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Purpose: Pulmonary edema following hyperbaric oxygen (HBO2) therapy is a rare clinical phenomenon. This case report describes such a patient – a 56-year-old woman who suffered from severe pulmonary edema after HBO2 therapy for carbon monoxide (CO) poisoning.  Case: Patient experienced ecphysesis and dyspnea suddenly after HBO2 therapy (100% oxygen at 0.25 MPa, for 60 minutes with a five-minute air break and decompression at 0.01 MPa/minute). Post therapy her heart rate (HR), blood pressure (BP), respiratory rate (RR) and oxygen saturation (SO2) were 140 bpm, 60/40 mmHg,  38 bpm and 84%, respectively. Diagnoses of acute pulmonary edema and shock were made.  Various treatments including antishock, tracheal intubation, mechanical ventilation for respiratory support, a diuretic, dexamethasone, asthma relief, and acidosis correction were administered. Pulmonary computed tomography (CT) indicated significant pulmonary edema. Due to active treatment, the patient showed gradual improvement. Pulmonary CT re-examination showed pulmonary edema markedly improved. At the two-year follow-up, the patient reported no abnormal mental or neurological symptoms.  Conclusion: Acute pulmonary edema is rare but can lead to serious side effects of HBO2 therapy in patients with severe acute CO poisoning. This complication must be must considered when administering HBO2 therapy to patients with severe CO poisoning. DOI: 10.22462/5.6.2017.11

Purpose: Pulmonary edema following hyperbaric oxygen (HBO2) therapy is a rare clinical phenomenon. This case report describes such a patient – a 56-year-old woman who suffered from severe pulmonary edema after HBO2 therapy for carbon monoxide (CO) poisoning. Case: Patient experienced ecphysesis and dyspnea suddenly after HBO2 therapy (100% oxygen at 0.25 MPa, for 60 minutes with a five-minute air break and decompression at 0.01 MPa/minute). Post therapy her heart rate (HR), blood pressure (BP), respiratory rate (RR) and oxygen saturation (SO2) were 140 bpm, 60/40 mmHg, 38 bpm and 84%, respectively. Diagnoses of acute pulmonary edema and shock were made. Various treatments including antishock, tracheal intubation, mechanical ventilation for respiratory support, a diuretic, dexamethasone, asthma relief, and acidosis correction were administered. Pulmonary computed tomography (CT) indicated significant pulmonary edema. Due to active treatment, the patient showed gradual improvement. Pulmonary CT re-examination showed pulmonary edema markedly improved. At the two-year follow-up, the patient reported no abnormal mental or neurological symptoms. Conclusion: Acute pulmonary edema is rare but can lead to serious side effects of HBO2 therapy in patients with severe acute CO poisoning. This complication must be must considered when administering HBO2 therapy to patients with severe CO poisoning. DOI: 10.22462/5.6.2017.10

A 57-year-old woman was admitted to the intensive care unit in a state of severe hypotensive shock following a session of hyperbaric oxygen (HBO2) therapy. Shock was attributed to gastric barotrauma, which resulted in a massive venous gas embolism. Gastric barotrauma was attributed to the presence of a filled gastric band/cuff during the HBO2 therapy that prevented expanding gas from escaping on decompression.  After deflation of the gastric band, two additional HBO2 sessions were performed and resulted in complete symptom resolution. Vasoactive drugs could be weaned, and the patient was discharged from hospital on Day Three with complete symptom resolution. Given the risk of gastric barotrauma and venous gas embolism, physicians should be aware of gastric band history before HBO2 therapy. DOI: 10.22462/5.6.2017.9

Introduction: In Yucatán, Mexico, during the sea cucumber season fishermen dive intensely to obtain good catches but are often at risk of decompression sickness (DCS). We present a single case fatality.  Objective: We analyzed the clinical course, medical assessment and recompression treatment plan of an untrained fisherman.  Case report: A 35-year-old male ascended rapidly using compressed-air diving. Before reaching the coast, he reported dizziness, shortness of breath, and pain in the abdomen and legs. Three hours later, when symptoms worsened, he went to the hospital. He was admitted with increased osteotendinous reflexes and cutis marmorata in the abdomen. The patient was diagnosed with carbon monoxide (CO) poisoning and Type I DCS, receiving the U.S. Navy Treatment Table 5 (USN TT5). Before completing his treatment at depth, he developed myocardial infarction and died. The death certificate indicated Type I DCS, thrombotic pulmonary embolism and cardiac arrest.  Discussion: Upon reviewing his medical records, we uncovered no evidence to support the diagnosis of CO poisoning and thrombotic pulmonary embolism. The clinical presentation seems to be compatible with a serious decompression insult, not a Type I hit. Based on the information gathered, it seems likely that the patient died as a result of cardiopulmonary DCS. This case report suggests a need to provide fishermen divers in ..

