if tension PNX is suspected, preferring the fourth or fifth intercostal space anterior to the adults’ midaxillary line to insert an 8-cm over-the-needle large-bore catheter (American College of Surgeons Committee on Trauma, 2018, p. 66). Once outside, further stabilization should be achieved through finger thoracostomy or chest drain insertion performed by an experienced provider, followed by an early transfer to the nearest facility. In the particular case of monoplace chambers, emergent chamber decompression and immediate chest decompression should be performed. Please see Supplementary Material 2 for the detailed case log.

Patients suffering from diabetes and complicated by non-healing lower extremity ulcers are among the most frequent populations treated with HBOT. This subset of patients seems to develop hypoglycemia during and after treatments, but the incidence is still unclear. Some studies confirmed the susceptibility of diabetics, especially if insulin-dependent (Ekanayake and Doolette, 2001; Trytko and Bennett, 2003; Al-Waili et al., 2006). The suggested pathophysiology involves increased secretion of insulin and an improved peripheral sensibility to insulin on target organs (Dedov et al., 1987; Wilkinson et al., 2012). On the other hand, Peleg et al. (2013) found no differences in blood sugar levels between diabetics and controls before and after HBOT in a controlled trial. Also, Stevens and colleagues, in a retrospective cohort analysis, found that hypoglycemic events were rare (1.5% on 3136 HBOT sessions), independently associated with Type 1 diabetes, and predicted by a pre-HBOT glucose level of 150 mg/dl (Stevens et al., 2015). Hypoglycemia can manifest with weakness, confusion, and sweating. If suspected, without the need of a stick glucose, plain sugar can be orally administered and the patient carefully evaluated: if improving, the patient can continue the treatment; otherwise, the patient can be decompressed. Please see Supplementary Material 3 for the detailed case log.

Cardiac arrest is a rare event in hyperbaric chambers (Kot, 2014), but a careful evaluation before each session should be carried out by the hyperbaric physician to prevent adverse events, especially for critical patients. Despite the fact that PaO2 levels during HBOT are higher than normal, and tissue survival time is prolonged—the so-called “grace period” (Wright et al., 2016)—basic life support must be started immediately after recognition (Merchant et al., 2020). There is no official recommendation regarding this special environment, but some considerations can be made based on the specific features of multiplace or monoplace chambers (Kot, 2014; Wright et al., 2016).

In the case of multiplace chambers, medical attendants should immediately start CPR while communicating the ongoing situation outside. The provider can consider recruiting other personnel or laypersons to ensure high-quality CPR. Decompression speed should consider the safety of other patients and healthcare personnel inside the chamber. The outer lock can be used to rapidly decompress an arrested patient while ensuring the safety of other people attending the main chamber. An oropharyngeal airway should be placed to avoid air trapping and consequent PNX. On the other hand, in monoplace chambers, the patient should be decompressed as fast as possible to minimize the no-flow time.

Defibrillation can be hazardous inside chambers, and only a few defibrillators have been certified for this purpose. Still, the safest way of delivering shocks seems to be the use of adhesive plates applied to the patient’s chest, connected to an external defibrillator through wires exiting the chamber and activated by a dedicated staff member. To further reduce inflammability, ambient air should be restored inside, a condition easily achieved in multiplace chambers where oxygen is inhaled through masks (Kot, 2014). Please see Supplementary Material 4 for the detailed case log.

Intubated patients are at increased risk of adverse events both for the severity of their disease and for the high number of medical equipment carried along with them. Particular attention should be paid while transferring a critical patient in a confined space such as hyperbaric chambers, avoiding any tube displacement or circuit/line disconnection. Once inside, the equipment should be accessible and visible at any moment because, during compression, the practitioner will be responsible for the patient’s adaptations. The high complexity of these treatments has been highlighted by several authors (Kot, 2015; Mathieu et al., 2015; Millar, 2015). Future simulation studies could validate a checklist to standardize the transport and medical assistance to intubated patients undergoing HBOT.

