Iatrogenic cerebral gas embolism, pneumocephalus and the concept of retrograde cerebral venous gas embolism

2019 ◽  
Vol 63 (6) ◽  
pp. 831-831
Author(s):  
Pieter A. Bothma ◽  
Christoph J. Schlimp
Keyword(s):  
Gas Embolism ◽  
Venous Gas Embolism

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.

Argon Pneumoperitoneum Is More Dangerous than CO2 Pneumoperitoneum During Venous Gas Embolism

1997 ◽  
Vol 85 (6) ◽  
pp. 1367-1371 ◽  
Author(s):  
Claude Mann ◽  
Gilles Boccara ◽  
Veronique Grevy ◽  
Francis Navarro ◽  
Jean M. Fabre ◽  
...  
Keyword(s):  
Gas Embolism ◽  
Co2 Pneumoperitoneum ◽  
Venous Gas Embolism

scholarly journals Venous gas embolism as a predictive tool for improving CNS decompression safety

2011 ◽  
Vol 112 (2) ◽  
pp. 401-409 ◽  
Author(s):  
A. Møllerløkken ◽  
S. E. Gaustad ◽  
M. B. Havnes ◽  
C. R. Gutvik ◽  
A. Hjelde ◽  
...  
Keyword(s):  
Gas Embolism ◽  
Predictive Tool ◽  
Venous Gas Embolism

Gas Embolism After Ingestion of Hydrogen Peroxide

PEDIATRICS ◽  
1990 ◽  
Vol 85 (4) ◽  
pp. 593-594
Author(s):  
WAYNE R. RACKOFF ◽  
DAVID F. MERTON
Keyword(s):  
Hydrogen Peroxide ◽  
Case Report ◽  
Venous System ◽  
Hydrogen Peroxide Solution ◽  
Portal Venous System ◽  
Gas Embolism ◽  
Colonic Irrigation ◽  
Radiographic Evidence ◽  
Portal Venous Gas ◽  
Venous Gas Embolism

Gas embolism to the portal venous system is a well-recognized radiographic sign in infants with necrotizing enterocolitis. It also has been seen after colonic irrigation with hydrogen peroxide solution.1,2 We present what we believe is the first reported patient with radiographic evidence of portal venous gas embolism after ingestion of hydrogen peroxide solution. This finding is important because gas embolism to the portal venous system after colonic irrigation with hydrogen peroxide has been associated with gangrenous and perforated bowel.1,2 CASE REPORT A 2-year-old boy ingested an unknown amount of 3% hydrogen peroxide solution. The child was found with foam around his mouth.

Hydrogen peroxide: an unusual cause of arterial and venous gas embolism

Anaesthesia ◽  
1996 ◽  
Vol 51 (11) ◽  
pp. 683-684
Author(s):  
S. P. W. Neff ◽  
L. Zulueta ◽  
R. Miller
Keyword(s):  
Hydrogen Peroxide ◽  
Gas Embolism ◽  
Venous Gas Embolism

scholarly journals Body fat does not affect venous bubble formation after air dives of moderate severity: theory and experiment

2013 ◽  
Vol 114 (5) ◽  
pp. 602-610 ◽  
Author(s):  
Nico A. M. Schellart ◽  
Tjeerd P. van Rees Vellinga ◽  
Rob A. van Hulst
Keyword(s):  
Body Fat ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Maximal Oxygen Consumption ◽  
Whole Body ◽  
Small Range ◽  
Gas Embolism ◽  
Blood Compartment ◽  
In Series ◽  
Venous Gas Embolism

For over a century, studies on body fat (BF) in decompression sickness and venous gas embolism of divers have been inconsistent. A major problem is that age, BF, and maximal oxygen consumption (V̇o2max) show high multicollinearity. Using the Bühlmann model with eight parallel compartments, preceded by a blood compartment in series, nitrogen tensions and loads were calculated with a 40 min/3.1 bar (absolute) profile. Compared with Haldanian models, the new model showed a substantial delay in N2 uptake and (especially) release. One hour after surfacing, an increase of 14–28% in BF resulted in a whole body increase of the N2 load of 51%, but in only 15% in the blood compartment. This would result in an increase in the bubble grade of only 0.01 Kisman-Masurel (KM) units at the scale near KM = I−. This outcome was tested indirectly by a dry dive simulation (air breathing) with 53 male divers with a small range in age and V̇o2max to suppress multicollinearity. BF was determined with the four-skinfold method. Precordial Doppler bubble grades determined at 40, 80, 120, and 160 min after surfacing were used to calculate the Kisman Integrated Severity Score and were also transformed to the logarithm of the number of bubbles/cm2 (logB). The highest of the four scores yielded logB = −1.78, equivalent to KM = I−. All statistical outcomes of partial correlations with BF were nonsignificant. These results support the model outcomes. Although this and our previous study suggest that BF does not influence venous gas embolism (Schellart NAM, van Rees Vellinga TP, van Dijk FH, Sterk W. Aviat Space Environ Med 83: 951–957, 2012), more studies with different profiles under various conditions are needed to establish whether BF remains (together with age and V̇o2max) a basic physical characteristic or will become less important for the medical examination and for risk assessment.

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