Spinal cord decompression sickness in an inside attendant after a standard hyperbaric oxygen treatment session

2021 ◽  
Vol 51 (1) ◽  
pp. 103-106
Author(s):  
Jacek Kot ◽  
◽  
Ewa Lenkiewicz ◽  
Edward Lizak ◽  
Piotr Góralczyk ◽  
...  

Medical personnel in hyperbaric treatment centres are at occupational risk for decompression sickness (DCS) while attending patients inside the multiplace hyperbaric chamber (MHC). A 51-year-old male hyperbaric physician, also an experienced diver, was working as an inside attendant during a standard hyperbaric oxygen therapy (HBOT) session (70 minutes at 253.3 kPa [2.5 atmospheres absolute, 15 metres’ seawater equivalent]) in a large walk-in MHC. Within 10 minutes after the end of the session, symptoms of spinal DCS occurred. Recompression started within 90 minutes with an infusion of lignocaine and hydration. All neurological symptoms resolved within 10 minutes breathing 100% oxygen at 283.6 kPa (2.8 atmospheres absolute) and a standard US Navy Treatment Table 6 was completed. He returned to regular hyperbaric work after four weeks of avoiding hyperbaric exposures. Transoesophageal echocardiography with a bubble study was performed 18 months after the event without any sign of a persistent (patent) foramen ovale. Any hyperbaric exposure, even within no-decompression limits, is an essential occupational risk for decompression sickness in internal hyperbaric attendants, especially considering the additional risk factors typical for medical personnel (age, dehydration, tiredness, non-optimal physical capabilities and frequent problems with the lower back).

2019 ◽  
Vol 9 (4) ◽  
pp. 235-238
Author(s):  
Altaf Saadi ◽  
Emily A. Ferenczi ◽  
Haatem Reda

Decompression sickness from diving is a rare but potentially reversible cause of spinal injury. Early treatment with hyperbaric oxygen is associated with a better neurologic outcome, making prompt recognition and management clinically important. We describe a case of a 65-year-old diver who presented with thoracic back pain and bilateral leg weakness after a 70 feet of sea water (fsw) (21 meters of sea water [msw]) dive, with no acute abnormality on spinal magnetic resonance imaging (MRI). He made a partial recovery after extended hyperbaric oxygen therapy. We discuss the epidemiology and pathophysiology of central nervous system injury in decompression sickness, as well as acute management and prognostic factors for recovery, including the role of adjunctive therapies and the implications of negative MRI. Ultimately, clinicians should make the diagnosis of spinal cord decompression sickness based primarily on clinical evaluation, not on MRI findings.


2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.


2019 ◽  
pp. 55-61
Author(s):  
Owen J. O’Neill ◽  
Elizabeth Smykowski ◽  
Jo Ann Marker ◽  
Lubiha Perez ◽  
drah Gurash ◽  
...  

Introduction: Eustachian tube dysfunction (ETD) and middle ear barotrauma (MEB) are the most common adverse effects of hyperbaric oxygen (HBO2) treatments. Patients practice equalization maneuvers to prevent ETD and MEB prior to hyperbaric exposure. Some patients are still unable to equalize middle ear pressure. This ETD results in undesirable consequences, including barotrauma, treatment with medications or surgical myringotomy with tube placement and interruption of HBO2. When additional medications and myringotomy are employed, they are associated with additional complications. Methods: A device known as the Ear Popper® has been reported to reduce complications from serous otitis media and reduce the need for surgical interventions (myringotomy). Patients unable to equalize middle ear pressure during initial compression in the hyperbaric chamber were allowed to use the device for rescue. All hyperbaric treatments were compressed using a United States Navy TT9, or a 45-fsw hyperbaric treatment schedule. Patients with persistent ETD and the inability to equalize middle ear pressure were given the Ear Popper upon consideration of terminating their treatment. Results: The Ear Popper allowed all patients to successfully equalize middle ear pressure and complete their treatments. Conclusion: This study substantiates the use of this device to assist in allowing pressurization of the middle ear space in patients otherwise unable to achieve equalization of middle ear pressure during HBO2 treatment in a multiplace chamber.


2019 ◽  
pp. 81-85
Author(s):  
Se Hyun Oh ◽  
◽  
Hui Dong Kang ◽  
Sang Ku Jung ◽  
Sangchun Choi ◽  
...  

