Cerebral arterial gas embolism (CAGE) during open water scuba certification training whilst practising a controlled emergency swimming ascent.

We report the case of a 23-year-old male novice diver who sustained cerebral arterial gas embolism (CAGE) during his open water certification training whilst practising a free ascent as part of the course. He developed immediate but transient neurological symptoms that had resolved on arrival to hospital. Radiological imaging of his chest showed small bilateral pneumothoraces, pneumopericardium and pneumomediastinum. In view of this he was treated with high flow normobaric oxygen rather than recompression, because of the risk of development of tension pneumothorax upon chamber decompression. There was no relapse of his neurological symptoms with this regimen. The utility and safety of free ascent training for recreational divers is discussed, as is whether a pneumothorax should be vented prior to recompression, as well as return to diving following pulmonary barotrauma.

A retrospective review of divers treated for inner ear decompression sickness at Fiona Stanley Hospital hyperbaric medicine unit 2014-2020.

Introduction: Inner ear decompression sickness (IEDCS) is increasingly recognised in recreational diving, with the inner ear particularly vulnerable to decompression sickness in divers with a right-to-left shunt, such as is possible through a persistent (patent) foramen ovale (PFO). A review of patients treated for IEDCS at Fiona Stanley Hospital Hyperbaric Medicine Unit (FSH HMU) in Western Australia was performed to examine the epidemiology, risk factors for developing this condition, the treatment administered and the outcomes of this patient population. Methods: A retrospective review of all divers treated for IEDCS from the opening of the FSH HMU on 17 November 2014 to 31 December 2020 was performed. Patients were included if presenting with vestibular or cochlear dysfunction within 24 hours of surfacing from a dive, and excluded if demonstrating features of inner ear barotrauma. Results: There were a total of 23 IEDCS patients and 24 cases of IEDCS included for analysis, with 88% experiencing vestibular manifestations and 38% cochlear. Median dive time was 40 minutes and median maximum depth was 24.5 metres. The median time from surfacing to hyperbaric oxygen treatment (HBOT) was 22 hours. Vestibulocochlear symptoms fully resolved in 67% and complete symptom recovery was achieved in 58%. A PFO was found in 6 of 10 patients who subsequently underwent investigation with bubble contrast echocardiography upon follow-up. Conclusions: IEDCS occurred predominantly after non-technical repetitive air dives and ongoing symptoms and signs were often observed after HBOT. Appropriate follow-up is required given the high prevalence of PFO in these patients.

A prospective single-blind randomised clinical trial comparing two treatment tables for the initial management of mild decompression sickness.

INTRODUCTION: Limited evidence suggests that shorter recompression schedules may be as efficacious as the US Navy Treatment Table 6 (USN TT6) for treatment of milder presentations of decompression sickness (DCS). This study aimed to determine if divers with mild DCS could be effectively treated with a shorter chamber treatment table. METHODS: All patients presenting to the Fremantle Hospital Hyperbaric Medicine Unit with suspected DCS were assessed for inclusion. Participants with mild DCS were randomly allocated to receive recompression in a monoplace chamber via either a modified USN TT6 (TT6m) or a shorter, custom treatment table (FH01). The primary outcome was the number of treatments required until resolution or no further improvement (plateau). RESULTS: Forty-one DCS cases were included, 21 TT6m and 20 FH01. Two patients allocated to FH01 were moved to TT6m mid-treatment due to failure to significantly improve (as per protocol), and two TT6m required extensions. The median total number of treatments till symptom resolution was 1 (IQR 1-1) for FH01 and 2 (IQR 1-2) for TT6m (P = 0.01). More patients in the FH01 arm (17/20, 85%) showed complete symptom resolution after the initial treatment, versus 8/21 (38%) for TT6m (P = 0.003). Both FH01 and TT6m had similar overall outcomes, with 19/20 and 20/21 respectively asymptomatic at the completion of their final treatment (P = 0.97). In all cases where two-week follow-up contact was made, (n = 14 FH01 and n = 12 TT6m), patients reported maintaining full symptom resolution. CONCLUSIONS: The median total number of treatments till symptom resolution was meaningfully fewer with FH01 and the shorter treatment more frequently resulted in complete symptom resolution after the initial treatment. There were similar patient outcomes at treatment completion, and at follow-up. We conclude that FH01 appears superior to TT6m for the treatment of mild decompression sickness.

