Undersea and Hyperbaric Medicine最新文献

Sudden sensorineural hearing loss (SSNHL) presents as the abrupt onset of hearing loss. Approximately 88% of SSNHL has no identifiable etiology and is termed idiopathic sudden sensorineural hearing loss (ISSHL). Hearing specialists have investigated ISSHL since the 1970s. Over the past 30 years, more than 800 articles, or one every two weeks, have been published in the English medical literature. ISSHL is the abrupt onset of hearing loss, usually unilaterally and upon wakening, that involves a hearing loss of at least 30 decibels (dB) occurring within three days over at least three contiguous frequencies. As most patients do not present with premorbid audiograms, the degree of hearing loss is usually defined by the presentation thresholds of the unaffected ear. Other associated symptoms include tinnitus, aural fullness, dizziness and vertigo. The historical incidence of ISSHL ranges from 5-20 cases/100,000 population, with approximately 4,000 new cases per annum in the United States. The true incidence is thought to be higher, as ISSHL is thought to be underreported. Interestingly, 4,000 cases annually calculate to 1.3 cases/ 100,000 in the United States; therefore, an incidence of 5-20/100,000 would translate to > 15,000 new ISSHL cases per annum in the United States. Recent literature has placed the annual ISSHL incidence in the United States as 27 cases/100,000, with a pediatric incidence of 11 cases/100,000. Other studies report that the incidence is increasing (160/100,000), especially in the elderly (77/100,000), and conclude that ISSHL is no longer rare. In 1984, Byl reviewed the literature and found the mean age of ISSHL presentation to be 46-49 years, with variation of incidence with age and an equal gender distribution. The presentation of ISSHL does not appear to have seasonal variations, uneven distributions of presentation throughout the year, or an association with upper respiratory infections, either prior to or following symptom onset. The spontaneous recovery is currently thought to be 30-60%.

Introduction: Arterial vascular occlusion is a rare complication of dermal filler injection. This case report describes the successful use of hyperbaric oxygen therapy in a patient with vascular occlusion after a permanent dermal filler was injected.

Case report: A 51-year-old woman underwent an injection of non-resorbable polymethylmethacrylate microspheres into her nasolabial folds. Several hours later, she experienced dusky discoloration of the right nasolabial fold and surrounding livedo skin changes, consistent with vascular occlusion. Treatment with warm compresses and topical nitroglycerin was initiated, and the patient was referred for hyperbaric oxygen therapy. The tissue discoloration improved significantly after the administration of six hyperbaric treatments.

Discussion: While hyaluronidase is recognized as a treatment option for vascular occlusion associated with using temporary fillers containing hyaluronic acid, it may also be beneficial for patients who experience vascular occlusion after administration of permanent fillers. Hyperbaric oxygen therapy, which results in hyperoxygenation of ischemic tissue and mitigation of the associated inflammatory response, may also benefit patients who experience vascular occlusion after permanent filler injection.

Conclusions: Administration of hyaluronidase and hyperbaric oxygenation should be considered for patients who develop arterial occlusions after dermal filler placement, regardless of the type of injected filler.

This report details a case study of a non-smoking 33-year-old female nurse who developed occupational asthma as an Inside Attendant (IA) in a hyperbaric chamber. The report analyzes the nurse's medical history, working environment, and potential causes. After beginning work in the hyperbaric chamber, an IA experienced respiratory symptoms, including coughing, wheezing, and fatigue. Her symptoms improved during a break attending a hyperbaric nursing certification program but returned when she resumed work in the IA hyperbaric chamber. Spirometry confirmed airflow obstruction, and the IA was subsequently diagnosed with occupational asthma. As a result, the IA had to terminate their employment in the hyperbaric chamber. The literature review indicates that diving and hyperbaric exposure can negatively affect respiratory function, particularly in individuals susceptible to respiratory issues. We emphasize the necessity for further research on the effects of hyperbaric exposure on the respiratory system of IAs.

