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PubMed1997

Viscoelastic relaxation and regional blood flow response to spinal cord compression and decompression.

STUDY DESIGN: To better understand the relationships between primary mechanical factors of spinal cord trauma and secondary mechanisms of injury, this study evaluated regional blood flow and somatosensory evoked potential function in an in vivo canine model with controlled velocity spinal cord displacement and real-time piston-spinal cord interface pressure feedback. OBJECTIVES: To determine the effect of regional spinal cord blood flow and viscoelastic cord relaxation on recovery of neural conduction, with and without spinal cord decompression. SUMMARY OF BACKGROUND DATA: The relative contribution of mechanical and vascular factors on spinal cord injury remains undefined. METHODS: Twelve beagles were anesthetized and underwent T13 laminectomy. A constant velocity spinal cord compression was applied using a hydraulic loading piston with a subminiature pressure transducer rigidly attached to the spinal column. Spinal cord displacement was stopped when somatosensory evoked potential amplitudes decreased by 50% (maximum compression). Six animals were decompressed 5 minutes after maximum compression and were compared with six animals who had spinal cord displacement maintained for 3 hours and were not decompressed. Regional spinal cord blood flow was measured with a fluorescent microsphere technique. RESULTS: At maximum compression, regional spinal cord blood flow at the injury site fell from 19.0 +/- 1.3 mL/100 g/min to 12.6 +/- 1.0 mL/100 g/min, whereas piston-spinal cord interface pressure was 30.5 +/- 1.8 kPa, and cord displacement measured 2.1 +/- 0.1 mm (mean +/- SE). Five minutes after the piston translation was stopped, the spinal cord interface pressure had dissipated 51%, whereas the somatosensory evoked potential amplitudes continued to decrease to 16% of baseline. In the sustained compression group, cord interface pressure relaxed to 13% of maximum within 90 minutes; however, no recovery of somatosensory evoked potential function occurred, and regional spinal cord blood flow remained significantly lower than baseline at 30 and 180 minutes after maximum compression. In the six animals that underwent spinal cord decompression, somatosensory evoked potential function and regional spinal cord blood flow recovered to baseline 30 minutes after maximum compression. CONCLUSIONS: Despite rapid cord relaxation of more than 50% within 5 minutes after maximum compression, somatosensory evoked potential conduction recovered only with early decompression. Spinal cord decompression was associated with an early recovery of regional spinal cord blood flow and somatosensory evoked potential recovery. By 3 hours, spinal cord blood flow was similar in both the compressed and decompressed groups, despite that somatosensory evoked potential recovery occurred only in the decompressed group.

Animals↗

PubMed1997

Intraoperative dermatomal evoked potential monitoring fails to predict outcome from lumbar decompression surgery.

STUDY DESIGN: Thirty-three patients with single-level, unilateral lumbosacral radiculopathy underwent micro-decompression and intraoperative dermatomal evoked potential monitoring. Side-to-side latency asymmetry was calculated. A criteria for "abnormal" was defined. Intraoperative dermatomal evoked potentials were obtained before and after decompression. The changes were correlated with clinical outcome at the 3-month follow-up examination. OBJECTIVES: To determine whether intraoperative dermatomal evoked potential latency asymmetry confirms nerve root compression and whether an improvement of latency asymmetry after decompression predicts a good clinical outcome. SUMMARY OF BACKGROUND DATA: Intraoperative dermatomal evoked potential has been proposed as a test to assess the adequacy of nerve root decompression. Initial reports suggested improvement of dermatomal evoked potential amplitude and latency after decompression. The clinical efficacy is controversial because of its technical difficulty and inherent variation. METHODS: Cervical recording was chosen to reduce the effects of anesthesia. The asymptomatic nerve root was used as a control. Quality of the tracings was determined by evoked potentials-to-noise amplitude ratio. Clinical outcome was based on patient's pain relief and satisfaction. RESULTS: Tracings of acceptable quality were obtained at baseline in 57.6% (19 of 33) of patients. A side-to-side latency asymmetry > 5% was defined as abnormal. Before decompression, 68.4% (13 of 19) of patients had an abnormal dermatomal evoked potential. After decompression, latency asymmetry returned to normal in every patient. Clinical outcome was good or excellent in 13 patients, fair in four patients, and poor in two patients. Dermatomal evoked potential latency improvements were not related to variation in clinical outcome. CONCLUSIONS: Intraoperative dermatomal evoked potential monitoring is technically demanding. Finding reproducible potentials is difficult. More research is necessary before general use of dermatomal evoked potentials for monitoring nerve root decompression.

