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.

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.

High-Altitude Decompression Sickness Treated with Hyperbaric Therapy and Extracorporeal Oxygenation

2020 ◽  
Vol 91 (2) ◽  
pp. 106-109
Author(s):  
Jacek Siewiera ◽  
Przemysław Szałański ◽  
Dariusz Tomaszewski ◽  
Jacek Kot
Keyword(s):  
Case Report ◽  
High Altitude ◽  
Decompression Sickness ◽  
Endothelial Damage ◽  
Neurological Deficits ◽  
Institute Of Medicine ◽  
First Case ◽  
Hyperbaric Therapy ◽  
Extracorporeal Oxygenation ◽  
Vv Ecmo

BACKGROUND: High-altitude decompression sickness (HADCS) is a rare condition that has been associated with aircraft accidents. To the best of our knowledge, the present paper is the first case report of a patient treated for severe HADCS using recompression therapy and veno-venous extracorporeal oxygenation (VV-ECMO) with a complete recovery.CASE REPORT: After depressurization of a cabin, the 51-yr-old jet pilot was admitted to the Military Institute of Medicine with a life-threatening HADCS approximately 6 h after landing from a high-altitude flight, in a dynamically deteriorating condition, with progressing dyspnea and edema, reporting increasing limb paresthesia, fluctuating consciousness, and right-sided paresis. Hyperbaric oxygen therapy in the intensive care mode was initiated. A therapeutic recompression with U.S. Navy Treatment Table 6 was performed with neurological improvement. Due to cardiovascular collapse, sedation, mechanical ventilation, and significant doses of catecholamines were started, followed by continuous veno-venous hemodialysis. In the face of disturbances in oxygenation, during the second day of treatment the patient was commenced on veno-venous extracorporeal oxygenation. Over the next 6 d, the patient’s condition slowly improved. On day 7, VV-ECMO was discontinued. On day 19, the patient was discharged with no neurological deficits.DISCUSSION: We observed two distinct stages during the acute phase of the disease. During the first stage, signs of hypoperfusion, neurological symptoms, and marbled skin were observed. During the second stage, multiple organ dysfunction dominated, including heart failure, pulmonary edema, acute kidney injury, and fluid overload, all of which can be attributed to extensive endothelial damage.Siewiera J, Szałański P, Tomaszewski D, Kot J. High-altitude decompression sickness treated with hyperbaric therapy and extracorporeal oxygenation. Aerosp Med Hum Perform. 2020; 91(2):106–109.

scholarly journals Deadly diving? Physiological and behavioural management of decompression stress in diving mammals

2011 ◽  
Vol 279 (1731) ◽  
pp. 1041-1050 ◽  
Author(s):  
S. K. Hooker ◽  
A. Fahlman ◽  
M. J. Moore ◽  
N. Aguilar de Soto ◽  
Y. Bernaldo de Quirós ◽  
...  
Keyword(s):  
Marine Mammal ◽  
Marine Mammals ◽  
Multiple Stressors ◽  
Decompression Sickness ◽  
Tissue Injury ◽  
Bubble Formation ◽  
Gas Bubbles ◽  
Breath Hold ◽  
Technological Advances ◽  
Measured Time

Decompression sickness (DCS; ‘the bends’) is a disease associated with gas uptake at pressure. The basic pathology and cause are relatively well known to human divers. Breath-hold diving marine mammals were thought to be relatively immune to DCS owing to multiple anatomical, physiological and behavioural adaptations that reduce nitrogen gas (N 2 ) loading during dives. However, recent observations have shown that gas bubbles may form and tissue injury may occur in marine mammals under certain circumstances. Gas kinetic models based on measured time-depth profiles further suggest the potential occurrence of high blood and tissue N 2 tensions. We review evidence for gas-bubble incidence in marine mammal tissues and discuss the theory behind gas loading and bubble formation. We suggest that diving mammals vary their physiological responses according to multiple stressors, and that the perspective on marine mammal diving physiology should change from simply minimizing N 2 loading to management of the N 2 load . This suggests several avenues for further study, ranging from the effects of gas bubbles at molecular, cellular and organ function levels, to comparative studies relating the presence/absence of gas bubbles to diving behaviour. Technological advances in imaging and remote instrumentation are likely to advance this field in coming years.

