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PubMed2003

[Observation of clinical results of orbital decompression in 30 cases of malignant exophthalmos].

OBJECTIVE: To evaluate the effectiveness and safety of orbital decompression for the treatment of malignant exophthalmos. METHODS: Thirty four eyes of malignant exophthalmos were followed-up for 3 months to 9 years (averaged 6 years) after orbital decompression (two walls decompression in 22 eyes, three walls decompression in 12 eyes). The postoperative vision, protrusion value and appearance of the patients were examined and analyzed. RESULTS: Complete closure of palpebral fissure was attained in all cases and the visual acuity was increased in 25 eyes, remained the same in 5 eyes and decreased in 4 eyes. The mean recession of exophthalmos after operation was 3.8 mm in two walls decompression and 7.1 mm in three walls decompression, respectively. CONCLUSION: Orbital decompression is an effective method for the treatment of malignant exophthalmos.

Adult↗
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↗
PubMed2000

Abdominal decompression for suspected fetal compromise/pre-eclampsia.

BACKGROUND: Abdominal decompression was developed as a means of pain relief during labour. It has also been used for complications of pregnancy, and in healthy pregnant women in an attempt to improve fetal wellbeing and intellectual development. OBJECTIVES: The objective of this review was to assess the effects of antenatal abdominal decompression for maternal hypertension or impaired fetal growth, on perinatal outcome. SEARCH STRATEGY: The Cochrane Pregnancy and Childbirth Group trials register and the Cochrane Controlled Trials Register were searched. Date of last search: February 1998. SELECTION CRITERIA: Randomised or quasi-randomised trials comparing abdominal decompression with no decompression in women with pre-eclampsia and/or fetuses thought to be compromised. DATA COLLECTION AND ANALYSIS: Eligibility and trial quality were assessed by one reviewer. MAIN RESULTS: Three studies were included, all with the possibility of containing serious bias. Therapeutic abdominal decompression was associated with the following reductions: persistent pre-eclampsia (relative risk 0.36, 95% confidence interval 0.18 to 0.72); fetal distress in labour (relative risk 0.37, 95% confidence interval 0.19 to 0.71); low birthweight (relative risk 0.50, 95% confidence interval 0.40 to 0. 63); Apgar scores less than six at one minute (relative risk 0.26, 95% confidence interval 0.12 to 0.56); and perinatal mortality (relative risk 0.39, 95% confidence interval 0.22 to 0.71). REVIEWER'S CONCLUSIONS: Due to the methodological limitations of the studies, the effects of therapeutic abdominal decompression are not clear. The apparent improvements in birthweight and perinatal mortality warrant further evaluation of abdominal decompression where there is impaired fetal growth and possibly for women with pre-eclampsia.

Female↗
PubMed2000

Abdominal decompression in normal pregnancy.

BACKGROUND: Abdominal decompression was developed as a means of pain relief during labour. It has also been used for complications of pregnancy, and in healthy pregnant women in an attempt to improve fetal wellbeing and intellectual development. OBJECTIVES: The objective of this review was to assess the effects of prophylactic abdominal decompression on admission for pre-eclampsia, fetal growth, perinatal morbidity and mortality and childhood development. SEARCH STRATEGY: The Cochrane Pregnancy and Childbirth Group trials register and the Cochrane Controlled Trials Register were searched. Date of last search: February 1999. SELECTION CRITERIA: Randomised trials comparing abdominal decompression with dummy decompression or no treatment in healthy pregnant women. DATA COLLECTION AND ANALYSIS: Eligibility and trial quality were assessed by one reviewer. MAIN RESULTS: Three studies were included. There was no difference between the abdominal decompression groups and the control groups for low birth weight (relative risk 0.69, 95% confidence interval 0.27 to 1.77) and perinatal mortality (relative risk 2.47, 95% confidence interval 0.77 to 7.92). There were no differences in admission for pre-eclampsia, Apgar score and childhood development. REVIEWER'S CONCLUSIONS: There is no evidence to support the use of abdominal decompression in normal pregnancies. Future research should be directed towards the use of abdominal decompression during labour, and during complicated pregnancies.

Female↗
PubMed2002

Decompressive craniectomy following traumatic brain injury: ICP, CPP and neurological outcome.