Oxygen toxicity seizure mimics.

INTRODUCTION: Oxygen toxicity seizures (OTS) are a well-recognised complication of hyperbaric oxygen treatment (HBOT). As such, seizure-like activity during HBOT is usually presumed to be a result of central nervous system oxygen toxicity (CNS-OT). Four cases are reported here where causes other than CNS-OT were determined as being the likely cause of the seizure; causes we have labelled 'OTS mimics'. Through review of the current literature, and our hyperbaric medicine unit's experience to date, we aimed to highlight the relevance of these OTS mimics, as the potential for significant morbidity and mortality exists with incorrect diagnoses. METHODS: A retrospective review of the medical records of all patients treated at the Fiona Stanley Hospital and Fremantle Hospital hyperbaric medicine units who had a seizure during HBOT between November 1989 and June 2020. These events were reviewed to determine whether causes for seizures other than oxygen toxicity were evident. RESULTS: Four OTS mimics were identified: posterior reversible encephalopathy syndrome, pethidine toxicity, previous subarachnoid haemorrhage with resultant epilepsy, and severe hypoglycaemia. CONCLUSIONS: This case series highlights the need for caution when diagnosing an apparent OTS. Multiple conditions may mimic the signs and symptoms of oxygen toxicity. This creates scope for misdiagnosis, with potential for consequent morbidity and mortality. A pragmatic approach is necessary to any patient exhibiting seizure-like activity during HBOT, with suspicion for other underlying pathologies.

Oxygen toxicity seizures during United States Navy Treatment Table 6: An acceptable risk in monoplace chambers?

INTRODUCTION: Hyperbaric oxygen treatment (HBOT) may be complicated by oxygen toxicity seizures, which typically occur with hyperbaric partial pressures of oxygen exceeding 203 kPa (2 atmospheres absolute). All other hyperbaric units in Australia exclusively use a multiplace chamber when treating with United States Navy Treatment Table 6 (USN TT6) due to this perceived risk. The purpose of this study was to determine the safety of a monoplace chamber when treating decompression illness (DCI) with USN TT6. METHODS: A retrospective review of the medical records of all patients treated at Fiona Stanley Hospital Hyperbaric Medicine Unit with USN TT6 between November 2014 and June 2020 was undertaken. These data were combined with previous results from studies performed at our hyperbaric unit at Fremantle Hospital from 1989 to 2014, creating a data set covering a 30-year period. RESULTS: One thousand treatments with USN TT6 were performed between 1989 and 2020; 331 in a monoplace chamber and 669 in a multiplace chamber. Four seizures occurred: a rate of 0.59% (1/167) in a multiplace chamber; and none in a monoplace chamber, indicating no statistically significant difference between seizures in a monoplace versus multiplace chamber (P = 0.31). CONCLUSIONS: The rate of oxygen toxicity seizures in a monoplace chamber is not significantly higher than for treatment in the multiplace chamber. We conclude that using the monoplace chamber for USN TT6 in selected patients poses an acceptably low seizure risk.

Acute spontaneous spinal cord infarction: Utilisation of hyperbaric oxygen treatment, cerebrospinal fluid drainage and pentoxifylline.

