Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “decompression”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 163 records · Page 9Linked to original sources
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↗
PubMed1991

Intraoperative monitoring of the facial nerve during decompressive surgery for hemifacial spasm.

In 11 consecutive patients, intraoperative electromyographic (EMG) recordings were made from the facial muscles during microvascular decompression for hemifacial spasm. In one patient, recordings could not be obtained for technical reasons, and two patients had no abnormality. In the remaining eight patients, the abnormal response resolved before decompression in two, resolved immediately at the time of decompression in five, and failed to resolve in one. All patients were relieved of their hemifacial spasm. In the five patients whose abnormalities resolved at the time of decompression, there was a precise intraoperative correlation between decompression of the nerve and disappearance of the abnormal EMG response. In three cases, this was a useful guide to the need to decompress more than one vessel. These results confirm the findings of Møller and Jannetta, support the use of this technique for intraoperative monitoring of facial nerve decompression procedures, and provide strong circumstantial evidence that vascular cross-compression is an important etiological factor in hemifacial spasm.

Electromyography↗
PubMed1994

Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression.

Thirty-one (2%) of 1404 consecutive patients with typical trigeminal neuralgia who underwent microvascular decompression between 1972 and 1993 were found to have vascular compression by the vertebral artery (VA) or the basilar artery (BA). Compared to the remaining 1373 patients, this subgroup was older (mean age 62 vs. 55 years, p < 0.001), was predominantly male (68% vs. 39%, p < 0.002), demonstrated left-sided predominance (65% vs. 39%, p < 0.002), was more likely to be hypertensive (65% vs. 18%, p < 0.001), and was more likely to have ipsilateral hemifacial spasm (16% vs. 0.6%, p < 0.001). The trigeminal nerve was compressed by the VA in 18 cases (the VA alone in three and the VA plus other vessels in 15), the BA in 12 cases (the BA alone in four and the BA plus other vessels in eight), and the vertebrobasilar junction in one case. Twenty-nine of the 31 patients underwent vascular decompression of the trigeminal nerve, one had a complete trigeminal root section, and one underwent partial root section with vascular decompression of the remaining nerve. All 31 patients were pain-free, off medication immediately after surgery, and this pain-free, medication-free status was maintained at 1 year after surgery in 96% of cases, at 3 years in 92%, and at 10 years in 86%, based on life-table analysis. Minor trigeminal hypesthesia/hypalgesia was present preoperatively in 52%. New or worsened minor hypesthesia/hypalgesia developed in 41% of patients, while transient diplopia as well as hearing loss developed in 23% and 13% in the overall series, respectively. No patient developed major trigeminal sensory loss or masseter weakness after vascular decompression alone. There was no operative mortality. Vascular decompression is an effective treatment for patients with trigeminal neuralgia who have vertebrobasilar compression of the trigeminal nerve. Patients should be warned that decompression of a tortuous vertebrobasilar system carries a higher risk of mild trigeminal dysfunction, diplopia, and hearing loss than standard microvascular decompression.

Age Factors↗
PubMed1995

Microvascular decompression for hemifacial spasm.

The authors report the results of 782 microvascular decompression procedures for hemifacial spasm in 703 patients (705 sides), with follow-up study from 1 to 20 years (mean 8 years). Of 648 patients who had not undergone prior intracranial procedures for hemifacial spasm, 65% were women; their mean age was 52 years, and the mean preoperative duration of symptoms was 7 years. The onset of symptoms was typical in 92% and atypical in 8%. An additional 57 patients who had undergone prior microvascular decompression elsewhere were analyzed as a separate group. Patients were followed prospectively with annual questionnaires. Kaplan-Meier methods showed that among patients without prior microvascular decompression elsewhere, 84% had excellent results and 7% had partial success 10 years postoperatively. Subgroup analyses (Cox proportional hazards model) showed that men had better results than women, and patients with typical onset of symptoms had better results than those with atypical onset. Nearly all failures occurred within 24 months of operation; 9% of patients underwent reoperation for recurrent symptoms. Second microvascular decompression procedures were less successful, whether the first procedure was performed at Presbyterian-University Hospital or elsewhere, unless the procedure was performed within 30 days after the first microvascular decompression. Patient age, side and preoperative duration of symptoms, history of Bell's palsy, preoperative presence of facial weakness or synkinesis, and implant material used had no influence on postoperative results. Complications after the first microvascular decompression for hemifacial spasm included ipsilateral deaf ear in 2.6% and ipsilateral permanent, severe facial weakness in 0.9% of patients. Complications were more frequent in reoperated patients. In all, one operative death (0.1%) and two brainstem infarctions (0.3%) occurred. Microvascular decompression is a safe and definitive treatment for hemifacial spasm with proven long-term efficacy.