Introduction: Indocyanine green fluorescent angiography (ICFA), commonly used to assess vascularity in patients with non-healing lower extremity wounds, is emerging as a useful adjunct for hyperbaric oxygen (HBO2) therapy patients. We describe the use of ICFA to measure vascularity and help tailor an appropriate HBO2 regimen in a patient with breast soft tissue radiation necrosis (STRN). Case report: A 67-year-old female with a history of right breast cancer treated two years previously with lumpectomy and radiation therapy (6200 cGy), developed open wounds in the right breast. A diagnosis of STRN was established; the patient completed 20 HBO2 treatments, followed by surgical closure of the right breast wounds. Intraoperative ICFA demonstrated a focal area of hypovascularity at the medial margin of the incision. Due to a concern of suboptimal vascularity, the patient returned for additional HBO2 treatments. ICFA was performed after eight post-operative HBO2 treatments, and showed improved vascularity in the previously identified area of concern. Discussion: Studies of patients previously irradiated for head and neck cancer suggest that HBO2-induced vascularity is apparent after approximately eight HBO2 treatments and peaks around 20 treatments. The results from this case indicate that the doses of HBO2 needed for adequate neovascularization in patients with STRN may be variable. Conclusion: The ..

Traumatic brain injury (TBI) may cause persistent cognitive dysfunction. A pilot clinical study was performed to determine if hyperbaric oxygen (HBO2) treatment improves cognitive performance. It was hypothesized that stem cells, mobilized by HBO2 treatment, are recruited to repair damaged neuronal tissue. This hypothesis was tested by measuring the relative abundance of stem cells in peripheral blood  and cognitive performance during this clinical trial. The subject population consisted of 28 subjects with persistent cognitive impairment caused by mild to moderate TBI suffered during military deployment to Iraq or Afghanistan. Fluorescence-activated cell sorting (FACS) analysis was performed for stem cell markers in peripheral blood and correlated with variables resulting from standard tests of cognitive performance and post-traumatic stress disorder: ImPACT, BrainCheckers and PCL-M test results. HBO2 treatment correlated with stem cell mobilization as well as increased cognitive performance. Together these results support the hypothesis that stem cell mobilization may be required for cognitive improvement in this population.  DOI: 10.22462/5.6.2017.6

This paper presents the replacement of a traditional wired communication link of the hyperbaric chambers with a wireless ZigBee-based system. This move allows a reduction in the costs of seals capable of withstanding the internal pressures and gives rise to a more versatile system. The new system is able to capture and process individual vital signs like the electrocardiography signal, and other analog sources, sending the data to an external computer and allowing analysis, representation and sharing with medical staff. This system solves such problems as the attenuation of the signal produced by the metal walls of the hyperbaric chamber and has a coverage area large enough to manage up to six patients with an effective data rate conversion of 2kHz. Furthermore, a battery-based and multiparameter platform is designed for multipatient hyperbaric chambers. DOI: 10.22462/5.6.2017.5

Objective: To explore the effect and mechanism of hyperbaric oxygen (HBO2) therapy of open tibial fractures in rabbits after transient seawater immersion. Methods: Forty-eight (48) New Zealand rabbits were randomly and averagely divided into an HBO2 therapy group (Group A) and a control group (Group B). All rabbits were subjected to unilateral open tibial fractures, while immersed in artificial seawater (20-22 °C) for three hours prior to debridement and external fixation. Group A was treated with HBO2 at 2 atmospheres absolute (ATA) for 50 minutes once daily for two weeks; Group B received postoperative routine treatments only. The fracture zone in each group was compared by radiological, histological and immunohistochemical examinations. Results: In Group A, bony callus and mature osteocytes without infiltration of inflammatory cells were observed in the fracture zone. Vascular endothelial growth factor (VEGF) was expressed mainly in the cytoplasm of osteoblasts, chondrocytes and osteocytes, and exhibited significant changes at different time points. The gray value of bony callus in Group A was 190.58 ± 7.52; that of Group B was 144 ± 8.11. Difference between the groups was statistically significant (P<0.01). The content of malondialdehyde (MDA) in Group A was significantly lower than Group B (P<0.01), and the activity of superoxide dismutase (SOD) ..