INTRODUCTION: Spinal cord infarction (SCI) is a potentially devastating disorder presenting with an acute anterior spinal artery syndrome, accounting for an estimated 1% of stroke presentations. Aetiologies include aortic surgical complications, systemic hypotension, fibrocartilaginous embolism and vascular malformations. Diagnosis is clinical combined with restriction on diffusion-weighted magnetic resonance imaging (MRI). There are no treatment guidelines for non-perioperative cases although there is limited literature regarding potential therapies, including hyperbaric oxygen treatment (HBOT) and cerebrospinal fluid (CSF) drainage. We describe 13 cases of acute SCI, five receiving HBOT, and three also receiving pentoxifylline and drainage of lumbar CSF. METHODS: Data for all patients with MRI-proven SCI at Fiona Stanley Hospital from 2014-2019 were reviewed. RESULTS: Thirteen patients, median age 57 years (31-74), 54% female, were identified. Aetiologies: two fibrocartilaginous emboli; seven likely atherosclerotic; two thromboembolic; two cryptogenic. All presented with flaccid paraplegia except one with Brown-Sequard syndrome. Levels ranged from C4 to T11. Five patients received HBOT within a median time of 40 hours from symptom onset, with an average 15 treatments (10-20). Three of these received triple therapy (HBOT, pentoxifylline, CSF drainage) and had median Medical Research Council manual muscle testing power of 5, median modified Rankin Score (mRS) of 1 and American Spinal Injury Association (ASIA) score of D on discharge, compared with 2 power, mRS 3.5 and ASIA B in those who did not. CONCLUSIONS: SCI can be severely disabling. Triple therapy with pentoxifylline, CSF drainage and HBOT may reduce disability and further prospective trials are required.

Effect of antiplatelet and/or anticoagulation medication on the risk of tympanic barotrauma in hyperbaric oxygen treatment patients, and development of a predictive model.

INTRODUCTION: Middle ear barotrauma (MEBt) is a common side effect of hyperbaric oxygen treatment (HBOT) and can result in pain, hearing loss, tinnitus and otorrhagia. The use of antiplatelet/anticoagulant drugs is thought to increase the risk and severity of MEBt during HBOT. METHODS: Single centre, retrospective observational cohort study of all patients treated with HBOT over a 4-year period (between 01 January 2015 to 31 December 2018) looking at the incidence of MEBt and the concurrent use of antiplatelet and/or anticoagulant drugs. MEBt was assessed by direct otoscopy of the tympanic membrane post-HBOT and scored using the modified Teed classification. Multivariate modelling assessed the relationship between antiplatelet and/or anticoagulation drug use, age, sex, and MEBt during HBOT. RESULTS: There was no evidence that antiplatelet and/or anticoagulation drugs increase the risk of tympanic barotrauma in HBOT patients. The prevalence of MEBt was higher in female patients than in males (χ2 P = 0.004), and increased with age (χ2 P = 0.048). No MEBt was recorded in patients undergoing recompression therapy for decompression sickness or cerebral arterial gas embolism. CONCLUSIONS: In this retrospective single-centre study, antiplatelet and/or anticoagulation drugs did not affect the risk of MEBt, but both age and sex did, with greater prevalence of MEBt among older patients and females compared with younger patients and males. A predictive model, requiring further validation, may be helpful in assessing the likelihood of MEBt in patients undergoing HBOT.

Cerebral arterial gas embolism proven by computed tomography following transthoracic echocardiography using bubble contrast.

A 75 year-old male developed features of an acute stroke following bubble contrast echocardiography, which was shown on emergent computed tomography scanning to be a result of cerebral arterial gas embolism (CAGE) to the left middle cerebral artery. Ischaemic stroke symptoms have previously been reported as a rare complication of bubble contrast echocardiography. Radiologically proven CAGE from bubble contrast echocardiography had not been reported at the time this case occurred. Immediate provision of 100% oxygen and administration of hyperbaric oxygen are recommended treatments for CAGE and were associated with a substantial recovery for this patient.

Fatal air embolism in a breath-hold diver.

Cerebral arterial gas embolism (CAGE) from breath-holding or inadequate exhalation during ascent is a well-recognised complication of scuba diving. It does not usually occur with breath-hold (BH) diving in those with normal lungs, as the volume of gas in the lungs on surfacing cannot exceed what it was on leaving the surface. However, a BH diver who breathes from a compressed gas supply at depth essentially becomes a scuba diver and is at risk of pulmonary barotrauma (PBt) and CAGE on ascent. In this case, a 26-year-old male experienced BH diver breathed from a scuba set at approximately 10 metres' sea water depth and ascended, sustaining massive PBt and CAGE with a fatal outcome. BH and scuba divers, especially those with less experience, need to be well-informed about this potential risk.