Adolescent↗
PubMed1992

Wide versus selective decompression in the operative treatment of lumbar spinal stenosis.

The early post-operative results of wide versus selective decompression in a group of 64 patients with lumbar spinal stenosis were studied with the aim of ascertaining whether a more limited approach gives comparable results to the more traditional method of wide decompression. Wide decompression involved complete removal of a vertebral lamina at the stenotic level. Selective decompression refers to removal of the lower part of the superior lamina and the upper part of the inferior lamina at the stenotic level together with limited facetectomies. Patients were compared with respect to post-operative relief of back pain and sciatica/claudication as well as the ability to return to their pre-morbid level of functional activity. Follow up ranged from 4 months to 26 months. Results showed that both wide and selective decompression were able to achieve complete or considerable relief of symptoms and return to pre-morbid level of activity in 74% to 84% of patients. The results in the 2 groups were not statistically different. It appears that within the first 2 years of surgery, the vast majority of our post-decompression patients had good results regardless of whether wide or selective decompression was used.

Adult↗
PubMed1991

1991 Volvo Award in experimental studies. Cauda equina syndrome: neurologic recovery following immediate, early, or late decompression.

An animal model of cauda equina syndrome was developed. Neurologic recovery was analyzed following immediate, early, and delayed decompression. Five experimental groups, each containing six dogs, were studied. Compression of the cauda equina was performed in all 30 dogs following an L6-7 laminectomy. The cauda equina was constricted by 75% in each group. The first group was constricted and immediately decompressed. The remaining groups were constricted for 1 hour, 6 hours, 24 hours, and 1 week, respectively, before being decompressed. Somatosensory evoked potentials were performed before and after surgery, before and immediately after decompression, and 6 weeks following decompression. Daily neurologic exams using the Tarlov grading scale were performed. At 6 weeks postdecompression, all dogs were killed, and the neural elements analyzed histologically. Following compression, all 30 dogs had significant lower extremity weakness, tail paralysis, and urinary incontinence. All dogs recovered significant motor function 6 weeks following decompression. The dogs with immediate decompression generally recovered neurologic function within 2-5 days. The dogs receiving 1-hour and 6-hour compression recovered within 5-7 days. The dogs receiving 24-hour compression remained paraparetic 5-7 days, with bladder dysfunction for 7-10 days and tail dysfunction persisting for 4 weeks. The dogs with compression for 1 week were paraparetic (Tarlov Grade 2 or 3) and incontinent during the duration of cauda equina compression. They recovered to walking by 1 week and Tarlov Grade 5 with bladder and tail control at the time of euthanasia. Immediately after compression, all five groups demonstrated at least 50% deterioration of the posterior tibial nerve evoked potential amplitudes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Pathogenetic aspects of decompression interventions in complicated injuries of the spine].

The paper is based on the analysis of the results of clinical, pathophysiological and roentgenological examinations and on the data of surgical verification of the causes of neurologic deficiency in 163 patients. Proceeding from the condition that the principal operations in cases of complicated fractures of the spine are decompression and stabilization interventions, the authors have elaborated a system of such interventions and stated the main principles of choice of the methods of decompression. In particular they have proposed the following extents of decompression interventions: decompression of the contents of the vertebral canal, decompression of the contents of the dural sac and intratrunk decompression of the spinal cord. The methods of decompression interventions may be correction, correction and stabilization, resection and resection and stabilization. The proposed scheme allows to eliminate the existing terminological discord and provides for objective evaluation of the efficiency of the intervention.

