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PubMed1986

Aseptic necrosis in caisson workers: a new set of decompression tables.

There is a high incidence of aseptic necrosis and decompression sickness among caisson workers due to inadequate decompression using the current OSHA decompression tables (1-7). Because of this, a new set of tables--Autodec III-O2--was developed which more effectively eliminates nitrogen from the body and, therefore, should decrease the incidence of both bends and aseptic necrosis. The Autodec III-O2 schedule's superiority was statistically significant at a level of 0.08 compared to the OSHA table. It is our conclusion that OSHA should adopt the Autodec III-O2 schedule as a replacement for the current decompression tables.

Adult↗
PubMed1979

Diffusion and nucleation of gas in gel and some implications for the development of decompression procedures.

Attention is directed to certain incongruities among accepted diving procedures in order to emphasize the need for a more complete understanding of the interactions between the factors involved in diving and decompression and in the onset of decompression sickness. It is suggested that physiological responses derived from the effects of diffusion and nucleation of gas in tissue might be interpreted in terms of similar events in specimens of gelatin subjected to patterns of compression and decompression. A model for behavior of specimens in gel is developed and conformity with the results of a program of experimentation is demonstrated. With the insight provided by this model, a substantial analogy between important aspects of the behavior of gel and tissue is claimed and application of this model to the refinement and development of diving and decompression procedures is proposed.

Decompression↗
PubMed1983

Analysis of gas composition of intravascular bubbles produced by decompression.

The gas composition of intravascular bubbles produced by decompression was investigated in rabbits using gas chromatography. The animals were exposed to 8 ATA for 30 min. All samples of bubbles were taken from the animals under 0.2 ATA pressure gradient so that no air could enter the sampling system from the outside. The percentage of carbon dioxide in the bubbles tended to decrease at first and then increased with post-decompression time. On the other hand, the percentage of oxygen tended to change in the opposite manner. Actual analysis of bubbles in the living decompressed animals indicates that carbon dioxide may be an outstanding factor in the initiation and early growth of bubbles. In view of this, Haldane's classical maximum supersaturation limit for avoiding decompression sickness should be examined and possibly modified for gases other than nitrogen.

Animals↗
PubMed1984

Decompression from a deep nitrogen/oxygen saturation dive--a case report.

Ten divers participated in a 4.5 d nitrogen/oxygen saturation dive to 165 fsw. There were daily 2 h excursions to 61 msw (200 fsw). The divers breathed air during the excursions and 0.51 bar (0.5 atm) oxygen in nitrogen at 50.3 msw (165 fsw). The final decompression began 6 h after the last excursion. The oxygen partial pressure was 0.51 bar (0.5 atm) from 50.3 to 13.7 msw (165 to 45 fsw), and air was used from 13.7 msw (45 fsw) to the surface. By 6.1 msw (20 fsw), four divers had developed decompression sickness. A fifth diver developed decompression sickness during a commercial air flight 68 h after surfacing. Comparison of ascent rates for this dive and for air or nitrogen/oxygen saturation dives reported in the literature suggests that deeper dives require slower rates of ascent. Dives shallower than 30.5 msw (100 fsw) had a mean ascent rate of 1 msw/h (3.2 fsw/h) and 14 decompression incidents in 107 man-exposures. Dives deeper than 30.5 msw (100 fsw) had a mean rate of 0.76 msw/h (2.5 fsw/h) and 14 incidents in 45 man-exposures.

Adaptation, Physiological↗
PubMed1983

Decompression incidence in air- and liquid-breathing hamsters.