Association of microparticles and neutrophil activation with decompression sickness.

Decompression sickness (DCS) is a systemic disorder, assumed due to gas bubbles, but additional factors are likely to play a role. Circulating microparticles (MPs)--vesicular structures with diameters of 0.1-1.0 µm--have been implicated, but data in human divers have been lacking. We hypothesized that the number of blood-borne, Annexin V-positive MPs and neutrophil activation, assessed as surface MPO staining, would differ between self-contained underwater breathing-apparatus divers suffering from DCS vs. asymptomatic divers. Blood was analyzed from 280 divers who had been exposed to maximum depths from 7 to 105 meters; 185 were control/asymptomatic divers, and 90 were diagnosed with DCS. Elevations of MPs and neutrophil activation occurred in all divers but normalized within 24 h in those who were asymptomatic. MPs, bearing the following proteins: CD66b, CD41, CD31, CD142, CD235, and von Willebrand factor, were between 2.4- and 11.7-fold higher in blood from divers with DCS vs. asymptomatic divers, matched for time of sample acquisition, maximum diving depth, and breathing gas. Multiple logistic regression analysis documented significant associations (P < 0.001) between DCS and MPs and for neutrophil MPO staining. Effect estimates were not altered by gender, body mass index, use of nonsteroidal anti-inflammatory agents, or emergency oxygen treatment and were modestly influenced by divers' age, choice of breathing gas during diving, maximum diving depth, and whether repetitive diving had been performed. There were no significant associations between DCS and number of MPs without surface proteins listed above. We conclude that MP production and neutrophil activation exhibit strong associations with DCS.

Joint position statement on persistent foramen ovale (PFO) and diving. South Pacific Underwater Medicine Society (SPUMS) and the United Kingdom Sports Diving Medical Committee (UKSDMC).

This consensus statement is the result of a workshop at the SPUMS Annual Scientific Meeting 2014 with representatives of the UK Sports Diving Medical Committee (UKSDMC) present, and subsequent discussions including the entire UKSDMC. Right-to-left shunt across a persistent or patent foramen ovale (PFO) is a risk factor for some types of decompression illness. It was agreed that routine screening for PFO is not currently justifiable, but certain high risk sub-groups can be identified. Divers with a history of cerebral, spinal, inner-ear or cutaneous decompression illness, migraine with aura, a family history of PFO or atrial septal defect and those with other forms of congenital heart disease are considered to be at higher risk. For these individuals, screening should be considered. If screening is undertaken it should be by bubble contrast transthoracic echocardiography with provocative manoeuvres, including Valsalva release and sniffing. Appropriate quality control is important. If a shunt is present, advice should be provided by an experienced diving physician taking into account the clinical context and the size of shunt. Reduction in gas load by limiting depth, repetitive dives and avoiding lifting and straining may all be appropriate. Divers may consider transcatheter device closure of the PFO in order to return to normal diving. If transcatheter PFO closure is undertaken, repeat bubble contrast echocardiography must be performed to confirm adequate reduction or abolition of the right-to-left shunt, and the diver should have stopped taking potent anti-platelet therapy (aspirin is acceptable).

Acute kidney injury due to decompression illness.

Decompression illness is a rare but serious complication of diving caused by intravascular or extravascular gas bubble formation. We report the first case of acute kidney injury in a 27-year-old diver following three rapid ascents. He presented with transient neurological symptoms and abdominal pain followed by rapidly progressive acute kidney injury (creatinine peak 1210 µmol/L) due to arterial air emboli. He received supportive care and 100% oxygen followed by hyperbaric therapy and recovered fully. Arterial air emboli caused by rapid decompression can affect multiple organs including the kidneys. Early transfer to a hyperbaric unit is important as complications may present delayed.

Livedoid vasculopathy successfully treated with hyperbaric oxygen.

Livedoid vasculopathy is a painful, ulcerating condition of the lower legs, ankles and feet with the typical histological feature of hyalinising vascular change of dermal blood vessels with minimal inflammation. Therapeutic interventions have been diverse and varyingly successful. We report a biopsy-proven case in a 27-year-old male, which responded rapidly and completely to hyperbaric oxygen therapy. A few such cases have been reported previously, but only in dermatological journals, not in the hyperbaric medicine literature.

