Decompression sickness in the rat following a dive on trimix: recompression therapy with oxygen vs. heliox and oxygen

2007 ◽  
Vol 102 (4) ◽  
pp. 1324-1328 ◽  
Author(s):  
R. Arieli ◽  
P. Svidovsky ◽  
A. Abramovich
Keyword(s):  
High Pressure ◽  
Body Mass ◽  
Rat Model ◽  
Death Rate ◽  
Decompression Sickness ◽  
Hyperbaric Chamber ◽  
Permanent Disability ◽  
Hyperbaric Treatment ◽  
Deep Diving ◽  
Time Required

Trimix (a mixture of helium, nitrogen, and oxygen) has been used in deep diving to reduce the risk of high-pressure nervous syndrome during compression and the time required for decompression at the end of the dive. There is no specific recompression treatment for decompression sickness (DCS) resulting from trimix diving. Our purpose was to validate a rat model of DCS on decompression from a trimix dive and to compare recompression treatment with oxygen and heliox (helium-oxygen). Rats were exposed to trimix in a hyperbaric chamber and tested for DCS while walking in a rotating wheel. We first established the experimental model, and then studied the effect of hyperbaric treatment on DCS: either hyperbaric oxygen (HBO) (1 h, 280 kPa oxygen) or heliox-HBO (0.5 h, 405 kPa heliox 50%-50% followed by 0.5 h, 280 kPa oxygen). Exposure to trimix was conducted at 1,110 kPa for 30 min, with a decompression rate of 100 kPa/min. Death and most DCS symptoms occurred during the 30-min period of walking. In contrast to humans, no permanent disability was found in the rats. Rats with a body mass of 100–150 g suffered no DCS. The risk of DCS in rats weighing 200–350 g increased linearly with body mass. Twenty-four hours after decompression, death rate was 40% in the control animals and zero in those treated immediately with HBO. When treatment was delayed by 5 min, death rate was 25 and 20% with HBO and heliox, respectively.

Hyperbaric treatment for decompression sickness: current recommendations

2019 ◽  
pp. 685-693
Author(s):  
Richard E. Moon ◽  
◽  
Simon Mitchell ◽  
◽  
Keyword(s):  
Decompression Sickness ◽  
Ambient Pressure ◽  
Dissolved Gas ◽  
Hyperbaric Chamber ◽  
Hyperbaric Treatment ◽  
Hypobaric Chamber ◽  
Rapid Ascent ◽  
Gas Pressures

Rationale Decompression sickness (DCS, “bends”) is caused by formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation) [1]. This may occur when ambient pressure is reduced during any of the following: • ascent from a dive; • depressurization of a hyperbaric chamber; • rapid ascent to altitude in an unpressurised aircraft or hypobaric chamber; • loss of cabin pressure in an aircraft [2] and • during space walks.

Norwegian deep diving trials

1984 ◽  
Vol 304 (1118) ◽  
pp. 143-149 ◽  
Keyword(s):  
High Pressure ◽  
North Sea ◽  
Thermal Protection ◽  
Decompression Sickness ◽  
The Other ◽  
Deep Diving ◽  
The North ◽  
Before And After ◽  
The North Sea

In 1983 NUTEC, together with two diving companies, completed two dives with 12 divers (6 in each dive) to pressures equivalent to 350 m s.w., one dive lasted for 17 d, and the other, 24 d. The purpose of the dives was to demonstrate that the diving companies were prepared for diving to 300 m depth in the North Sea. No major medical or physiological problems arose during the dives, although all divers had minor symptoms of high pressure nervous syndrome during compressions. During decompression three decompression sickness incidents occurred, which involved pain only, and all were successfully treated. All divers went through comprehensive medical physiological examinations before and after the dives. No significant changes from values measured before diving have been found in the six divers who have so far been examined after diving, except that five of them were considerably more sensitive to CO 2 after the dive than before. Several problems arose in connection with the divers’ breathing equipment, thermal protection and communication, which need to be improved.