Fractures, Bone↗
PubMed1994

Graves ophthalmopathy. Results of transantral orbital decompression performed primarily for cosmetic indications.

PURPOSE: Transantral orbital decompression is effective treatment for excessive proptosis and optic neuropathy due to Graves ophthalmopathy. In these sight-threatening circumstances, patients willingly accept the side effects of orbital decompression. When transantral orbital decompression is performed for cosmetic indications, patients' acceptance of side effects may be different. This study reports detailed results of transantral decompression for 34 patients in whom the indications were primarily cosmetic. METHODS: The medical records of 34 patients with Graves ophthalmopathy who had transantral orbital decompression primarily for cosmetic indications were reviewed. Preoperative and postoperative physical features of the eyes were compared. Long-term assessment was formulated from follow-up examination and a follow-up questionnaire. RESULTS: The most notable improvement was in the reduction of proptosis (mean decrease, 5.2 mm). The frequency of asymmetry of proptosis, however, did not improve. Asymmetry was more than 1 mm in 44% of patients preoperatively and in 54% postoperatively. Although the palpebral fissure was decreased by an average of 2.7 mm, upper lid retraction became worse in 12 (43%) of 28 eyes. Of 15 patients who had no diplopia preoperatively, continuous diplopia developed postoperatively in 73%. The patients underwent a total of 37 eye muscle operations and 31 eyelid operations after decompression. Of 29 patients who responded to a long-term follow-up questionnaire, 69% were satisfied with the appearance of the eyes and 31% found it acceptable. No patient was dissatisfied. Symptomatic diplopia was present in 6.9% of patients at the time of the follow-up questionnaire. CONCLUSION: Transantral orbital decompression performed for cosmetic indications in Graves ophthalmopathy may need to be followed by eye muscle and lid operations. These procedures result in a high degree of patient satisfaction. However, a small percentage of patients experience persistent diplopia, despite multiple eye muscle procedures.

Adolescent↗
PubMed1976

The response of fish blood cells, particularly thrombocytes, to decompression.

The effects of decompression on various blood-cell types in chinook salmon (Oncorhynchus tshawytscha) were investigated using a 4-liter hyperbaric chamber. Thrombocytes (platelets) were found to decrease significantly in numbers following lethal and nonlethal decompressions. The response was highly dependent on depth, gas solubility, and rate of decompression, whereby increasing depth or gas solubility caused greater and faster declines of thrombocyte levels. Return of thrombocyte numbers to normal values usually occurred within 48 hours, except after the more severe decompressions where recovery was never fully attained during the sampling period. Erythrocyte levels increased significantly 1 day after a severe decompression, suggesting hemoconcentration. Leucocytes appeared not to respond to decompression; they were not decreased compared to normal levels, although they were significantly decreased compared to levels of the chamber controls in the nonpressurized chamber. The results are discussed in relation to possible involvement of the fish's blood-coagulation system after decompression.

Animals↗
PubMed1984

Ultrasonic monitoring of decompression procedures.

p6rly detection of bubbles may provide clues to the mechanism of their formation, and a knowledge of their extent during a decompression may allow the prevention of decompression sickness. We have used ultrasound imaging to study bubble formation in peripheral tissues. The results suggest that: (a) a threshold supersaturation for bubble formation exists; (b) the earliest bubbles are intravascular; (c) before signs of decompression sickness a substantial accumulation of stationary bubbles occurs. Despite the success of Doppler methods in detecting moving bubbles after decompressions normally considered safe, recent studies have shown that the correlation between number of bubbles detected and symptoms of decompression sickness is often poor. We have used a time integral of the ultrasound images, which avoids laborious image analysis, to follow the extent of both moving and stationary bubbles. Human trials involving a wide variety of decompressions suggest that correct prediction of symptoms is possible.