Decompression sickness is a disease caused by abrupt pressure change and presents various symptoms. To date, acute kidney injury associated with decompression sickness has been reported frequently, but there is no report of hepatic infarction associated with decompression sickness. We report a case of acute kidney injury and acute hepatic infarction treated with hyperbaric oxygen (HBO2) therapy and dialysis in a patient with severe decompression sickness after work diving.


2021 ◽  
pp. 287-295
Author(s):  
Ya Li ◽  
◽  
Xiaona Xu ◽  
Junxiang Bao Bao ◽  
Wenlan Wang ◽  
...  

Objective: Decompression sickness (DCS) causes serious brain hypoxic-ischemic injury. This experiment was designed to observe whether hyperbaric oxygen (HBO2) pretreatment played a neuroprotective effect in decompression sickness rat models and to explore the mechanism of protective effects. Methods: Sprague-Dawley (SD) male rats were pretreated with HBO2 and then underwent decompression to establish the DCS rat model. Antioxidant capacities were evaluated by detecting peroxides (GPx), superoxide dismutase (SOD), catalase (CAT) activity and malondialdehyde (MDA) content in brains. The levels of metal elements manganese (Mn), zinc (Zn), iron (Fe) and magnesium (Mg) in brain tissues were assessed by flame atomic absorption spectrometry. Necrosis and apoptosis of neurons were assessed by H-E staining and immunohistochemical staining. Results: HBO2 pretreatment reduced the degree of necrosis and apoptosis in brain tissues of decompression sickness rat models. In addition, HBO2 pretreatment increased GPx, SOD and CAT activities and reduced MDA accumulation. It also increased the content of Mn, Zn, Fe and Mg in brain tissue, which are all related to free radical metabolism. Conclusion: These results suggested that HBO2 pretreatment has protective effects on brain injury of rats with decompression sickness. The mechanism of the protective effects may be related to reducing oxidative damage by affecting metal elements in vivo.


Author(s):  
Retno Budiarti ◽  
Siti Qamariyah Khairunisa ◽  
Nasronudin ◽  
Kuntaman ◽  
Guritno

Cellular immune has an important role in response HIV infection, which is attack the infected cells to activate signaling molecule. Hyperbaric Oxygen (HBO) worked as complementary treatment for HIV infection. The production of ROS and RNS molecules during hyperbaric exposure can affect gene expression which contributes to cellular adaptative response. This study was conducted to explore the mechanisms of cellular adaptive response to HIV infection during hyperbaric exposure. This study was carried on in vitro using healthy volunteers’ PBMCs (Peripheral Blood Mononuclear Cells) cultures infected with HIV-1. The study was conducted as a post- test only group design. The experimental unit was PBMC from venous blood of healthy volunteers which were cultured in vitro and infected by co-culturing with HIV-1 in MT4 cell line. The experimental unit consist of treatment and control group. Each group examined the expression of transcription factor NFκB, Interferon α, reverse transcriptase inhibitors (p21), and the amount of HIV-1 p24 antigen. There were increasingly significant differences in the expression of the trancription factor of NFκB, p21, and HIV-1 p24 antigen,as well as mRNA transcription of interferon α2 between treatment and controlgroup. By decreasing p24 antigen showed that HBO exposure was able to suppress HIV-1 replication. The exposure to hyperbaric oxygen at the pressure of 2.4 ATAand 98% oxygen wasable to produce ROS and RNS molecules, which play a role in cellular adaptive responses through increasing the expression of nfĸb, p21 and mRNA of interferon α2 plays a role in inhibition mechanism of HIV-1 replication in cells.


2019 ◽  
Vol 7 (11) ◽  
pp. 2231-2234
Author(s):  
Sami Ullah ◽  
Ahmad Zaheer Qureshi ◽  
Kholoud Kedowah ◽  
Afnan AlHargan ◽  
Asim Niaz

2008 ◽  
Vol 79 (12) ◽  
pp. 1112-1116 ◽  
Author(s):  
Emmanuel Gempp ◽  
Jean-Eric Blatteau ◽  
Eric Stephant ◽  
Jean-Michel Pontier ◽  
Pascal Constantin ◽  
...  

2018 ◽  
Vol 65 (4) ◽  
pp. 7-24
Author(s):  
Ryszard Kłos

Abstract Recently, the Polish Navy has extended its capability for the implementation of underwater works with autonomous dives conducted beyond the saturation zone to a depth of 80 mH2O. In the near future it is also planned to introduce long-term dives within typical depths of the saturation plateau. One of the activities resulting from the analysis of the risk associated with the extension of these competences is the need to conduct a critical review of the system for securing hyperbaric treatment of cases of decompression sickness1.


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