Definitive Treatment of Neurological Decompression Sickness in a Resource Limited Location

2021 ◽  
Vol 92 (1) ◽  
pp. 47-49
Author(s):  
Matthew J. Petruso ◽  
Samuel M. Philbrick
Keyword(s):  
Air Force ◽  
Decompression Sickness ◽  
Definitive Treatment ◽  
Military Bases ◽  
Hyperbaric Chamber ◽  
Hyperbaric Treatment ◽  
Course Of Action ◽  
Resource Limited ◽  
Close Proximity ◽  
Air Force Base

BACKGROUND: While Fairbanks, AK, USA, is a remote location with significant constraints on medical resources and specialty care, a small U.S. Air Force clinic was able to provide a pilot with definitive care for neurological decompression sickness.CASE REPORT: A 31-yr-old female patient presented to her flight surgeon in Anchorage, AK, USA, with migrating polyarthropathy and headaches 48 h after a flight which included planned aircraft decompression for high altitude low opening (HALO) jump operations. In order to get definitive treatment in a hyperbaric chamber, the patient typically would have to be flown to Seattle, WA, USA. This transfer of care would cost the Air Force approximately 150,000 and may have led to more complicated disease. Fortunately, Eielson Air Force Base (AFB) in Fairbanks had previously procured a Hyperlite hyperbaric chamber specifically for this situation. After consultation with a hyperbaric specialist, the team decided that the most appropriate course of action was to transfer her by car 6 h north from Anchorage to Fairbanks. On initiation of the Hart treatment table, she experienced immediate reduction in joint pain with a reversal of neurological symptoms.DISCUSSION: This patients care could not have been done without the procurement of a hyperbaric chamber. This case demonstrates the utility and necessity for these capabilities at more facilities that manage significant flying operations. Military bases should ensure that hyperbaric treatment capabilities are available within a close proximity.Petruso MJ, Philbrick SM. Definitive treatment of neurological decompression sickness in a resource limited location. Aerosp Med Hum Perform. 2021; 92(1):4749.

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.

Prediction of signs/symptoms of decompression sickness following submarine tower escape

2019 ◽  
pp. 17-33
Author(s):  
Joel Edney ◽  
Geoffrey Loveman ◽  
Fiona Seddon ◽  
Julian Thacker ◽  
Karen Jurd ◽  
...  
Keyword(s):  
Body Mass ◽  
Marked Effect ◽  
Decompression Sickness ◽  
Outcome Data ◽  
Calibration Data ◽  
Limb Pain ◽  
Pulmonary Barotrauma ◽  
Escape Depth ◽  
Different Types ◽  
Risk Curves

Crew survival in a distressed submarine (DISSUB) scenario may be enhanced by the knowledge of the risks of different types of decompression sickness (DCS) should the crew attempt tower escape. Four models were generated through calibration against DCS outcome data from 3,919 pressure exposures, each for the prediction of one of four categories of DCS: neurological, limb pain, respiratory and cutaneous. The calibration data contained details of human, goat, sheep and pig exposures to raised pressure while breathing air or oxygen/nitrogen mixtures. No exposures had substantial staged decompression or cases of suspected pulmonary barotrauma. DCS risk was scaled between species and with body mass. A parameter was introduced to account for the possibility of the occurrence of some symptom types masking others. The calibrated models were used to estimate likelihood of DCS occurrence for each symptom category following submarine tower escape. Escape depth was found to have a marked effect only on predicted rates of neurological DCS. Saturation at raised internal DISSUB pressure prior to escape was found to affect predicted rates of all symptom types. The iso-risk curves presented are offered as guidance to submarine crews and rescue forces in preparation for, or in the event of, a DISSUB scenario.

scholarly journals Decompression sickness risk in rats by microbial removal of dissolved gas

