Decompression-Related Disorders: Decompression Sickness, Arterial Gas Embolism, and Ebullism Syndrome

2008 ◽  
pp. 223-246 ◽  
Author(s):  
William T. Norfleet
Keyword(s):  
Decompression Sickness ◽  
Gas Embolism ◽  
Arterial Gas Embolism

scholarly journals Surfactant reduction of cerebral infarct size and behavioral deficit in a rat model of cerebrovascular arterial gas embolism

2013 ◽  
Vol 115 (6) ◽  
pp. 868-876 ◽  
Author(s):  
David M. Eckmann ◽  
Stephen C. Armstead
Keyword(s):  
Morris Water Maze ◽  
Rat Model ◽  
Water Maze ◽  
Decompression Sickness ◽  
Infarct Volume ◽  
Neurological Dysfunction ◽  
Morris Water Maze Test ◽  
Placement Test ◽  
Gas Embolism ◽  
Arterial Gas Embolism

Gas embolism occurs commonly in cardiac and vascular surgery and decompression sickness. The goals of this study were to develop a new in vivo rat model of cerebrovascular arterial gas embolism and to determine the effects of exogenous surfactants on resultant brain infarct volume and accompanying long-term neurological dysfunction using the model. Unilateral cerebral arterial gas embolism was induced in Sprague Dawley rats, including groups receiving intravenous Pluronic F-127 (PF-127) and Oxycyte perflourocarbon surfactant pretreatment. Magnetic resonance imaging (MRI) was performed at 24 and 72 h postembolism to determine infarct volume. The elevated body swing test (EBST), limb-placement test, proprioception forelimb and hindlimb tests, whisker tactile test, and Morris Water Maze test were performed to assess motor behavior, somatosensory deficit, and spatial cognitive function out to 29 days after embolization. A stable stroke model was developed with MRI examination revealing infarction in the ipsilateral cerebral hemisphere. Gas embolized rats had significant cognitive and sensorimotor dysfunction, including approximately threefold increase in Morris Water Maze latency time, ∼20% left-sided biasing in EBST performance, 0.5 to 1.5 (mean) point score elevations in the proprioception and whisker tactile tests, and 3.0 point (mean) elevation in the limb-placement test, all of which were persistent throughout the postembolic period. Surfactant prophylaxis with either PF-127 or Oxycyte rendered stroke undetectable by MRI scanning and markedly reduced the postembolic deficits in both cognitive and sensorimotor performance in treated rats, with normalization of EBST and whisker tactile tests within 7 days.

Arterial Gas Embolism and Decompression Sickness

Physiology ◽  
2002 ◽  
Vol 17 (2) ◽  
pp. 77-81 ◽  
Author(s):  
Tom S. Neuman
Keyword(s):  
Gas Phase ◽  
Decompression Sickness ◽  
Ambient Pressure ◽  
The Body ◽  
Pulmonary Vasculature ◽  
Gas Embolism ◽  
Pulmonary Barotrauma ◽  
Arterial Gas Embolism ◽  
Underlying Pathophysiology

Decompression sickness occurs when a sufficiently large gas phase forms within the tissues of the body after a reduction in ambient pressure. Arterial gas embolism occurs secondary to pulmonary barotrauma when gas is forced into the pulmonary vasculature. Although they may clinically present in a similar fashion, the underlying pathophysiology of the two conditions is quite different.

Hyperbaric treatment of air or gas embolism: current recommendations

2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  
Keyword(s):  
Animal Studies ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Endothelial Damage ◽  
Neurological Deficits ◽  
Breath Hold ◽  
Gas Embolism ◽  
Hyperbaric Treatment ◽  
Pulmonary Capillaries ◽  
Venous Gas Embolism

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.

Accuracy of a SET of Screening Parameters Developed for the Diagnosis of Arterial Gas Embolism: The SANDHOG Criteria

2015 ◽  
Vol 49 (5) ◽  
pp. 792-798
Author(s):  
Stephen R. Hayden ◽  
Kevin C. Buford ◽  
Edward M. Castillo
Keyword(s):  
Gas Embolism ◽  
Arterial Gas Embolism

Iatrogenic Arterial Gas Embolism From Esophagogastroduodenoscopy

2019 ◽  
Vol 57 (5) ◽  
pp. 683-688
Author(s):  
Daniel Popa ◽  
Ian Grover ◽  
Stephen Hayden ◽  
Peter Witucki
Keyword(s):  
Gas Embolism ◽  
Arterial Gas Embolism

Cerebral gas embolism absorption during hyperbaric therapy: theory

2001 ◽  
Vol 90 (2) ◽  
pp. 593-600 ◽  
Author(s):  
Annette B. Branger ◽  
Christian J. Lambertsen ◽  
David M. Eckmann
Keyword(s):  
Decompression Sickness ◽  
Initial Step ◽  
External Pressure ◽  
Neurological Dysfunction ◽  
Inert Gas ◽  
Gas Embolism ◽  
Royal Navy ◽  
Absorption Time ◽  
Hyperbaric Therapy

Cerebral gas embolism is a serious consequence of diving. It is associated with decompression sickness and is assumed to cause severe neurological dysfunction. A mathematical model previously developed to calculate embolism absorption time based on in vivo bubble geometry is used in which various conditions of hyperbaric therapy are considered. Effects of varying external pressure and inert gas concentrations in the breathing mixtures, according to US Navy and Royal Navy diving treatment tables, are predicted. Recompression alone is calculated to reduce absorption times of a 50-nl bubble by up to 98% over the untreated case. Lowering the inhaled inert gas concentration from 67.5% to 50% reduces absorption time by 37% at a given pressure. Bubbles formed after diving and decompression with He are calculated to absorb up to 73% faster than bubbles created after diving and decompression with air, regardless of the recompression gas breathed. This model is a useful alternative to impractical clinical trials in assessing which initial step in hyperbaric therapy is most effective in eliminating cerebral gas embolisms should they occur.

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