Decompressive craniectomy is often the final option in the management of posttraumatic intracranial hypertension. Aim of this study was to investigate the effect of secondary decompression on intracranial pressure (ICP), cerebral perfusion pressure (CPP) and neurological outcome. 62 patients decompressed after severe head injury were included in the retrospective study. Decompression was performed when ICP could not be controlled by non-surgical treatment. Mean age was 36.6 yrs, 77.4% were male. Initial Glasgow Coma Score (GCS) was 6. Outcome was determined 6 months after trauma according to the Glasgow Outcome Scale (GOS) and the functional Barthel-Index (BI). In the last hour before decompression ICP was 40.5 +/- 1.6 mmHg and CPP was 65.3 +/- 2.1 mmHg (being maintained, if necesary, by catecholamines). ICP was significantly reduced to 9.8 +/- 1.3 mmHg by surgery and CPP improved to 78.2 +/- 2.3 mmHg. 12 hrs following decompression mean ICP rose to 21.6 +/- 1.7 mmHg again (CPP: 73.6 +/- 1.7 mmHg), but in the following period ICP could be kept below 25 mmHg in the majority of patients. 6 months after trauma 22.5% of the patients had died (except one all these patients were aged more than 50 yrs). 48.4% of patients survived with an unfavourable outcome (GOS 2 + 3), while 29.1% had a favourable outcome (GOS 4 + 5). Decompressive craniectomy is highly effective to treat otherwise uncontrollable intracranial hypertension and improves CPP. A satisfactory outcome, however, is only achieved under strict consideration of negative predictors (e.g. age).

Adolescent↗
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↗
PubMed1999

The influence of spinal canal narrowing and timing of decompression on neurologic recovery after spinal cord contusion in a rat model.

STUDY DESIGN: The effect of spinal canal narrowing and the timing of decompression after a spinal cord injury were evaluated using a rat model. OBJECTIVE: To evaluate whether progressive spinal canal narrowing after a spinal cord injury results in a less favorable neurologic recovery. Additionally, to evaluate the effect of the timing of decompression after spinal cord injury on neurologic recovery. SUMMARY OF BACKGROUND DATA: Results in previous studies are contradictory about whether the amount of canal narrowing or the timing of decompression after a spinal cord injury affects the degree of neurologic recovery. METHODS: Forty adult male Sprague-Dawley rats were equally divided into a control group, in which spacers of 20%, 35%, and 50% were placed into the spinal canal after laminectomy, and an injury group in which the spacers were placed after a standardized incomplete spinal cord injury. After spacer removal, neurologic recovery in both was monitored by Basso, Beattie, Bresnahan (BBB) Locomotor Rating Scale (Ohio State University, Columbus, OH) motor scores and transcranial magnetic motor evoked potentials for 6 weeks followed by histologic examination of the spinal cords. Subsequently, 42 rats were divided into five groups in which, after spacer placement, the time until decompression was lengthened 0, 2, 6, 24, and 72 hours. Again, serial BBB motor scores and transcranial magnetic motor evoked potentials were used to assess neurologic recovery for 6 weeks until the animals were killed for histologic evaluation. RESULTS: Spacer placement alone in the control animals resulted in no neurologic injury until canal narrowing reached 50%. All of the control groups (spacer only) exhibited significantly better (P < 0.05) motor scores compared with the injury groups (injury followed by spacer insertion). Within the injury groups the motor scores were progressively lower as spacer sizes increased from the no-spacer group to the 35% group. The results in the 35% and 50% groups were not statistically different. The results of the time until decompression demonstrated that the motor scores were consistently better the shorter the duration of spacer placement (P < 0.05) for each of the time groups (0, 2, 6, 24, and 72 hours) over the 6-week recovery period. Histologic analysis showed more severe spinal cord damage as both spinal canal narrowing and the time until decompression increased. CONCLUSION: The results in this study present strong evidence that the prognosis for neurologic recovery is adversely affected by both a higher percentage of canal narrowing and a longer duration of canal narrowing after a spinal cord injury. The tolerance for spinal canal narrowing with a contused cord appears diminished, indicating that an injured spinal cord may benefit from early decompression. Additionally, it appears that the longer the spinal cord compression exists after an incomplete spinal cord injury, the worse the prognosis for neurologic recovery.

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↗