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PubMed1978

Relationship between CO2 levels and decompression sickness: implications for disease prevention.

Extensive data concerning the incidence of decompression sickness among workers participating in the deepest caisson operation in Japan to date have been collected and analyzed for the period April through August, 1976. When the bottom pressure was between 3.0 and 3.2 ATA, the incidence of decompression sickness was 3.05%; subsequently, the incidence was only 0.96% between 3.2 and 3.4 ATA. The man lock (i.e., decompression chamber) had never been ventilated during the former group of decompressions and the level of CO2 had ranged between 1.8 and 2.3% (v/v); in the latter group of decompressions, the CO2 level ranged between 0.3 and 0.8% with ventilation. All other conditions, including the decompression table used, were the same. Moreover, based upon the nature of the muscular activity required of the caisson workers just prior to decompression, their most common site of affliction was found to lie within the body region where the highest tissue tensions of CO2 would be expected during decompression.

Adult↗

PubMed1982

Evaluation of different decompression schedules by an agarose gel bubble technique.

It is well known that diving decompression schedules vary according to country and that Navy schedules are often different from civilian ones. Furthermore, it is difficult to compare them effectively, because the bends incidence for each schedule is rarely known accurately. We have evaluated various decompression schedules by an agarose gel bubble technique in which the appearance of bubbles in a dry chamber at a controlled temperature was used, and we report this as a useful method of evaluating decompression tables. It is generally accepted that decompression sickness symptoms are due to bubble formation and the body's subsequent physiological reaction. Individual differences and physical conditions are also influential factors. However, bubble formation appears to be the most important factor in initiating symptoms. As the number of bubbles is influenced by the physical decompression ratio, it can be estimated which decompression schedule is more likely to minimize the number of bubbles. Nine decompression schedules were studied in this experiment: U.S. Navy Table, French Navy Table, Japanese Standard Decompression Schedule Numbers 1 and 2, Royal Naval Physiological Laboratory Table, French Ministry of Labor Table, Model 1 Table by Mano et al., Washington State Table, and Blackpool Table.

Decompression↗

PubMed1995

Cardiovascular pressures with venous gas embolism and decompression.

Venous gas embolism (VGE) is reported with decompression to a decreased ambient pressure. With severe decompression, or in cases where an intracardiac septal defect (patent foramen ovale) exists, the venous bubbles can become arterialized and cause neurological decompression illness. Incidence rates of patent foramen ovale in the general population range from 25-34% and yet aviators, astronauts, and deepsea divers who have decompression-induced venous bubbles do not demonstrate neurological symptoms at these high rates. This apparent disparity may be attributable to the normal pressure gradient across the atria of the heart that must be reversed for there to be flow patency. We evaluated the effects of: a) venous gas embolism (0.025, 0.05 and 0.15 ml.kg-1.min-1 for 180 min.); b) hyperbaric decompression; and c) hypobaric decompression on the pressure gradient across the left and right atria in anesthetized dogs with intact atrial septa. Left ventricular end-diastolic pressure was used as a measure of left atrial pressure. In a total of 92 experimental evaluations in 22 dogs, there were no reported reversals in the mean pressure gradient across the atria; a total of 3 transient reversals occurred during the peak pressure gradient changes. The reasons that decompression-induced venous bubbles do not consistently cause serious symptoms of decompression illness may be that the amount of venous gas does not always cause sufficient pressure reversal across a patent foramen ovale to cause arterialization of the venous bubbles.

Altitude↗

PubMed1990

Endoscopic transnasal orbital decompression.

Orbital decompression for dysthyroid orbitopathy has traditionally been performed through either an external or a transantral approach. The advent of intranasal endoscopes allowed for the development of a transnasal approach for medial and inferior orbital wall decompression. Using this approach, orbital decompressions were performed on 13 orbits in eight patients with severe complicated dysthyroid orbitopathy. Simultaneous bilateral lateral orbitotomies were performed on five patients. Walsh-Ogura decompressions and lateral orbitotomies were performed on two orbits. When combined with lateral orbitotomy, Hertel measurements improved an average of 5.7 mm in orbits decompressed transnasally and 4.5 mm in orbits decompressed with a Walsh-Ogura approach. Transnasal decompression alone improved Hertel measurements an average of 4.7 mm. Visual acuity improved in three of four patients with optic neuropathy, and in all patients with exposure keratopathy. We conclude that the endoscopic transnasal approach provides comparable decompression to traditional methods while avoiding the morbidity of an external ethmoidectomy or Caldwell-Luc antrotomy.

Adult↗

PubMed1993

Orbital fat removal. Decompression for Graves orbitopathy.