Nitrogen tensions in brachial vein blood of Korean ama divers

1992 ◽  
Vol 73 (6) ◽  
pp. 2592-2595 ◽  
Author(s):  
P. Radermacher ◽  
K. J. Falke ◽  
Y. S. Park ◽  
D. W. Ahn ◽  
S. K. Hong ◽  
...  
Keyword(s):  
Decompression Sickness ◽  
Bubble Formation ◽  
Compartment Model ◽  
Breath Hold ◽  
Computer Assisted ◽  
Half Time ◽  
Single Compartment ◽  
Single Compartment Model ◽  
Effective Depth ◽  
Forearm Muscle

Intravascular bubble formation and symptoms of decompression sickness have been reported during repetitive deep breath-hold diving. Therefore we examined the pattern of blood N2 kinetics during and after repetitive breath-hold diving. To study muscle N2 uptake and release, we measured brachial venous N2 partial pressure (PN2) in nine professional Korean breath-hold divers (ama) during a 3-h diving shift at approximately 4 m seawater depth and up to 4 h after diving. PN2 was determined with the manometric Van Slyke method. Diving time and depth were recorded using a backpack computer-assisted dive longer that allowed calculating the surface-to-depth time ratio to derive the effective depth. With the assumption that forearm muscle N2 kinetics follow the general Haldanian principles of compression and decompression, i.e., forearm muscle is a single compartment with a uniform tissue PN2 equal to venous PN2, PN2 data were fitted to monoexponential functions of time. In the early phase of the diving shift, PN2 rapidly increased to 640 Torr (half time = 6 min) and then slowly declined to baseline levels (half time = 36 min) after the work shift. Peak PN2 levels approximated the alveolar PN2 derived from the effective depth. We conclude that forearm muscle N2 kinetics are well described by a Haldanian single-compartment model. Decompression sickness is theoretically possible in the ama; it did not occur because the absolute PN2 remained low due to the shallow working depth of the ama we studied.

Ultrastructure of pulmonary microvasculature in acute endotoxemia

1978 ◽  
Vol 36 (2) ◽  
pp. 470-471
Author(s):  
R. G. Gerrity ◽  
M. Richardson
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Alveolar Epithelium ◽  
Endothelial Damage ◽  
Capillary Endothelium ◽  
Type Ii Cells ◽  
Type Ii ◽  
Interstitial Edema ◽  
Pulmonary Capillaries ◽  
Lung Ultrastructure ◽  
Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

Blood platelet-derived microparticles release and bubble formation after an open-sea air dive

2012 ◽  
Vol 37 (5) ◽  
pp. 888-892 ◽  
Author(s):  
Jean-Michel Pontier ◽  
Emmanuel Gempp ◽  
Mihaela Ignatescu
Keyword(s):  
Platelet Aggregation ◽  
Decompression Sickness ◽  
Blood Platelets ◽  
Water Immersion ◽  
Bubble Formation ◽  
Blood Platelet ◽  
Field Conditions ◽  
Control Group ◽  
Open Sea ◽  
Experimental Group

Bubble-induced platelet aggregation offers an index for evaluating decompression severity in humans and in a rat model of decompression sickness. Endothelial cells, blood platelets, or leukocytes shed microparticles (MP) upon activation and during cell apoptosis. The aim was to study blood platelet MP (PMP) release and bubble formation after a scuba-air dive in field conditions. Healthy, experienced divers were assigned to 1 experimental group (n = 10) with an open-sea air dive to 30 msw for 30 min and 1 control group (n = 5) during head-out water immersion for the same period. Bubble grades were monitored with a pulsed doppler according to Kissman Integrated Severity Score (KISS). Blood samples for platelet count (PC) and PMP (annexin V and CD41) were taken 1 h before and after exposure in both groups. The result showed a decrease in post-dive PC compared with pre-dive values in experimental group with no significant change in the control group. We observed a significant increase in PMP values after the dive while no change was revealed in the control group. There was a significant positive correlation between the PMP values after the dive and the KISS bubble score. The present study highlighted a relationship between the post-dive decrease in PC, platelet MP release, and bubble formation. Release of platelet MPs could reflect bubble-induced platelet aggregation and could play a key role in alteration of the coagulation. Further studies must investigate endothelial and leukocyte MP release in the same field conditions.

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.

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