The effects of hyperbaric compression on heart rate, rectal temperature, respiratory rate, bubble formation, and survival were studied in three groups of anesthetized golden hamsters (Mesocricetus auratus). Group I (15 animals) breathed air while exposed to 7 ATA of pressure for 1 h in a hyperbaric chamber; Group II (13 animals), at the same pressure level (7 ATA) and for the same time period (1 h), breathed an oxygenated fluorocarbon liquid (temperature 27 degrees C) that was open to the chamber atmosphere; Group III (10 animals), at the same pressure and time period as the other groups, were sealed in a flexible plastic bag filled with oxygenated fluorocarbon as a breathing mixture. A fourth, Group IV (12 animals), breathed oxygenated fluorocarbon for 1 h at 1 ATA. Survival after rapid decompression in each group varied, 9 animals died in Group I, 12 animals in Group II, whereas none of the animals died in either Groups III or IV. Thirty minutes after decompression postmortem examinations of all the animals demonstrated the presence of large amounts of gas bubbles in the right ventricle and some gas bubbles in the left ventricle of all the hamsters in Groups I and II. No gas bubbles were found in the hearts of the Group III animals. Group III animals, breathing a liquid unsaturated by an inert gas, survived rapid explosive decompression without the signs and symptoms of decompression sickness. Immersion in the liquid fluorocarbon produced a profound decrease in heart rate, rectal temperature, and respiration in Groups II, III, and IV.

Air↗
PubMed1994

Protective effect of oxygen and heliox breathing during development of spinal decompression sickness.

A rat model of spinal decompression sickness (DCS) allows study of spinal cord function for at least 3 h after decompression to 1 atm abs (101 kPa) after an exposure to air at 3.8 atm abs (385 kPa) for 1 h. During these 3 h, spinal evoked potentials (SEPs) elicited by peroneal nerve stimulation may be reduced or disappear, and histologic lesions in the spinal cord are observed. Three groups of animals were given either air, oxygen, or heliox (80/20) to breathe at 1 atm abs for 3 h after decompression. Both oxygen and heliox breathing impeded the development of DCS significantly as judged by the mortality of the animals and disappearance of the SEPs. The effect of heliox seemed to be superior to that of oxygen. The latency time from stimulation to the first SEP peak increased significantly during both air and oxygen breathing, whereas no significant increase was seen during heliox breathing. Histologic examination of the spinal cords of animals breathing air, oxygen, or heliox (80/20) showed focal lesions in the white and gray matter. In the white matter, degenerated myelin sheaths as well as expanded extracellular spaces compatible with bubble formation were seen. In the gray matter, perikaryal degeneration was observed. The extracellular space in the white matter was increased in all decompressed animals compared with controls (P < 0.01). Oxygen and heliox breathing caused a smaller increase in extracellular space as compared with air-breathing animals (P < 0.05) and (0.10 > P > 0.05), respectively. It is concluded that breathing of oxygen or heliox (80/20) at 1 atm abs has a preventive effect on the development of DCS when compared with air breathing; the effect of heliox seems to be superior to that of oxygen.

Air↗
PubMed1996

Reduction of decompression illness risk in pigs by use of non-linear ascent profiles.

An established swine model of neurologic decompression illness (DCI) was adapted to investigate the influence of no-stop ascent profile shape on DCI risk after deep air and heliox dives. Pigs underwent a simulated air dive in a dry chamber to 200 fsw (613 kPa) for 24 min bottom time. They were then decompressed at either a linear rate of 20 fsw/min (61 kPa/min) or on a non-linear, fast-deep/slow-shallow profile. Both decompressions lasted 10 min. In the linear group, there were 11/20 cases of neurologic DCI, including 1 death and 8 severe cases, compared to 5/20 cases (1 severe) in the fast/slow group. Thirteen out of 20 from the linear group, vs. 6/20 of the non-linear group, had moderate or severe skin DCI affecting > 20% skin surface area. A similar study, but of paired, randomized, investigator-blind, and sequential design was performed with pigs breathing 80/20% heliox: Pigs were compressed to 250 fsw (766 kPa) for 8 min 50 s, then decompressed at either a linear 30 fsw/min (92 kPa/min), or on a fast/slow profile. Neurologic DCI occurred more frequently (P = 0.024) in the linear group (16/20; 1 death and 11 severe) than in the fast/slow group (8/20; 3 severe). Moderate or severe skin DCI affected 16/20 of the linear group compared to 3/20 of the fast/slow group (P = 0.0002). The study findings suggest that substantial reductions in DCI risk may be obtainable by manipulating the ascent profile after deep no-stop diving. This finding has potential application in both military and civil diving operations.

Air↗
PubMed1996

Complement system response to decompression.

A role for the activated complement system in the pathogenesis of decompression sickness has recently been suggested. In this study we aimed at evaluating the response of the complement system to decompression in 24 human volunteers. A significant reduction was observed in the levels of iC3, which is a conformationally changed form of the third complement component (C3), and C3A after decompression (P < 0.001). The levels of total C3 did not change during the experiment. A relatively mild decompression has thus led to a distinct change in the complement activation profile in human volunteers.

Adult↗
PubMed1976

Blood viscosity in man following decompression: correlations wiht hematocrit and venous gas emboli.

Whole blood viscosities were measured in U.S. Navy personnel before and after chamber compressions to 5 ATA (132FSW) and 7.4 ATA (210 FSW) by a new method described here. Bubble scores as a quantitative measure of venous gas emboli were determined during decompression and for 30 min thereafter. Hematocrit was measured both before and after each dive. There were five cases of decompression sickness in the two groups. No significant changes in whole blood viscosity, or hematocrit, were noted either in the group that was affected by decompression sickness or in all of the subjects taken as a group. No correlations between total bubble score and changes in viscosity or hematocrit could be made. These results imply that no major changes in viscosity occur in the usual forms of decompression sickness encountered in human beings.

Blood Viscosity↗
PubMed1998

Rapid decompression in the EA-6B.

A Grumman EA-6B aircraft experienced a rapid pressurization failure at 27,000 feet. All four crew members had removed their oxygen masks and were breathing cabin air pressurized to 8,000 feet before the incident. Although none of the crew members developed signs or symptoms of decompression sickness, the potential for adversity was realized by all. Altitude decompression sickness (DCS) and pulmonary overinflation syndrome (POIS) represent potentially fatal complications of rapid decompression or uncontrolled ascent in aircraft. The signs and symptoms of DCS range from mild joint pain to eventual cardiopulmonary collapse and death. The symptoms of POIS are usually more abrupt and lethal. The medical management of DCS and POIS includes (1) maintenance of airway and cardiopulmonary resuscitation if necessary: (2) administration of 100% oxygen; (3) descent as per Naval Aviation Training and Operating Procedures Standardization guidelines; (4) horizontal body position; (5) maintenance of fluid intake; and (6) early medical evaluation by a flight surgeon or other physician qualified in the management of DCS. Symptoms of DCS may appear up to 24 hours after decompression, and continued monitoring or grounding of exposed individuals during this time is essential. Many controllable factors may predispose to DCS/POIS, and preventive measures should be taken to ensure maximum reduction of risk.

Aerospace Medicine↗
PubMed1994

Role of extravascular gas bubbles in spinal cord injury induced by decompression sickness in the rat.

We have evaluated the contribution of extravascular gas bubbles to spinal cord injury in decompression sickness. For this purpose, a model of decompression sickness was developed by subjecting rats to simulated dives using compressed air. Various diving profiles were tested and the presence of spinal cord injury was demonstrated by electrophysiologic measurements. To evaluate the space occupying lesions induced by gas bubbles in the white matter, the spinal cord was fixed by perfusion with 10% buffered formalin. Tissue blocks from cervical, thoracic, and lumbar spinal cords were embedded in paraffin. Tissue sections were double stained with luxol fast blue and hematoxylin and eosin. The space occupying lesions were quantified with a digitizer tablet. The fractional area of the lesions was 0.009% in controls and 0.026% in rats subjected to diving. We conclude that the volume of extravascular free gas present in the cord of rats with spinal decompression sickness is small and that artifacts of tissue preparation contribute to the volume estimate. As far as can be judged from the results in this animal model, the contribution of extravascular gas bubbles to spinal cord decompression injury is minor.

Animals↗
PubMed2006

Decompressive craniectomy in traumatic brain injury: outcome following protocol-driven therapy.

Although decompressive craniectomy following traumatic brain injury is an option in patients with raised intracranial pressure (ICP) refractory to medical measures, its effect on clinical outcome remains unclear. The aim of this study was to evaluate the outcome of patients undergoing this procedure as part of protocol-driven therapy between 2000-2003. This was an observational study combining case note analysis and follow-up. Outcome was assessed at an interval of at least 6 months following injury using the Glasgow Outcome Scale (GOS) score and the SF-36 quality of life questionnaire. Forty-nine patients underwent decompressive craniectomy for raised and refractory ICP (41 [83.7%] bilateral craniectomy and 8 [16.3%] unilateral). Using the Glasgow Coma Scale (GCS), the presenting head injury grade was severe (GCS 3-8) in 40 (81.6%) patients, moderate (GCS 9-12) in 8 (16.3%) patients, and initially mild (GCS 13-15) in 1 (2.0%) patient. At follow-up, 30 (61.2%) patients had a favorable outcome (good recovery or moderate disability), 10 (20.48) remained severely disabled, and 9 (18.4%) died. No patients were left in a vegetative state. Overall the results demonstrated that decompressive craniectomy, when applied as part of protocol-driven therapy, yields a satisfactory rate of favorable outcome. Formal prospective randomized studies of decompressive craniectomy are now indicated.

Adolescent↗
PubMed2006

Decompressive craniectomy for severe head injury in patients with major extracranial injuries.

Neurosurgical therapy aims to minimize secondary brain damage after a severe head injury. This includes the evacuation of intracranial space-occupying hematomas, the reduction of intracranial volumes, external ventricular drainage, and aggressive therapy in order to influence increased intracranial pressure (ICP) and decreased P(ti)O2. When conservative treatment fails, a decompressive craniectomy might be successful in lowering ICP. From September 1997 until December 2004, we operated on 836 patients with severe head injuries, of whom 117 patients (14%) were treated by means of a decompressive craniectomy. The prognosis after decompression depends on the clinical signs and symptoms at admission, patient age, and the existence of major extracranial injuries. Our guidelines for decompressive craniectomy after failure of conservative interventions and evacuation of space-occupying hematomas include: patient age below 50 years without multiple trauma, patient age below 30 years in the presence of major extracranial injuries, severe brain swelling on CT scan, exclusion of a primary brainstem lesion or injury, and intervention before irreversible brain stem damage.

Comorbidity↗
PubMed2005

The importance of major extracranial injuries by the decompressive craniectomy in severe head injuries.

Neurosurgical therapy aims to minimise the secondary brain damage after a severe head injury. This includes the evacuation of an intracranial space occupying bleeding, the reduction of intracranial volumes, in hematocephalus an external ventricular drainage, and the conservative therapy in order to influence an increased intracranial pressure (ICP) and a decreased p(ti)02. When conservative treatment fails to act a decompressive craniectomy might be successful in lowering ICP. From September 1997 until July 2004 we operated on 737 patients with severe head injuries. 103 patients (14%) were treated by means of a decompressive craniectomy. The prognosis after decompression depends on the clinical signs and symptoms on admission, the patients age and the existence of major extracranial injuries. Our guidelines for an indication for decompressive craniectomy after failure of conservative interventions and evacuation of space occupying hematomas include a patients age below 50 years without multiple trauma, a patients age below 30 years in the presence of major extracranial injuries, a severe brain swelling on CT scan, the exclusion of a primary brainstem lesion or injury and the intervention before irreversible brainstem damage and secondarily while monitoring ICP and p(ti)02 in an interval up to 48 hours after the accident before irreversible brainstem damage or generalised brain damage has occurred.

Adult↗
PubMed2005

Preliminary report on spiegelberg pre and post-operative monitoring of severe head-injured patients who received decompressive craniectomy.

The monitoring of craniospinal compliance is uncommonly used clinically despite it's value. The Spiegelberg compliance monitor calculates intracranial compliance (C = deltaV/deltaP) from a moving average of small ICP perturbations (deltaP) resulting from a sequence of up to 200 pulses of added volume (deltaV = 0.1 ml, total V = 0.2 ml) made into a double lumen intraventricular balloon catheter. The objective of this study was thus to determine the effectiveness of the decompressive craniectomy done on the worst brain site with regard to compliance (Cl), pressure volume index (PVI), jugular oximetry (SjVo2), autoregulation abnormalties, brain tissue oxygen (TiO2) and cerebral blood flow (CBF). This is a prospective cohort study of 17 patients who were enrolled after consent and approval of the ethics committee between the beginning of the year 2001 and end of the year 2002. For pre and post assessment on compliance and PVI, all 12 patients who survived were reported to become normal after decompressive craniectomy. There is no significant association between pre and post craniectomy assessment in jugular oxymetry (p > 0.05), autoregulation (p > 0.05), intracranial brain oxymetry (p = 0.125) and cerebral blood flow (p = 0.375). Compliance and PVI improved dramatically in all alive patients who received decompressive craniectomy. Compliance and PVI monitoring may be crucial in improving the outcome of severe head injured patients after decompressive craniectomy.

Adolescent↗
PubMed2003

The importance of decompressive craniectomy for the management of severe head injuries.

Neurosurgical therapy aims to minimize the secondary brain damage after a severe head injury. This includes the evacuation of an intracranial space occupying bleeding, the reduction of intracranial volumes, in hematocephalus an external ventricular drainage, and the conservative therapy in order to influence an increased intracranial pressure (ICP) and a decreased p(ti)02. When conservative treatment fails to act a decompressive craniectomy might be successful in lowering ICP. From September 1997 until August 2001 we operated on 439 patients with severe head injuries. 50 patients (11%) were treated by means of a decompressive craniectomy. The prognosis after decompression depends on the clinical signs and symptoms on admission, the patients age and the existence of major extracranial injuries. Our guidelines for an indication for decompressive craniectomy after failure of conservative interventions and evacuation of space occupying hematomas include a patients age below 50 years without multiple trauma, a patients age below 30 years in the presence of major extracranial injuries, a severe brain swelling on CT scan, the exclusion of a primary brainstem lesion or injury and the intervention before irreversible brainstem damage and secondarily while monitoring ICP and p(ti)02 in an interval up to 48 hours after the accident before irreversible brainstem damage or generalized brain damage has occurred.

Adult↗
PubMed2000

The role of decompressive craniectomy in the treatment of uncontrollable post-traumatic intracranial hypertension.

The benefit of decompressive craniectomy for the treatment of uncontrolled post-traumatic intracranial hypertension seems to be encouraging if medical management fails. We present our experience in 22 cases of cerebral edema due to head trauma. The edema alone was rarely the direct consequence of head trauma. Frequently it was associated with an acute subdural or extradural hematoma and contusion (with or without mass effect). First of all we treated the mass effect of the hematoma and contusion when the diameter was more than 3 cm. Intracranial pressure was monitored in the majority of patients. Bone decompression was performed in the operating theatre depending on the values of intracranial pressure. In our series 41% of patients had a good recovery, 18% a severe disability, 23% a vegetative state and 18% died. The findings showed that the bony decompression must be performed early before the situation becomes irreversible. We suggest that if intracranial pressure values remain greater than 30 mmHg with cerebral perfusion pressure below 70 mmHg, despite vigorous anti-edema therapy, decompressive craniectomy should be considered.

Adolescent↗
PubMed2000

The use of decompressive craniectomy for the management of severe head injuries.

The aim of Neurosurgical care is to minimise the secondary brain damage that occurs after a severe head injury. This includes the evacuation of an intracranial space occupying haematoma, the reduction of intracranial volume, external ventricular drainage with hydrocephalus, and conservative therapy to reduce intracranial pressure (ICP) and to maintain tissue oxygen p(ti)O2. When conservative treatment fails, a decompressive craniectomy might be successful in lowering ICP. From September 1997 until April 1999 we operated on 128 patients with severe head injuries. 19 patients (15%) were treated by means of a decompressive craniectomy. The prognosis after decompression depends on clinical signs and symptoms on admission, patients' age and the existence of major extracranial injuries. Our guidelines for decompressive craniectomy after failure of conservative intervention and evacuation of space occupying hematomas included: a patient's age below 50 years without multiple trauma or a patient's age below 30 years in the presence of major extracranial injuries; severe brain swelling on CT scan (primary brainstem injuries were excluded). In 8 patients conservative 1TU treatment had failed.

Adolescent↗