Adult↗

PubMed1993

Effects of decompressive craniectomy on regional cerebral blood flow in severe head trauma patients.

The effect of decompressive craniectomy on regional cerebral blood flow (rCBF) was investigated in five patients with severe head trauma who underwent decompressive craniectomy. Repeated rCBF studies using single photon emission computed tomography with 99mtechnetium-hexamethylpropyleneamine oxime observed that a hyperperfusion area (focal CBF increase) occurred in the decompressed brain within 24 hours after decompressive craniectomy. The hyperperfusion area in the decompressed brain enlarged and increased in severity by 1 week after surgery. However, it attenuated and disappeared by 1 month after surgery. The chronology of the hyperperfusion area corresponded to the change in the swelling of decompressed brain observed by x-ray computed tomography. Patient consciousness showed a significant and progressive improvement in the postoperative 1 month period. Decompressive craniectomy may cause a focal CBF increase in the decompressed brain related to the beneficial effect in patients with acute severe head trauma.

Adolescent↗

PubMed1993

The effect of surgical decompression on neurologic outcome after lumbar fractures.

From 1980 until 1989, 69 patients with lumbar fractures resulting in incomplete paraparesis were admitted to the authors' medical center for treatment. Thirty had anterior vertebrectomy, including 18 who had posterior instrumentation and four who had anterior instrumentation. Twenty-two patients were treated with a posterolateral decompression and fusion, including four who also required an anterior decompression. Nineteen of the remaining 21 patients required posterior spine instrumentation and fusion only. The American Spinal Injury Association (ASIA) motor index score was determined for each patient pre- and postoperatively and used to compare these three treatment groups. Average follow-up period for the patients was 19 months. The improvement in ASIA motor score for all patients treated with decompression averaged 10 and similar improvement was obtained in those who were treated with posterior decompression (10.2 points). The average improvement in those who had vertebrectomy was 9.9 points. For those who had fusion without decompression, average improvement was 4.2 points. Comparing those patients who were surgically decompressed, either anteriorly or posteriorly, with those patients who only underwent fusion, the difference in neurologic improvement was statistically significant. Neurologic outcome after lumbar fractures is improved by surgical decompression. The neurologic outcome results were similar after anterior and posterior decompression.

Follow-Up Studies↗

PubMed1996

The effect of early craniocervical decompression on functional outcome in neonates and young infants with myelodysplasia and symptomatic Chiari II malformations: results from a prospective series.

The indications for hindbrain decompression in neonates and young infants with spinal dysraphism who experience brain stem dysfunction in association with Chiari II malformations have remained controversial. This largely reflects the fact that the postoperative outcome in such patients has often been poor, which has supported the belief that much of the brain stem compromise in these patients is congenital and inherently irreversible. However, in a previous retrospective review of our operative results between 1975 and 1989, we noted that a significant component of the brain stem dysfunction in these children was an acquired phenomenon that potentially was reversible with prompt operative intervention. Accordingly, we hypothesized that with early craniocervical decompression, excellent functional outcome could be achieved in a majority of neonates and young infants with symptomatic Chiari II malformations. On the basis of this premise, we prospectively treated all such patients since 1989 with urgent brain stem decompression after other potential causes for brain stem dysfunction, such as progressive hydrocephalus, had been ruled out. All children underwent limited suboccipital craniectomies, cervical laminectomies extending beneath the inferior extent of the cerebellar tissue, and dural decompressions. The outcome in these patients has been favorable in comparison with previous studies. Ten of the 13 children treated according to this protocol recovered normal or nearly normal brain stem function shortly after decompression; 1 child had mild residual unilateral lower cranial nerve paresis. None of these children required a tracheostomy for ventilatory support, and only one required a temporary gastrostomy. The other three children all exhibited bilateral vocal cord paralysis and severe central hypoventilation by the time decompression was performed and failed to have any meaningful recovery of function. We conclude that early recognition of the symptoms of brain stem compromise in neonates and young infants with spinal dysraphism coupled with urgent evaluation and decompression are effective in producing prompt resolution of the brain stem dysfunction in most affected patients. Conversely, the prognosis for recovery is poor in children who exhibit bilateral vocal cord paralysis by the time of decompression.

Arnold-Chiari Malformation↗

PubMed1991

Decompression comparison of N2 and O2 in rats.