1998 ◽  
Vol 275 (3) ◽  
pp. R677-R682 ◽  
Author(s):  
Susan R. Kayar ◽  
Terry L. Miller ◽  
Meyer J. Wolin ◽  
Eugenia O. Aukhert ◽  
Milton J. Axley ◽  
...  
Keyword(s):  
Gas Chromatography ◽  
High Pressures ◽  
Decompression Sickness ◽  
Body Burden ◽  
The Body ◽  
Dissolved Gas ◽  
Hyperbaric Chamber ◽  
Methanobrevibacter Smithii ◽  
Water Rate ◽  
Microbial Removal

We present a method for reducing the risk of decompression sickness (DCS) in rats exposed to high pressures of H2. Suspensions of the human colonic microbe Methanobrevibacter smithii were introduced via a colonic cannula into the large intestines of the rats. While the rats breathed H2in a hyperbaric chamber, the microbe metabolized some of the H2diffusing into the intestine, converting H2and CO2to methane and water. Rate of release of methane from the rats, which was monitored by gas chromatography, varied with chamber H2pressure. This rate was higher during decompression than during compression, suggesting that during decompression the microbe was metabolizing H2stored in the rats’ tissues. Rats treated with M. smithii had a 25% (5 of 20) incidence of DCS, which was significantly lower ( P < 0.01) than the 56% (28 of 50) incidence of untreated controls, brought on by a standardized compression and decompression sequence. Thus using a microbe in the intestine to remove an estimated 5% of the body burden of H2reduced DCS risk by more than one-half. This method of biochemical decompression may potentially facilitate human diving.

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 ◽  
...  
Keyword(s):  
Hyperbaric Oxygen ◽  
Decompression Sickness ◽  
Transoesophageal Echocardiography ◽  
Medical Personnel ◽  
Treatment Session ◽  
Occupational Risk ◽  
Additional Risk ◽  
Hyperbaric Treatment ◽  
Hyperbaric Exposure ◽  
Spinal Cord Decompression

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).

Single-Dose Pharmacokinetics of Intraperitoneal Ofloxacin in Patients on Continuous Ambulatory Peritoneal Dialysis

1993 ◽  
Vol 13 (2_suppl) ◽  
pp. 383-385 ◽  
Author(s):  
Ignatius Kum-Po Gheng ◽  
Pak-Yin Ghau ◽  
Gyrus R. Kumana ◽  
Ghing-Ying Ghan ◽  
Maybelle Kou ◽  
...  
Keyword(s):  
High Pressure ◽  
Renal Function ◽  
Liquid Chromatography ◽  
Single Dose ◽  
Peritoneal Dialysis ◽  
Serum Concentration ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Total Serum ◽  
Serum Clearance ◽  
Time Required

The present study examines the pharmacokinetics of ofloxacin given In a single dose of 200 mg intraperitoneally (Ip) In the first bag of three 2-L 8-hour exchanges. Ofloxacin was measured using high-pressure liquid chromatography (HPLC) in the serum and peritoneal effiuent over 24 hours. Six patients without and 3 patients with peritonitis were studied. Ofloxacin given Ip was almost completely absorbed after an 8-hour dwell, and this was not affected by peritonitis. The time required to reach peak serum concentration was longer than that reported previously following oral administration. Elimination halflife (11/2) of ofloxacln was markedly prolonged compared to patients with normal renal function. Peritoneal clearance accounted for only one-tenth of total serum clearance. Peritonitis appeared to shorten the T112 of ofloxacln, but this was mainly due to an Increase In total serum clearance rather than a change In peritoneal clearance. Peritoneal drug concentration >0.5 mg/L was reached In the second and third exchange by the second hour. No Bide effects from Ip ofloxacin were observed. We concluded that ofloxacin given in a single dose of 200 mg is safe and provides adequate therapeutic serum and peritoneal concentration for more than 24 hours in patients on continuous ambulatory peritoneal dialysis (CAPD) with 8-hour exchanges.

scholarly journals Vitamin D Promotes Adiposity But Improves Associated Metabolic Derangements In An Obese Rat Model