Animals↗
PubMed1976

Decompression-induced decrease in nitrogen elimination rate in awake dogs.

Formulation of safe decompression procedures still requires unproven assumptions regarding both gas equilibration rates and the associated ascent criteria. Although the assumption of symmetry of uptake and elimination rates has been suspect for several years, few data are available. Measurements of actual mixed venous blood nitrogen content [vN2] during compression and following decompression in chronically catheterized awake dogs have clearly demonstrated that desaturation is markedly slower than saturation, and that this effect can be imposed by decompression. The disappearance of arteriovenous nitrogen concentration differences during desaturation following a decompression that produced decompression sickness indicates that cardiopulmonary and cardiovascular changes induced by mechanisms associated with decompression per se can potentiate its deleterious effects. Current US practices do not provide for such asymmetry, while those used in the UK have incorporated this in their models for the last decade.

Animals↗
PubMed2001

The physiological kinetics of nitrogen and the prevention of decompression sickness.

Decompression sickness (DCS) is a potentially crippling disease caused by intracorporeal bubble formation during or after decompression from a compressed gas underwater dive. Bubbles most commonly evolve from dissolved inert gas accumulated during the exposure to increased ambient pressure. Most diving is performed breathing air, and the inert gas of interest is nitrogen. Divers use algorithms based on nitrogen kinetic models to plan the duration and degree of exposure to increased ambient pressure and to control their ascent rate. However, even correct execution of dives planned using such algorithms often results in bubble formation and may result in DCS. This reflects the importance of idiosyncratic host factors that are difficult to model, and deficiencies in current nitrogen kinetic models. Models describing the exchange of nitrogen between tissues and blood may be based on distributed capillary units or lumped compartments, either of which may be perfusion- or diffusion-limited. However, such simplistic models are usually poor predictors of experimental nitrogen kinetics at the organ or tissue level, probably because they fail to account for factors such as heterogeneity in both tissue composition and blood perfusion and non-capillary exchange mechanisms. The modelling of safe decompression procedures is further complicated by incomplete understanding of the processes that determine bubble formation. Moreover, any formation of bubbles during decompression alters subsequent nitrogen kinetics. Although these factors mandate complex resolutions to account for the interaction between dissolved nitrogen kinetics and bubble formation and growth, most decompression schedules are based on relatively simple perfusion-limited lumped compartment models of blood: tissue nitrogen exchange. Not surprisingly, all models inevitably require empirical adjustment based on outcomes in the field. Improvements in the predictive power of decompression calculations are being achieved using probabilistic bubble models, but divers will always be subject to the possibility of developing DCS despite adherence to prescribed limits.

Algorithms↗
PubMed1994

Cerebral imaging of decompression injury patients with 18-F-2-fluoro-2-deoxyglucose positron emission tomography.

The objective assessment of the extent of cerebral insult and the effects of therapy in decompression injury patients has proven to be difficult by most imaging modalities. In this pilot study we evaluated the ability of 18-F-2-fluoro-2-deoxyglucose (FDG) positron emission tomography (PET) to identify metabolic brain abnormalities in decompression injury patients. Twenty-two patients who were evaluated at our institution for decompression accidents were evaluated with FDG-PET. Four of the 22 patients had no neurologic symptoms and no neurologic findings on clinical exam at the time of the FDG-PET study. No statistically significant correlations were found between the presence of symptoms and the demonstration of abnormalities on the PET study and no statistically significant correlation was found between the location of the decompression injury and the demonstration of abnormalities on the PET study. We conclude that FDG-PET imaging of the brain cannot reliably identify cerebral abnormalities in patients with decompression injuries and would be of limited benefit for monitoring therapy in patients with decompression illness.

Adult↗
PubMed1997

Exercise during decompression reduces the amount of venous gas emboli.