Comparison of venous glucose to finger-prick glucose in patients with diabetes under hyperbaric hyperoxic conditions: a pilot study.

INTRODUCTION: Blood glucose is commonly measured in diabetic patients undergoing hyperbaric oxygen treatment (HBOT) from a 'finger-prick' capillary sample. Although this method is an accurate reflection of venous glucose under normal conditions it has not been validated under hyperbaric, hyperoxic conditions. METHODS: Four patients with diabetes mellitus undergoing HBOT had venous blood samples drawn simultaneously with routine capillary samples before, during and immediately after three of four HBOT sessions. The Bland-Altman method of assessing agreement between these two measures was used separately for the three time periods. RESULTS: The relationship between venous and finger-prick glucose at room air was altered significantly by HBOT. The bias (finger-prick minus venous measurements) was significantly less than zero during the HBOT session but not immediately after completion of the session. Owing to the small sample size, the limits of agreement straddled zero at all time points, although the lower limit was close to zero during treatment (finger measurement appeared to be higher than venous measurement on room air and lower than venous undergoing HBOT). CONCLUSION: Finger-prick capillary sampling may not be an accurate reflection of venous glucose during HBOT.

Oxygen toxicity seizures: 20 years' experience from a single hyperbaric unit.

INTRODUCTION: Oxygen toxicity seizures (OTS) are a known complication of hyperbaric oxygen therapy (HBOT). The incidence of OTS has been variously reported and appears to be related to the duration and pressure of exposure in addition to individual susceptibility factors. METHOD: All OTS occurring in patients undergoing HBOT during the first 20 years of operation of the Fremantle Hospital Hyperbaric Medicine Unit were reviewed. RESULTS: During 41,273 HBOT in 3,737 patients, 25 OTS occurred; a rate of 0.06% (1/1,650 or 6 per 10,000) HBOT exposures. For the initial treatment of dysbarism with United States Navy Treatment Table 6, the rate was 0.56%. (4/714) and for the treatment of carbon monoxide (CO) poisoning was 0.18% overall but 0.49% for the first HBOT. There was an increasing OTS rate with increasing pressure with a statistically significant difference (P < 0.001) in OTS rate at 203 kPa or less versus > 203 kPa (OR 8.5, 95% confidence intervals (CI) 2.0 to 36.1), and for comparison of two commonly used pressures of 203 kPa versus 243 kPa (P = 0.028, OR 5.1, 95% CI 1.1 to 22.8), but not with first versus follow-up HBOT at 284 kPa for dysbarism (P = 0.061) nor CO (P = 0.142). CONCLUSIONS: This study reports all OTS in a single hyperbaric unit over a 20-year period, the longest observational study period yet reported for OTS during HBOT for all indications. The incidence of OTS in this study compares favourably to previously reported rates, and shows an increasing OTS rate with increasing pressure.

A double-blind, randomized trial of intravenous versus intramuscular antivenom for red-back spider envenoming.

OBJECTIVE: To compare the efficacy of intravenous versus intramuscular antivenom (AV) in the treatment of Red-back spider (RBS) envenoming. METHODS: Randomized, double-dummy, double-blind, multicentre trial of patients with red-back spider envenoming requiring AV treatment recruited from five hospital EDs in Western Australia. RESULTS: Thirty-five patients were recruited; two were excluded; 33 were available for initial analysis, but two who were unblinded after one ampoule of trial AV and given i.v. AV had limited data; 31 remained in the study and had more complete data. After AV, pain scores for both i.m. and i.v. groups improved rapidly. At 24 h, the i.v. group was better with a 55% absolute difference (76% vs. 21%; 95% CI 25-85% difference) in the proportion pain-free. There were no safety issues. CONCLUSIONS: Red-back spider antivenom was initially effective by both i.m. and i.v. routes. The study generates the hypothesis that at 24 h, significantly more patients are pain-free with i.v. administration. Definitive recommendations on the optimal route of administration of RBS AV await the results of further studies.