Arieli has previously demonstrated that the exposure metric K could be used to predict pulmonary oxygen toxicity (POT) based on changes in Vital Capacity (VC). Our previous findings indicate that the Equivalent Surface Oxygen Time (ESOT) allows the estimation of POT without loss of accuracy compared to K. In this work, we have further investigated POT recovery. The K metric assumes that the recovery of POT is to be controlled by exposure to pO₂. This results in a counterintuitively slow estimated recovery after exposure to low pO₂. Similarly, K overestimates POT during intermittent hyperoxic exposures. We used results from previous studies to train the parameters of a new ESOT recovery model. The predicted recovery of ESOT (ESOT_rec) after initial hyperoxic exposure (ESOT_I) of duration t_exp (h) and recovery time t (h) can be calculated as ESOT_rec=ESOT_I · e^-f with f=0.439 · t · 0.906^t_exp. For intermittent exposures, the function ESOT(n)=(n · a · ln(b · n+1)+c) · t_exp · pO₂^2.285 will approximate POT (ESOT(n)) after n sessions of pO₂ (atm) for time t_exp (min) in each cycle. Parameters a, b, and c are specific for each cycling pattern. These ESOT functions will better predict the development of POT during intermittent hyperoxic exposures as well as recovery after a broader range of continuous hyperoxic exposures than K. We recommend limiting hyperoxic exposures in surface-oriented diving to ESOT=660, 500, and 450 for a maximum of one, five, and seven consecutive days, respectively. A minimum of 48 hours of recovery should follow. These limits can probably be relaxed for intermittent exposures.

Objective: To determine the outcomes of patients receiving hyperbaric oxygen therapy for sudden sensorineural hearing loss and the impact of patient comorbidities on outcomes.

Study design: Retrospective chart review.

Setting: Tertiary referral center.

Methods: All patients over 18 diagnosed with sudden sensorineural hearing loss between 2018 and 2021 who were treated with hyperbaric oxygen therapy were included. Demographic information, treatment regimens and duration, and audiometric and speech perception outcomes were recorded and analyzed.

Results: 19 patients were included. The median age was 45 years. 53% were female and 21% had pre- existing rheumatologic disorders. The mean duration between hearing loss onset and physician visits was 9.6 days. All patients received an oral steroid course, while 95% also received a median of 3 intratympanic steroid injections. Patients began hyperbaric oxygen therapy an average of 34.2 days after the hearing loss onset for an average of 13 sessions. No significant relationships were found between patient comorbidities and outcomes. Of those who reported clinical improvement, 57% demonstrated complete recovery per Siegel's criteria. There was significant improvement after hyperbaric oxygen therapy for pure tone averages (50.3dB vs. 36.0dB, p<0.01) and word discrimination scores (73% vs 79%, p<0.05) for all patients regardless of reported clinical improvement.

Conclusion: Hyperbaric oxygen therapy, as an adjunct to steroids, significantly improves recovery from sudden sensorineural hearing loss. The Charlson comorbidity index was not significantly associated with patient outcome, but patients with rheumatologic disorders were less likely to respond. Differentiating the natural history of the disease from hyperbaric oxygen therapy-associated improvements remains a challenge.

The term "intracranial abscess" (ICA) includes cerebral abscess, subdural empyema, and epidural empyema, which share many diagnostic and therapeutic similarities and, frequently, very similar etiologies. Infection may occur and spread from a contiguous infection such as sinusitis, otitis, mastoiditis, or dental infection; hematogenous seeding; or cranial trauma. Brain abscess usually results from predisposing factors such as HIV infection, immunosuppressive drug treatment, surgery, adjacent infection (i.e., mastoiditis, sinusitis, dental infection), or systemic infection causing bacteremia. Approximately 30% to 50% of infections are caused by contiguous spread of local infections. Hematogenous spread is responsible in around a third of cases, with the mechanism for the remainder not identifiable.

Objective: To investigate the effect of 6 ATA air/ oxygen treatment scheme and 2.8 ATA oxygen inhalation scheme on cerebral gas embolism.

Methods: 29 patients with cerebral gas embolism admitted from January 2014 to June 2022 were retrospectively included. The patients were divided into 6 ATA air/ oxygen treatment scheme group (14 cases) and 2.8 ATA oxygen inhalation therapy scheme group (15 cases). Glasgow Coma Scale (GCS) was used to evaluate the therapeutic effect before and after treatment. The effective standard of treatment: recovery of consciousness (GCS scores>8).