We have previously reported that O2 in the breathing gas mixture contributed significantly to the risk of decompression sickness (DCS) in rats after rapid (less than 10 s) decompression to the surface from depth. The rate of O2 uptake was extremely fast (less than 1 min estimated for equilibrium after a pressure change) compared to much slower rates for He and N2. To further define the role that O2 plays in diving, the present investigation examined decompression outcome in unanesthetized male albino rats after 60-min N2-O2 dives (1-3 atm abs O2, depth 6.26 or 7.26 atm abs). Slower decompression profiles were used to determine the elimination rates of N2 and O2 as pressure was reduced and included "stops" of up to 20 min. The probability of DCS was modeled using the maximum likelihood technique. O2 again contributed significantly to the risk of DCS, although O2 was eliminated very rapidly during decompression; the washout of N2 was considerably longer. These findings support the view that O2 can add significantly to decompression risk. However, this phenomenon may not normally be encountered during human diving operations where relatively slower decompression and lower PO2's are used.

Animals↗

PubMed1979

Evaluation of standard decompression schedule by agarose gel method.

The Standard Decompression Schedule was evaluated by the method of bubble formation in agarose gel, the result of which can be summarized as follows: 1) The number of bubbles formed in agarose gel corresponded well with the exposed pressure. 2) The technique of this method was simple and the number of bubbles was accurately counted. 3) Eventually, this method was useful for examining the decompression schedules. 4) It is not always safe to follow the Standard Decompression Schedule in some pressure conditions. 5) As to the period of time that a person is able to tolerate a high pressure condition, the prescription of the Standard Decompression Schedule is not necessarily correct. 6) The number of bubbles was small by the proper decompression schedule, for example, in the cases of exposure above the 60-meter depth of water. 7) This method can be applied for the prevention of decompression sickness when the agarose gel samples are attached to the workers during the compressed air work. 8) The number of bubbles was inconsistent with the coefficient of body pressure (1. N2 in the body), therefore it is not necessarily safe to rely only on the coefficient of body pressure. 9) To prevent osteonecrosis, the Standard Decompression Schedule is not proper, a deeper first stop and slower ascent being recommended.

Decompression↗

PubMed1985

Air and nitrox saturation decompression: a report of 4 schedules and 77 subjects.

Seventy-seven subjects were decompressed from air or nitrogen-oxygen (nitrox) saturation exposures at 18.3 to 40.2 meters sea water (msw) [60 to 132 feet sea water (fsw)] using four different decompression schedules. A h schedule for decompression from an air saturation-excursion profile at 18.3 msw (60 fsw) resulted in pain-only decompression sickness (DCS) symptoms in 2 of 23 subjects. A 32 and 35 h schedule from a different air saturation profile at 19.8 and 22.9 msw (65 and 75 fsw), respectively, resulted in DCS symptoms in 1 of 24 subjects. A third and fourth schedule for air or nitrox saturation at 40.2 msw (132 fsw) resulted in DCS symptoms in 3 of 12 and 1 of 18, respectively. No serious (type II) symptoms were observed as a result of any of the decompressions. All DCS cases consisted of knee pain occurring either in the last 3 msw of the decompression or shortly after surfacing. Doppler ultrasound monitoring revealed venous gas emboli (VGE) in several subjects, but generally only shallow to 6.1 msw (20 fsw). Results demonstrate an overall DCS incidence of 9%, and all cases were pain-only and localized to the knee. The third schedule (U.S. Navy heliox saturation decompression schedule) seems to produce a higher incidence of DCS than the other schedules when used in air or nitrox exposures. Differentiation between the schedules designed for nitrox was impossible due to the limited number of subjects in each and the variable nature of the exposures.

Adult↗

PubMed1996

[A method for evaluating the safety of decompression regimens for divers].

The authors offer a way of estimation of safety modes of decompression, based on definition of intensity of venous gas embolism (VGE) at each decompression and account of probability of illness of divers in series of tests. Intensity of VGE was determined with the help of ultrasonic gas bubbles Doppler radar. Comparative safety of standard modes of decompression of divers of the Navy was estimated, and also the modes, designed in accordance with mathematical model of decompression, offered by I. A. Voĭtsekhovich (1990), were done. The results testify, that use of ultrasonic radar for estimation of intensity of VGE at decompression and account of average and maximum probability of decompression illness in series of tests of modes permit to receive the comparative characteristic of safety of modes at small number of decompressions.

Adult↗

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↗

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↗