In breath-hold divers, PaO₂ significantly increases due to lung compression and accumulation of O2 in the blood (Bosco et al., 2018a). Conversely, during ascent, the re-expansion of alveoli determines significant hypoxemia (Bosco et al., 2020). The reduced amount of oxygen to the brain can therefore result in neurologic symptoms ranging from focal weaknesses to seizure-like uncontrolled movements (the so-called “taravana” or “samba” phenomenon) or loss of consciousness (also called “shallow water blackout” or “ascent syncope”) (Lindholm and Lundgren, 2009). A breath-hold diver experiencing neurologic symptoms should be placed on high oxygen concentration with a non-rebreather mask and transferred to the nearest ED. When syncope occurs, rescue by a peer and standard basic life support should be enacted to ensure airway patency while transferring the patient on oxygen. Please see Supplementary Material 5 for the detailed case log.

Drowning is a process resulting in respiratory impairment from submersion or immersion in a fluid, and is a public health issue (van Beeck et al., 2005). Water activities and sports are at particular risk of drowning, especially those performed underwater. In SCUBA diving, drowning occurs mostly after losing consciousness for medical reasons or problems with the air supplies (wrong gas mixtures; equipment failure; entrapment in caves/relicts, and depletion of supplies). Instead, in activities requiring breath-hold, drowning is due to the subjects’ and athletes’ attempt to prolong their time submerged. Drowning is a complication of BHD syncope due to water entering the subject’s unprotected airways while still submerged. Before a breath-hold dive, voluntary hyperventilation has been demonstrated to predispose to ascent syncope—leading to water aspiration—by reducing PaCO₂. Since hypercarbia has greater influence on the respiratory drive than hypoxemia, voluntary hyperventilation hampers the alarm mechanism giving the subjects a wrong perception of their endurance capability (Lindholm and Lundgren, 2009). Prevention and early recognition are the first steps. The victim should be rescued by trained personnel if the scene if safe. Basic and advanced life support should be performed as early as possible (Szpilman and Morgan, 2020). Please see Supplementary Material 6 for the detailed case log.

Another problem faced during underwater activities is lung volume reduction (“lung squeeze” descending) and re-expansion (ascending) due to the varying environmental pressure. Pulmonary barotrauma usually occurs in SCUBA divers rapidly ascending and holding their breath or when air is trapped inside the lungs (e.g., obstructive pulmonary disease or asthma) (Russi, 1998). In BHD, barotrauma is less frequent since the volume at the end of the dive cannot be larger than it was initially. However, symptoms of barotrauma can range from a simple cough to life-threatening conditions such as pulmonary edema, hemoptysis, PNX, or gas embolism in the worst cases (Ferrigno and Lundgren, 2003). Ferrigno and Lundgren synthesized two possible explanations regarding the pathophysiology of lung damage in breath-hold divers. First, the blood shift experienced underwater causes blood engorgement of pulmonary vessels, thus reducing lung compliance and interfering with re-expansion. Second, compliance could vary across different lung areas, thus predisposing to shear forces development and direct damage or deformation of airways and consequent transient obstruction. Moreover, athletes performing “lung packing” to reach total lung capacity before a dive are particularly predisposed (Ferrigno and Lundgren, 2003). The management of barotrauma in BHD and SCUBA diving should promptly identify and stabilize complications while organizing a timely transfer to the nearest facility. Practitioners should also consider swim-induced pulmonary edema (SIPE) in the differential since this condition has a specific treatment and is potentially fatal (Moon et al., 2016). Please see Supplementary Material 7 for the detailed case log.

Gases at pressure dissolve in biological liquids and tissues and form bubbles during decompression. Bubbles are composed of inert gases, mostly nitrogen, and can form in tissues or in the bloodstream causing local damage or distal embolization. The manifestations of DCI are broad and non-specific, potentially involving every system. The most frequent presentations are neurologic (e.g., paresthesias/numbness/tingling, focal neurologic deficit), cutaneous (e.g., itching or marbling), or pain in the affected area (Nochetto et al., 2019). Recent activity in the hyperbaric environment (e.g., SCUBA diving, repetitive BHD, HBOT) is fundamental to suspect DCI. The mainstay of treatment is immediate oxygen administration through a non-rebreathing mask and transfer to the nearest hyperbaric facility (Mitchell et al., 2018). Since SCUBA diving is often practiced in remote areas, an urgent transfer by air could be needed. In this case, a pressurized aircraft should be used for long-haul flights, while the maximum recommended fight altitude for helicopters is 300 m (1,000 ft). The standard recommended treatment is the US Navy Treatment Table 6 using oxygen at 2.8 ATA (Naval Sea Systems Command, 2016). Please see Supplementary Material 8 for the detailed case log.