BACKGROUND: Orbital decompression has been used to describe surgical procedures that remove some portion of the orbital walls to reduce pressure on the orbital contents. Substantial morbidity associated with these procedures includes infraorbital anesthesia, worsened extraocular motility, globe displacement, and blindness. The authors believe that orbital contents also may be decompressed by removing orbital fat. METHODS: Eighty-one patients with nonactive Graves orbitopathy were selected for orbital fat decompression based on the presence of proptosis and associated signs and symptoms to avoid bone removal. Soft-tissue analysis by computed tomography (CT) scan showed distended pockets of fat extending into the intraconal space, which were removed through medial-upper and lateral-lower anterior orbitotomies. Decompression with bone removal was reserved for those few patients with compressive optic neuropathy unresponsive to medical treatment and those patients with residual deforming exophthalmos after fat removal. RESULTS: One hundred fifty-eight fat decompressions were performed on 81 patients over 9 years. The authors measured an average reduction in proptosis of 1.8 mm (range, 0-6.0 mm). The greatest average reduction in proptosis (3.3 mm) was produced in patients with preoperative Hertel measurements of greater than 25.0 mm. Morbidity was limited to temporary motility impairment of the inferior oblique in two patients. CONCLUSION: The concept of orbital decompression can include removal of orbital fat to reduce proptosis, eliminate symptoms, and improve appearance with far less morbidity than when bone decompression is used as the primary decompressive procedure.

Adipose Tissue↗

PubMed1993

A comparison of active compression-decompression cardiopulmonary resuscitation with standard cardiopulmonary resuscitation for cardiac arrests occurring in the hospital.

BACKGROUND: Recent studies have demonstrated improved cardiopulmonary circulation during cardiac arrest with the use of a hand-held suction device (Ambu CardioPump) to perform active compression-decompression cardiopulmonary resuscitation (CPR). The purpose of this study was to compare active compression-decompression with standard CPR during cardiac arrests in hospitalized patients. METHODS: All patients over the age of 18 years who had a witnessed cardiac arrest while hospitalized at our center were enrolled in this trial; they were randomly assigned according to their medical-record numbers to receive either active compression-decompression or standard CPR. The study end points were the rates of initial resuscitation, survival at 24 hours, hospital discharge, and neurologic outcome. Compressions were performed according to the recommendations of the American Heart Association (80 to 100 compressions per minute; depth of compression, 3.8 to 5.1 cm [1.5 to 2 in.]; and 50 percent of the cycle spent in compression). RESULTS: Sixty-two patients (45 men and 17 women) with a mean age (+/- SE) of 68 +/- 2 years were entered into the trial. Sixty-two percent of the patients who underwent active compression-decompression were initially resuscitated, as compared with 30 percent of the patients who received standard CPR (P < 0.03); 45 percent of the patients who underwent active compression-decompression survived for at least 24 hours, as compared with 9 percent of patients who underwent standard CPR (P < 0.004). Two of the 62 study patients survived to hospital discharge; both were randomly assigned to receive active compression-decompression. Neurologic outcome, as measured by the Glasgow coma score, was better with active compression-decompression (8.0 +/- 1.3) than with standard CPR (3.5 +/- 0.3; P < 0.02). CONCLUSIONS: In this preliminary study, we found that, as compared with standard CPR, active compression-decompression CPR improved the rate of initial resuscitation, survival at 24 hours, and neurologic outcome after in-hospital cardiac arrest. Larger trials will be required to assess the potential benefit in terms of long-term survival.

Aged↗

PubMed1995

A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy.

OBJECTIVE: A meta-analysis of all published clinical trials comparing selective versus routine nasogastric decompression was performed in an attempt to evaluate the need for nasogastric decompression after elective laparotomy. BACKGROUND: Many studies have suggested that routine nasogastric decompression is unnecessary after elective laparotomy and may be associated with an increased incidence of complications. Despite these reports, many surgeons continue to practice routine nasogastric decompression, believing that its use significantly decreases the risk of postoperative nausea, vomiting, aspiration, wound dehiscence, and anastomotic leak. METHODS: A comprehensive search of the English language medical literature was performed to identify all published clinical trials evaluating nasogastric decompression. Twenty-six trials (3964 patients) met inclusion criteria. The outcome data extracted from each trial were subsequently "pooled" and analyzed for significant differences using the Mantel-Haenszel estimation of combined relative risk. RESULTS: Fever, atelectasis, and pneumonia were significantly less common and days to first oral intake were significantly fewer in patients managed without nasogastric tubes. Meta-analysis based on study quality revealed significantly fewer pulmonary complications, but significantly greater abdominal distension and vomiting in patients managed without nasogastric tubes. Routine nasogastric decompression did not decrease the incidence of any other complication. CONCLUSIONS: Although patients may develop abdominal distension or vomiting without a nasogastric tube, this is not associated with an increase in complications or length of stay. For every patient requiring insertion of a nasogastric tube in the postoperative period, at least 20 patients will not require nasogastric decompression. Routine nasogastric decompression is not supported by meta-analysis of the literature.

Elective Surgical Procedures↗

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↗

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↗

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↗

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↗