To determine the effects of moderate, intermittent exercise during decompression on the Doppler detectable amount of venous gas emboli (VGE), 29 healthy male volunteers performed 44 wet (8 degrees +/- 2 degrees C) dives to 45 msw (450 kPa) for 30 min with standard air decompression. During compression and the bottom period, all subjects were inactive; during decompression, 28 remained inactive, 11 performed leg exercise, and 5 did arm exercise. Intermittent exercise was controlled at approximately 50% of each subject's arm or leg aerobic capacity. At 30-min intervals after surfacing, subjects were monitored with a Doppler ultrasonic bubble detector. The Doppler scores were used to calculate the Kisman Integrated Severity Score (KISS). The KISS were log transformed (with zeroes being equivalent to log 0.01) and analyzed with a one-way analysis of variance. No significant differences (P < or = .05) between mean KISS scores after arm or leg exercise were observed, thus these data were pooled and compared to those of the inactive controls. The mean pooled KISS after exercising during decompression were significantly lower than those of the inactive controls. Moderate, intermittent exercise during decompression apparently reduces the amount of Doppler-detectable VGE after diving. The incidence rate of decompression sickness in both groups was not significantly different (P < 0.05).

Adult↗
PubMed1993

Spinal cord decompression sickness in sport diving.

OBJECTIVE: To summarize 16 years' experience in the diagnosis and treatment of spinal cord decompression sickness in Israel. DESIGN: The survey data were collected firsthand by physicians trained in underwater diving medicine. SETTING: The Israeli Naval Medical Institute, Israel's national hyperbaric referral center. PATIENTS: Sixty-eight sport divers diagnosed as having spinal cord decompression sickness. INTERVENTIONS: Hydration and 100% oxygen breathing until the patient reached the hyperbaric chamber. All patients received recompression therapy on US Navy treatment tables using oxygen, except for six who were treated by Comex Treatment Table CX-30, which uses helium in addition to oxygen. MAIN OUTCOME MEASURES: Neurological examination after the completion of recompression therapy. RESULTS: Forty-one percent of the dives were performed within the decompression limits of the US Navy standard decompression tables. Risk factors were fatigue, circumstances suggesting dehydration, and extreme physical effort. The most common presenting symptoms were paresthesias, weakness of the legs, lower back pain, or abdominal pain. Full recovery was achieved in 79% of the patients. Spinal symptoms appeared immediately on surfacing in six of the eight patients who continued to have multiple neurological sequelae. CONCLUSIONS: United States Navy air decompression tables appear not to be completely safe for sport divers. Even mild spinal symptoms identified on surfacing should be treated vigorously. High-pressure oxygen-helium therapy seems to be a promising alternative in cases of severe spinal cord decompression sickness.

Adult↗
PubMed1982

The permeability alteration of brain and spinal cord vasculature to horseradish peroxidase during experimental decompression sickness as compared to the alteration in permeability induced by hyperosmolar solution.

The permeability of microvasculature in the cerebral cortex, neostriatum, and spinal cord to i.v. injected horseradish peroxidase (HRP) has been investigated in rats following experimental compression to 6.1 bars (abs.) air for 90 min, and subsequent decompression to the ambient pressure in 1 min. For comparison, 1 ml of 2.0 M urea was injected into the right common carotid artery of rats during 15 s. After exposure to compression-decompression, under the light microscope focal leaky areas were found in all the regions examined. The leakage was most prominent in the grey matter of the spinal cord, and the cerebral cortex. In decompressed rats, arterioles were most often the site of peroxidase extravasation, whereas extravasation of HRP was less frequently displayed by capillaries and venules. In urea-treated rats, capillaries and venules frequently displayed extravasation of HRP as well. Parenchymal cells accumulated the trace adjacent to the leaky areas. Under the electron microscope, the extravasation of HRP was associated with peroxidase-containing pleomorphic vesicular structures in the endothelium, both in decompressed and urea-injected rats. Moreover, in contrast to decompressed rats, the junctions between endothelial cells were penetrated by the trace in urea-treated rats. Accordingly, the results indicate that during decompression sickness the pathway for the extravasation of proteins is through vesicular transfer, whereas the injection of hyperosmolar urea induces extravasation, both through vesicular transfer and junctions between the endothelial cells.

Animals↗