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
N A Mohamed ◽  
A A Seif ◽  
M S Abdelhamid ◽  
R S A Eissa
Keyword(s):  
Body Mass Index ◽  
Vitamin D ◽  
Adipose Tissue ◽  
Lipid Profile ◽  
Body Mass ◽  
Visceral Adipose Tissue ◽  
Rat Model ◽  
Dose Group ◽  
Tnf Α ◽  
Visceral Adipose

Abstract Background Obesity is a worldwide problem and is a major risk factor for chronic diseases. The relation between obesity and vitamin D is not completely understood. Obesity is associated with vitamin D insufficiency. Some studies claim that vitamin D may reduce lipogenesis and others claim that vitamin D can promote adipogenesis. Aim of the study This study was planned to evaluate the effect of alteration in vitamin D level on body weight and adipose tissue metabolism in an obese rat model. Methods 32 Female Albino-rats were randomly allocated into: control group (C, n = 8), fed on control diet containing 1000 IU vitamin D/kg diet, and a high caloric diet group (HCD, n = 32). The HCD group was further subdivided into 3 groups according to the vitamin D dose into: standard vitamin D dose group (HCD+SVD) containing 1000 IU vitamin D/kg diet, low vitamin D dose group (HCD+LVD) containing 25 IU vitamin D/kg diet and high vitamin D dose group (HCD+HVD) containing 5169 IU vitamin D/kg diet. Body mass index, serum vitamin D, glucose, lipid profile, TNF-α and adipose tissue UCP-1 were measured. Different fat depots were weighed and histopathologically assessed. Results HCD+HVD group showed a significant increase in the final body mass index and in the different fat depot weights compared to all groups. Compared to the HCD+SVD group, the HCD+HVD group showed significantly lower serum total cholesterol and LDL-c levels, while it showed a non-significant change in serum glucose, TNF-α and visceral adipose tissue UCP-1. A significant negative correlation was found between serum 25(OH)D and visceral adipose tissue UCP-1. HCD+LVD showed the highest visceral adipose tissue UCP-1 compared to all groups. Conclusion Vitamin D promoted adiposity and decreased visceral adipose tissue UCP-1 but improved the associated derangements in lipid profile.

scholarly journals Application of Multifrequency Bioelectrical Impedance Analysis Method for the Detection of Dehydration Status in Professional Divers

Medicina ◽  
2012 ◽  
Vol 48 (4) ◽  
pp. 29 ◽  
Author(s):  
Sermin Sengun ◽  
Atilla Uslu ◽  
Salih Aydin
Keyword(s):  
Bioelectrical Impedance Analysis ◽  
Decompression Sickness ◽  
Bioelectrical Impedance ◽  
Impedance Analysis ◽  
Extracellular Water ◽  
Analysis Method ◽  
Fluid Shift ◽  
Predisposing Factor ◽  
Deep Diving ◽  
Total Body

Background and Objective. The level of dehydration has been known to be a predisposing factor for the development of decompression sickness in divers. The aim of this study was to determine the level of dehydration in divers who dove with heliox and to determine whether the source of this dehydration was intracellular and/or extracellular by means of multifrequency bioelectrical impedance analysis (MF-BIA). Material and Methods. Eleven male professional divers were enrolled in the study. In order to determine the level of dehydration, MF-BIA was carried out (at 5, 50, and 100 kHz) and capillary hematocrit (Hct) was measured two times: one before diving and the other after leaving the pressure room. Results. When prediving and postdiving parameters were compared, significant increases in the resistance at 5 kHz (P<0.001), 50 kHz, (P<0.001), and 100 kHz (P<0.01) and Hct (P<0.01) were observed after the diving. Similarly, a statistically significant fluid shift was found: total body water, –1.30 L (P<0.001), extracellular water, –0.85 L (P<0.001); and intracellular water, –0.45 L (P=0.011). Conclusions. Our results showed that mild dehydration occurred both in the intracellular and extracellular compartments in divers after deep diving. This study also indicates that MF-BIA could be a reliable new method for determining the dehydration status in divers.

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