Purpose: To determine the effects of a blockade of nitric oxide (NO) synthesis on hyperbaric oxygen (HBO2) therapy during cyanide (CN) intoxication. Methods: 39 anesthetized female Sprague-Dawley rats were exposed to CN intoxication (5.4 mg/kg intra-arterially) with or without previous nitric oxide synthase (NOS) inhibition by L-NG-nitroarginine methyl ester (L-NAME) injection (40 mg/kg intraperitoneally). Subsequently, either HBO2 therapy (284 kPa/90 minutes), normobaric oxygen therapy (100% oxygen/90 minutes) or nothing was administered. Intracerebral microdialysis was used to measure the interstitial brain concentration of lactate, glucose, glycerol and lactate/pyruvate ratios.  Results: L-NAME potentiated CN intoxication by higher maximum and prolonged lactate (in mM: 0. 5+/- 0.3 vs. 0.7 +/- 0.4, P < 0.005) concentrations compared with solely CN-intoxicated rats. The same trend was found for mean glucose, glycerol and lactate/pyruvate ratio levels.During HBO2 treatment a sustained reduction occurred in mean lactate levels (in mM: 0.5 +/- 0.5 vs. 0.7 +/- 0.4, P < 0.01) regardless of NOS blockade by L-NAME. The same trend was found for mean glucose and glycerol levels. Conclusion: The results suggest that blocking NOS using L-NAME can worsen acute CN intoxication. HBO2 treatment can partially overcome this block and continue to ameliorate CN intoxication. DOI: 10.22462/5.6.2017.3

The venous bubble load in the body after diving may be used to infer risk of decompression sickness (DCS). Retrospective analysis of post-dive bubbling and DCS was made on seven studies. Each of these investigated interventions, using an 18 meters of sea water (msw) air dive profile from Royal Navy Table 11 (Mod Air Table), equivalent to the Norwegian Air tables.  A recent neurological DCS case suggested this table was not safe as thought. Two-hundred and twenty (220) man-dives were completed on this profile. Bubble measurements were made following 219 man-dives, using Doppler or 2D ultrasound measurements made on the Kisman-Masurel and Eftedal-Brubakk scales, respectively.  The overall median grade was KM/EB 0.5 and the overall median maximum grade was KM/EB 2. Two cases of transient shoulder discomfort (“niggles”) were observed (0.9% (95% CL 0.1% – 3.3%)) and were treated with surface oxygen. One dive, for which no bubble measurements were made, resulted in a neurological DCS treated with hyperbaric oxygen. The DCS risk of this profile is below that predicted by models, and comparison of the cumulative incidence of DCS of these data to the large dataset compiled by DCIEM [1, 2], show that the incidence is lower than might be expected. DOI: 10.22462/5.6.2017.2

Carbon dioxide (CO2) retention, or hypercapnia, is a known risk of diving that can cause mental and physical impairments leading to life-threatening accidents. Often, such accidents occur due to elevated inspired carbon dioxide. For instance, in cases of CO2 elimination system failures during rebreather dives, elevated inspired partial pressure of carbon dioxide (PCO2) can rapidly lead to dangerous levels of hypercapnia. Elevations in PaCO2 (arterial pressure of CO2) can also occur in divers without a change in inspired PCO2. In such cases, hypercapnia occurs due to alveolar hypoventilation. Several factors of the dive environment contribute to this effect through changes in minute ventilation and dead space. Predominantly, minute ventilation is reduced in diving due to changes in respiratory load and associated changes in respiratory control. Minute ventilation is further reduced by hyperoxic attenuation of chemosensitivity. Physiologic dead space is also increased due to elevated breathing gas density and to hyperoxia. The Haldane effect, a reduction in CO2 solubility in blood due to hyperoxia, may contribute indirectly to hypercapnia through an increase in mixed venous PCO2. In some individuals, low ventilatory response to hypercapnia may also contribute to carbon dioxide retention. This review outlines what is currently known about hypercapnia ..