Results: There was no significant difference between two groups in terms of gender, age, cause of disease, time of onset and GCS score before treatment (P>0.05). There was not significant difference between two groups in terms of GCS score after 1 day and 1 week of treatment (P>0.05). After 1 week of treatment, 78.6% (11/14) of patients in the 6 ATA group and 80.0% (12/15) in the 2.8 ATA group improved.

Conclusion: The 2.8 ATA oxygen inhalation scheme can effectively treat cerebral gas embolism, and effect is similar to the 6 ATA air/ oxygen treatment scheme.

The assessment of rectal temperature and behavior is an important parameter in all patients for whom hyperbaric oxygen (HBO₂) therapy is used. The study aims to verify if there is less reduction in body temperature after HBO₂ therapy in restless patients and their behavior during the therapeutic session. Clinical data from 217 HBO₂ therapy sessions with 2 to 2,5 atmospheres absolute (ATA) were reviewed under therapy protocols of 30 (P1) or 45 (P2) minutes, covering 29 canines and 13 felines. Behavioral data, initial rectal temperature (iRT), final (fRT), and variation between them (RTv) of each patient were recorded. Parameters of oxygen concentration, humidity, temperature, and chamber flow rate were also recorded. Three of 217 patients experienced major adverse effects (seizure and auto-trauma). 144/217 HBO₂ therapy session records were selected for statistical analysis. In P1 sessions, 33.3% of the canine and 33.3% of the feline patients were restless. In P2 sessions, 40.7% of the canine and 28.1% of the feline patients were restless. The study did not observe a correlation between vRT and patients' behavior (p> 0.089) or differences in vRT between quiet and restless patients. There was a difference between iRT and fRT only in canines submitted to P1 (p<0.001) and felines submitted to P2 (p<0.001). Older canine patients were more restless than young canine patients at P1 (p= 0.02). We conclude that there may be a reduction in the fRT of dogs and cats submitted to 2 ATA for 30 minutes and 2.5 ATA for 45 minutes, respectively.

Introduction: Submersion results in blood redistribution into the pulmonary circulation, causing changes in pulmonary compliance and increased cardiac preload. Few studies have compared incremental exercise to exhaustion (VO₂ max testing) in a dry environment with exercise underwater. We hypothesized that the physiological effects of submersion would result in lower heart rate (HR), minute ventilation (V_E), and peak oxygen uptake (VO₂ peak) compared with dry conditions.

Methods: Fourteen male and four female volunteers completed two VO₂ peak testing sessions with approximately two hours between trials: first in the dry laboratory on a cycle ergometer and second while fully submersed in a prone position with zero static lung load. HR was monitored via ECG, and inspiratory and expiratory gas compositions were recorded using a metabolic cart. The tests were terminated once the subject reached exhaustion.

Results: Absolute VO₂ peak was lower in the submersed VO₂ max trial (37.1 ± 7.0 mL•kg^-1•min^-1) compared with dry exercise (45.8 ± 8.9 mL•kg^-1•min^-1) p < 0.001. HR and V_E were also lower in the submersed trial.

Conclusions: VO₂ peak while submersed is reduced relative to dry VO₂ peak, which may be partly due to a decrease in heart rate and a reduction in V_E.

Despite established exposure limits and safety standards, and the availability of carbon monoxide (CO) alarms, each year an estimated 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO or from longer exposures to lower levels. If the CO exposure is sufficiently high, unconsciousness and death occur quickly, and without symptoms. With non-lethal exposures to CO, common symptoms include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath, and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often develop brain injury. As with brain injury from non- CO causes such as traumatic brain injury, the clinical expression of brain injury caused by CO poisoning includes the domains of cognition, affect, neurological, and somatic. Common problems are neurological: imbalance, motor weakness, neuropathies, hearing loss, tinnitus, Parkinson's-like syndrome, vestibular, gaze, auditory processing, cognitive, anxiety and depression, posttraumatic stress, personality change, persistent headaches, dizziness, sleep problems, and others. In addition, some will have cardiac or other problems. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO₂) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by CO-induced adduct formation of myelin basic protein. Based upon supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO₂ should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation.