SEARCH · PubMed Health

Results for “Decompression”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed1997

Compressed air tunneling and caisson work decompression procedures: development, problems, and solutions.

Multinational experience over many years indicates that all current air decompression schedules for caisson and compressed air tunnel workers are inadequate. All of them, including the Occupational Safety and Health Administration tables, produce dysbaric osteonecrosis. The problem is compounded because decompression sickness (DCS) tends to be underreported. Permanent damage in the form of central nervous system or brain damage may occur in compressed air tunnel workers, as seen on magnetic resonance imaging, in addition to dysbaric osteonecrosis. Oxygen decompression seems to be the only viable method for safely decompressing tunnel workers. Oxygen decompression of tunnel workers has been successfully used in Germany, France, and Brazil. In Germany, only oxygen decompression of compressed air workers is permitted. In our experience, U.S. Navy tables 5 and 6 usually prove adequate to treat DCS in caisson workers despite extremely long exposure times, allowing patients to return to work following treatment for DCS. Tables based on empirical data and not on mathematical formulas seem to be reasonably safe. U.S. Navy Exceptional Exposure Air Decompression tables are compared with caisson tables from the United States and Great Britain.

Decompression↗

PubMed1994

Comparison of haemodynamic effects during venous air infusion and after decompression in pigs.

We have compared haemodynamic effects of venous gas emboli during continuous air infusion into the right atrium and after rapid decompression in pigs. Eight anaesthetized and spontaneously breathing pigs received continuous air infusion at a rate of either 0.05 ml.kg-1.min-1 (six pigs, air infusion group) or 0.10 ml.kg-1.min-1 (two pigs). Another eight pigs (decompression group) underwent a 30-min compression to 5 bar (500 kPa, absolute pressure), followed by a rapid decompression (2 bar.min-1). Haemodynamic variables were measured or calculated, and bubbles in the pulmonary artery were monitored using transoesophageal echocardiography. The results showed less variation in the maximal increase in mean pulmonary arterial pressure (BPa,pulm) during air infusion (0.05 ml.kg-1.min-1) than after decompression, although the mean maximal increase did not differ between the two groups [28.0 mmHg (3.73 kPa), 95% confidence interval (CI) 23.5-32.5, vs 32.0 mmHg (4.27 kPa), 95% CI 25.3-38.7, P = 0.3]. The BPa,pulm stabilized or decreased very slowly after peak values were reached in the air infusion group, whereas the BPa,pulm decreased rapidly during the same period in the decompression group. No significant changes in mean arterial pressure were observed during air infusion (0.05 ml.kg-1.min-1), in contrast to the rapid increase and the subsequent decrease, that appeared after decompression. Finally, the maximal bubble count was much lower in the air infusion group than in most of the pigs in the decompression group. The two pigs that received 0.10 ml.kg-1.min-1 stopped breathing after 5-min infusion, developed arterial hypotension and died.

Animals↗

PubMed1997

Decompression comparison of helium and hydrogen in rats.

The hypothesis that there are differences in decompression risk between He and H2 was examined in 1,607 unanesthetized male albino rats subjected to dives on 2% O2-balance He or 2% O2-balance H2 (depths < or = 50 ATA, bottom times < or = 60 min). The animals were decompressed to 10.8 ATA with profiles varying from rapid to slow, with up to four decompression stops of up to 60 min each. Maximum likelihood analysis was used to estimate the relative decompression risk on a per unit pressure basis (termed "potency") and the rate of gas uptake and elimination, both factors affecting the decompression sickness risk, from a specific dive profile. H2 potency for causing decompression sickness was found to be up to 35% greater than that for He. Uptake rates were unresolvable between the two gases with the time constant (TC) estimated at approximately 2-3 min, leading to saturation in both cases in < 15 min. Washout of both gases was significantly slower than uptake, with He washout (TC approximately 1.5-3 h) substantially slower than H2 washout (TC approximately 0.5 h). It is unknown whether the decompression advantage of the faster washout of H2 or the disadvantage of its increased potency, observed in the rat, would be important for human diving.

Animals↗

PubMed1989

Decompression: English tables.

The formulation of decompression procedures has generally been based on the observation that divers can be decompressed without stoppages to surface, from steady-state exposures of about twice the atmospheric pressure. Because decompression sickness rarely develops from this "no-stop decompression", it has been assumed that no gas is liberated. It is therefore assumed, in the calculation of the majority of decompression tables, that using a 2:1 decompression ratio allows the additional gas load from the hyperbaric exposure to be transported to the lungs in solution. Ultrasonic scanning and Doppler techniques have shown that this is not the case. Decompression tables must therefore be formulated so as to take into account the presence of gas, the critical diameter of circulating bubbles and the inherent unsaturation introduced by oxygen.

Decompression↗

PubMed1986

An effect of CO2 on the maximum safe direct decompression to 1 bar from oxygen-nitrogen saturation.

An investigation into the maximum safe decompression step from oxygen nitrogen saturation to 1 bar was carried out with and without the presence of 0.02 bar carbon dioxide. The series, Islander 1, involved 13 teams of 5, fully informed, male volunteers carrying out simulated dives. One group of 6 teams carried out dives in an atmosphere of 0.4 bar oxygen, balance nitrogen (O2-N2); another group of 7 teams used an atmosphere of 0.38 bar oxygen, 0.02 bar carbon dioxide, balance nitrogen (O2-N2-CO2). The dives consisted of a 48-h stay at 1.7 or 1.8 bar to saturate the tissues, followed by decompression to 1 bar air at 0.5 bar/min. Two decompression parameters were studied; the incidence of decompression sickness (DCS) in the 24 h postdecompression, and the incidence and grade of venous gas emboli (VGE) in the first 6 h postdecompression. The grade of VGE was assessed using the Kisman-Masurel scoring system which produces a bubble grade with the subject at rest and after movement. No significant difference was found in the incidence of DCS between the two groups. Twenty subjects were decompressed from 1.7 bar using each mixture, without signs or symptoms of DCS. However, after decompression from 1.8 bar there were 2 cases of DCS in 10 subjects in the O2-N2 group and 2 cases in 15 subjects in the O2-N2-CO2 group. The incidence of detectable VGE was always lower in the O2-N2-CO2 group at both saturation pressures; at 1.7 bar the VGE incidence was lower by 40% (P less than 0.05) at rest and by 55% (P less than 0.001) after movement. At 1.8 bar the reduction was 3% (NS) at rest and 30% (NS) after movement. The results indicate that decompression from 1.8 bar to 1 bar, with or without the presence of 0.02 bar carbon dioxide, is likely to produce more than 5% DCS.

Adult↗

PubMed1983

Hyperbaric exposure during pregnancy in sheep: staged and rapid decompression.

Hyperbaric exposure during pregnancy in sheep: staged and rapid decompression. Undersea Biomed Res 1983; 10(1): 11-15. --Twelve sheep with dated pregnancies were exposed for 20 min to hyperbaric pressure comparable to 165 feet of sea water weekly between the 49th and 133rd days of pregnancy. Six were decompressed in stages and six directly without decompression stops. Those that were decompressed gradually delivered normally at or near term. One lamb was abnormal, but the relationship to pressurization is unclear. Three of those decompressed rapidly aborted dead fetuses, and two others delivered mature, but affected, lambs. Under the conditions of this study staged decompression after repeated hyperbaric exposures protected the fetuses from the destructive effects of rapid decompression. Hyperbaric pressure did not alter gross anatomic development.

Abortion, Incomplete↗

PubMed1997

Reversibility in blood-brain barrier, microcirculation, and histology in rat brain after decompression.

To examine the changes in blood-brain barrier (BBB), cerebral microcirculation, and histology from 15 min to 72 h after decompression, 90 rats were exposed to experimental compression to 6 atm abs air for 90 min and subsequent rapid decompression. The disruption of BBB was examined by Evans blue extravasation. The cerebral microcirculation was demonstrated by perfusion with India ink. The area stained with Evans blue and the regions of defective filling with India ink, observed immediately after decompression decreased in size with time and were undetectable 3-24 h after decompression. The edematous brain tissue with enlarged perivascular space and darkly stained nerve cells also decreased to the uncompressed control level 1-24 h after decompression. These reversible dysbaric changes, however, reappeared 48-72 h after decompression. The different mechanisms, the physicochemical effects of microbubbles, and the maturation phenomenon after temporary brain ischemia induced by dysbaric microbubbles may be involved in the brain damage after decompression sickness.

Animals↗

PubMed1998

[Follow-up monitoring with magnetic resonance tomography after decompressive trephining in experimental "malignant" hemispheric infarct].

Acute ischemia in the complete territory of the carotid or the middle cerebral artery may lead to cerebral edema with raised intracranial pressure and progression to coma and death. Although clinical data suggest benefit for patients undergoing decompressive surgery for massive space occupying hemispheric stroke, little data about the effects of this procedure on morbidity and outcome is available. The experimental data support an early surgical approach. For early and probably most effective treatment of severe, space-occupying cerebral ischemia, the "malignant" character of the brain edema has to be recognized early after onset of vessel occlusion. Hereby magnetic resonance imaging (MRI) may allow to determine the clinical significance of brain edema early after onset, simultaneously allowing to monitor the evolution of ischemia. We performed serial SE-MRI in rats with acute hemispheric infarctions treated by decompressive craniectomy. Focal cerebral ischemia was induced in 36 rats using an endovascular occlusion technique. Decompressive craniectomy was performed 4 and 24 hours after vessel occlusion in groups of 12 animals each. Twelve animals were not treated by decompressive craniectomy (control group). Four, 24, 48, 72 and 168 hours after MCAO all animals were examined with conventional T1- and T2-weighted SE-MRI. Shift of the midline structures and compression of the ventricles were scored. Changes in weight and neurological performance were measured daily. The infarction volume was calculated by triphenyltetrazolium chloride staining 168 hours after MCAO. While mortality in the untreated group was 33.3%, none of the animals treated by a decompressive craniectomy died (mortality 0%). Neurological behaviour, weight loss and infarction volume were significantly better in the animals treated by early decompressive craniectomy (p < 0.05). Four hours after MCAO all untreated animals showed a massive shift of the midline structures and a massive compression of the ventricles; only 7 of 12 animals treated early by craniectomy showed mild mass effects. Correlation of the histological brain damage with T2-weighted MRI 4 hours after MCAO was poor (r = 0.41); later than 24 hours there was a good correlation (r > 0.7). Our results suggest that decompressive craniectomy in malignant cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. In the acute phase of hemispheric infarction conventional SE-MRI is not sensitive in estimation of infarction size. Later than 24 hours, conventinal SE-MRI proved to be useful in monitoring brain edema and infarction size in this rat model of malignant hemispheric stroke.

Animals↗

PubMed1994

Simultaneous active compression-decompression and abdominal binding increase carotid blood flow additively during cardiopulmonary resuscitation (CPR) in pigs.

The effects of adding active compression-decompression and abdominal binding separately or combined to standard compression CPR was tested in a randomized cross-over design during ventricular fibrillation in eight pigs. The flow and pressure effects of the two techniques appeared to be additive with no interference between the two. Carotid blood flow increased 22% with active compression-decompression, 34% with abdominal binding and 59% with the combination compared to flow with standard compression. Peak antegrade carotid flow occurred in early systole with retrograde flow in early diastole and close to zero in late diastole with no profound alterations induced by active decompression or abdominal binding. Abdominal binding increased the intrathoracic pressure during the compression phase as estimated from the esophageal pressure, while active decompression caused a negative esophageal pressure during the decompression phase. Neither active decompression nor abdominal binding caused any changes in the coronary perfusion pressure, nor in the left ventricular transmural pressure except for a rise in mid-diastolic pressure with active decompression.

Animals↗

PubMed1994

Active compression-decompression resuscitation: effect on resuscitation success after in-hospital cardiac arrest.

OBJECTIVES: The purpose of this study was to test the hypothesis that active compression-decompression would improve resuscitation success in human subjects after cardiac arrest. BACKGROUND: Active compression-decompression cardiopulmonary resuscitation is a new method that improves cardiopulmonary hemodynamic function in animal models and humans after cardiac arrest. METHODS: We conducted a prospective randomized clinical trial in patients with in-hospital cardiac arrest. Patients were assigned to receive standard manual or active compression-decompression cardiopulmonary resuscitation. The primary study end points were spontaneous return of circulation, 24-h survival and survival to hospital discharge. RESULTS: Fifty-three consecutive patients after cardiac arrest undergoing 64 resuscitation attempts were studied (30 women, 23 men; mean [+/- SD] age 71 +/- 13 years, range 38 to 96). Spontaneous return of circulation was observed in 24 (47%) of 53 patients and was increased in patients receiving active compression-decompression compared with those receiving standard manual cardiopulmonary resuscitation (15 [60%] of 25 vs. 9 [32%] of 28, respectively, p = 0.042); 24-h survival was increased (12 [48%] of 25 vs. 6 [21%] of 28, respectively, p = 0.041); and there was a trend toward improved survival to hospital discharge (6 [24%] of 25 vs. 3 [11%] of 28, respectively, p = 0.198) when active compression-decompression was compared with standard manual cardiopulmonary resuscitation. CONCLUSIONS: Active compression-decompression cardiopulmonary resuscitation improves return of spontaneous circulation and 24-h survival after in-hospital cardiac arrest. Active compression-decompression cardiopulmonary resuscitation appears to be a beneficial adjunct to standard manual cardiopulmonary resuscitation.

Aged↗

PubMed1991

Treatment of pseudotumor cerebri by primary and secondary optic nerve sheath decompression.

We performed optic nerve sheath decompression in 53 patients (101 eyes) with pseudotumor cerebri and visual loss. Sixty-nine eyes (85 patients) with acute papilledema uniformly had improved visual function after optic nerve sheath decompression. Of 32 eyes with chronic papilledema (18 patients), only ten had improved visual function after optic nerve sheath decompression. This difference was significant (P = .0001). Thirteen eyes required secondary or tertiary optic nerve sheath decompression after an initial successful result. Eleven of 13 eyes had improved visual function after repeat optic nerve sheath decompression. We believe that patients with acute papilledema and visual loss should be offered optic nerve sheath decompression, and if symptoms recur, repeat optic nerve sheath decompression is a safe and effective treatment option.

Acute Disease↗

PubMedDate not supplied

Treatment of acute nontoxic megacolon during colonoscopy: tube placement versus simple decompression.

The study compares the efficacy of colonoscopic decompression versus decompression and tube placement in the treatment of Ogilvie's syndrome. Nine patients were treated with a single colonoscopic decompression which resulted in four recurrences. In contrast, there were no recurrences observed in 11 patients who underwent decompression and subsequent tube placement (p less than 0.05). There was no morbidity observed from either decompression or tube placement. Tube placement added less than 10 min of additional procedure time to the colonoscopy. The tube utilized in this study was an enteroclysis tube with sideholes cut in the distal 20 cm. The tube was easily inserted over a Teflon-coated flexible guide wire inserted through the colonoscope into the cecum following decompression. This study demonstrates that colonoscopic decompression followed by tube placement is the preferred treatment modality for acute nontoxic megacolon.

Acute Disease↗

PubMed1997

The risk of diplopia following orbital floor and medial wall decompression in subtypes of ophthalmic Graves' disease.

We preoperatively divided 58 ophthalmic Graves' disease patients into types I and II categories before two-wall orbital decompression. Type I classification was given to patients who had no diplopia and essentially normal versions. Type II classification was assigned to patients with restrictive motility loss and diplopia within 20 degrees of the primary position. Ocular motility was assessed before and after two-wall orbital decompression. Only one of 25 type I patients (4%) experienced diplopia after orbital decompression, while seven of 14 (50%) (p = 0.001) type II patients without preoperative primary-position diplopia had primary diplopia postoperatively. Of 12 type II patients who had preoperative primary-position diplopia, esotropia increased by an average of 12.4 diopters postoperatively. Vertical deviation increased an average of 13.4 diopters for 10 patients who underwent unilateral two-wall decompression. The likelihood of new or worsening diplopia in all type II patients following decompression was 22 of 36 (61%). We conclude that adverse motility change following two-wall orbital decompression is rare in type I disease patients, but it occurs 61% of the time in type II disease patients. Predicting preoperatively which patients are likely to develop adverse motility change and diplopia may help clarify indications and risks of orbital decompression surgery in patients with ophthalmic Graves' disease.

Adolescent↗

PubMedDate not supplied

Lumbar spinal instability (olisthesis) after extensive posterior spinal decompression.

Twenty-seven patients who underwent extensive posterior spinal decompression procedures were reviewed to investigate the incidence, the clinical significance and contributing factors of the postdecompression olisthesis, and indication for spinal fusion at the time of extensive decompression. Eleven patients were female and 16 were male. The mean age was 49.4 years. Twenty-two patients were treated with extensive decompression and spinal fusion, and five patients were treated with decompression alone without spinal fusion. The average follow-up time was 2 1/2 years (1-4 1/2). The incidence of newly developed postdecompression olisthesis was 3.7% (1/27) and all four patients with preoperative spondylolisthesis progressed further postoperatively. The author was neither able to identify definitive contributing factors for olisthesis, nor able to confirm the previously reported factors: young age, normal disc heights, and multiple level decompression in this review study. The incidence rate of pseudarthrosis was high (27.3%) after the extensive posterior decompression and fusion. The concomitant spinal fusion is not routinely indicated to patients with extensive posterior spinal decompression. Furthermore, it does not appear to be effective in prevention of olisthesis. The concomitant spinal fusion should be exceptional rather than routine.

Adult↗

PubMed1994

Axon regeneration after decompression of the conus medullaris.

STUDY DESIGN: The effect of acute spinal stenosis (simulating fracture) and decompression of stenosis on axon regeneration was evaluated in an animal model. OBJECTIVES: Clinical function and quantitative histomorphometry were used to gain insight into the clinicopathologic effects of acute spinal stenosis and decompression. SUMMARY OF BACKGROUND DATA: Decompression of extrinsic compression after thoracolumbar fractures has been suggested to maximize recovery of neurologic function. Clinical studies seem to support this, but the histologic results of decompression are poorly understood. METHODS: Experimental spinal stenosis was created in 5 female beagle dogs, followed by decompression in three of the beagles at 6 weeks. Clinical function and histologic appearance were analyzed using a monoclonal antibody to neurofilaments. RESULTS: Stenosis consistently produced significant neurologic deficit and axon degeneration within motor roots distal to the stenosis. Decompression resulted in improved neurologic function and a tendency for the axons to return to normal number and volume based on quantitative histomorphometry. CONCLUSION: This study provides an animal model and functional and histologic data that support the use of decompression of acute spinal stenosis of 50% or more canal compromise at the level of the conus medullaris and a neurologic deficit. This may be seen clinically in thoracolumbar fractures.

Animals↗

PubMed1994

Optic nerve sheath decompression for the treatment of visual failure in chronic raised intracranial pressure.

The records of all patients undergoing optic nerve sheath decompression for visual failure in chronic raised intracranial pressure performed over a 15 year period have been reviewed. The aim was to study the visual outcome and relation to any shunting procedures. Fourteen patients (20 eyes) were identified in whom follow up information of at least one year was available. Eleven patients had benign intracranial hypertension (idiopathic intracranial hypertension) and three had dural venous sinus occlusive disease. Eight patients had unilateral surgery and six had bilateral surgery. Visual acuity and fields either improved or stabilised in 17 out of 20 eyes and three deteriorated. Of the eight patients undergoing unilateral surgery, the other eye remained stable in seven and deteriorated in one. Four patients required optic nerve sheath decompression despite previous shunting or subtemporal decompression. Five patients required shunts or subtemporal decompression after optic nerve sheath decompression because of persistent headache in three cases and for uncontrolled visual failure in two cases. No patients lost vision as a direct consequence of surgery. It is concluded that optic nerve sheath decompression is a safe and important therapeutic option in the management of chronic raised intracranial pressure complicated by visual loss. Vision can be saved after shunt failure, and in other cases may be maintained without the need for a shunt. Shunts may still be required, however, after optic nerve sheath decompression, especially for persistent headache.

Adult↗

PubMedDate not supplied

Equalization of amniotic fluid volumes after decompression amniocentesis for treatment of the twin oligohydramnios-polyhydramnios sequence.

OBJECTIVE: To measure acute and chronic changes in the placenta and amniotic fluid associated with performance of decompression amniocentesis in pregnancies with the twin oligohydramnios-polyhydramnios sequence (TOPS). METHODS: Amniotic fluid pressures, placental thickness, placental perfusion, and amniotic fluid volumes were measured in each sac of a monochorionic diamniotic twin gestation before and after decompression amniocentesis. Indigo carmine was injected into the polyhydramnic sac after decompression, and fluid from the oligohydramnic sac was sampled after equilibration. Spectrophotometric analysis of amniotic fluid specimens was performed for dye detection. Amniotic fluid volume and placental perfusion studies were repeated 1 week later. RESULTS: Three patients with TOPS were enrolled, and decompression amniocentesis was performed in the midtrimester. After decompression, amniotic fluid volume decreased in the polyhydramnic sac, amniotic fluid pressures decreased in both sacs, placental thickness increased, and umbilical artery Doppler velocimetry was unaffected. The amniotic fluid volume increased acutely in only one oligohydramnic sac after decompression, and ultrasonographic examination, amniotic fluid spectrophotometric analysis, and placental pathologic examination all identified interfetal membrane disruption as the etiology. CONCLUSIONS: Decompression amniocentesis as a treatment for TOPS does not result in acute or chronic changes in the amniotic fluid volume of the oligohydramnic sac in the absence of interfetal membrane disruption.

Adult↗

PubMedDate not supplied

Arthroscopic shoulder decompression development and application. A five year experience.

The purpose of this study was to critically evaluate the results of 80 consecutive subacromial decompressions in 76 patients with impingement syndrome and to assess the value of arthroscopy for subacromial decompression. The average followup was 32 months. The charts, radiographs, and clinical findings of all patients were reviewed. There were 57 males and 19 females, with a mean age of 41 years. Subjective, objective, and functional results were assessed. The greatest improvement was seen in the areas of pain with activity, pain at night, and use of medications. Impingement signs had decreased significantly at final followup. The procedure allowed an early return to work and competitive athletics. Repeat surgery was necessary in eight cases: three full thickness rotator cuff repairs, two stabilization procedures, two open debridements, and one biceps tenodesis and excision of the distal clavicle. An important finding was the number of unsuspected diagnoses that were made during arthroscopy. Twelve patients had significant labral tears, seven patients had complete rotator cuff tears, four patients had biceps tendon fraying, and two patients had loose bodies in the glenohumeral joint. In most of these shoulders the intraarticular lesions would not have been diagnosed by open subacromial decompression. Radiographic evaluation suggested that the "outlet view" can be helpful in determining depth of bony resection and may be a prognostic indicator. Patients who underwent simple decompression rather than bony resection tended to be younger and had less Stage III impingement changes, and they generally had a slightly better final outcome. Patients who had compensation injuries generally had a poorer outcome. In reviewing our results, it appears that arthroscopic subacromial decompression can be a successful alternative to open decompression. The key to success for closed decompression is related to 1) accurate diagnosis, 2) selective treatment, 3) adequate bone resection when required, and 4) repair of full thickness rotator cuff tears in the active patient. Postoperative rehabilitation, which includes early range of motion, is critical.

Acromion↗