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PubMedDate not supplied

[Effect of decompression on the compliment system].

Decompression effects on the complement system were studied in healthy male volunteers who made 39 "ascents" to 7000-9000 m and 13 "descents" to 30 m. Hemolytic activity of the complement system components was determined in the blood serum taken from the cubital vein of the subjects immediately before and after decompression. The results of this study showed that in the absence symptoms of decompression sickness (DCS) and doppler-detected gas bubbles (GB) the subjects reduced activities of C1 and C4. In the event of altitude joint pains the activity of the complement system components was significantly unchanged. In subjects with circulating GB the complement status was more markedly altered following simulated descents rather than ascents pointing to an alternative activation of the system. Subject with the skin DCS had a two-fold reduction of the complement system activity by the alternative mechanism and a reduction of C5 activity whereas there were no changes in the activities of C1, C2, C3, C4, CH50. It is concluded that alternative activation of the complement system may be involved in the genesis of those DCS forms whose emergence relates to gaseous embolism of veins and pulmonary capillaries.

Adult↗
PubMed1994

Influence of carbon dioxide on venous gas emboli production during altitude decompression in goats.

Goats (N = 7) were decompressed from 1,500 m to 9,150, 9,750, or 10,400 m simulated altitude while breathing CO2 tensions of 0, 15, 30, or 46 mm Hg in O2 during 15-min prebreathing and 30-min peak altitude exposures. Risk of decompression sickness was determined by detecting venous gas emboli (VGE) in the pulmonary artery with an implanted Doppler cuff. VGE scores were calculated using the ratio of cardiac cycles containing VGE to total cardiac cycles. The VGE scoring methodology proved sensitive to standard treatment effects (air versus O2 prebreathing). No significant change in VGE scores as a result of varying the inspired CO2 level was detected. Further, no significant change in cardiac index occurred during the various CO2 exposures, and VGE scores were not correlated with cardiac index. Ground-level studies revealed the tension of end-tidal CO2 was significantly elevated at all three levels of inspired CO2, but no change in cardiac index was observed. Short-duration breathing of CO2 in oxygen failed to significantly reduce the risk of decompression sickness as assessed by VGE production.

Altitude↗
PubMedDate not supplied

[Prevention of altitude decompression sickness during short flights in a depressurized cabin at high altitudes].

Forty altitude chamber experiments were carried out in which 18 test subjects participated. The purpose of the experiments was to prevent decompression sickness in a pilot using an altitude compensatory suit and oxygen mask. It was demonstrated that oxygen breathing on the ground and at an altitude of 8 km for 20 and 50-60 min eliminated severe symptoms and lowered the frequency of occurrence of mild symptoms of decompression sickness during the subsequent 10-20 and 60-120 min exposures to altitudes of 40,000 and 11,000 m respectively. An increase in the absolute pressure to 240-290 mm Hg in the altitude garment prevented decompression sickness of altitudes of 11,000-15,000 m and eliminated it if it occurred at lower barometric pressure.

Adult↗
PubMedDate not supplied

[Development of decompression regimens for excursion dives after a prolonged exposure to 21 ata].

Decompression regimens for excursion dives from a depth of 20, 50, 100 or 200 m were developed and tested in a dry altitude chamber. Each dive continued for about 2 weeks, during which test subjects performed 10 excursion dives to a lower depth. No cases of decompression sickness were observed during 246 man/excursions whereas two cases of decompression sickness occurred in a field study.

Adult↗
PubMed1995

[A mathematical model of permissible integral supercritical supersaturation of tissues by gases under decompression].

A criterion of permissible integral supercritical gas oversaturation of the body tissues was established using mathematical modelling. The heart of this criterion is that if integral supercritical oversaturation of tissues by gases does not go beyond a permissible level, gas bubbles do not reach critical volumes and give rise to decompression sickness symptoms. An equation was also built to calculate integral supercritical oversaturation of tissues during and after decompression. Permissible integral supercritical saturation values were determined for animals from mice to dogs and humans basing on literary threshold pressures with saturation and follow-on one-step decompression.

Animals↗
PubMed1997

Nature and incidence of bubbles in the spinal cord of decompressed goats.

The nature of so-called autochthonous bubbles was investigated. Their presence in compressed/decompressed goats was compared with that in animals killed before decompression and in controls. Ten goats (group 1) were subjected to compression/decompression in air. Clinical signs of spinal decompression sickness usually occurred. Within 35 min of surfacing, the animals were given a lethal dose of thiopentone sodium, i.v.. Spinal cords were fixed by immersion in 10% formol saline. Histologically autochthonous bubbles appeared to arise from rupture of over-distended blood vessels. The incidence of grossly dilated empty vessels (GDEV) was recorded. Seven goats (group 2) were similarly compressed but killed before decompression. In five animals of group 1 there was a greater number of GDEV than in controls (group 3, seven animals) but in the other five animals the incidence was similar to the controls. The incidence of GDEV in group 2 was greater than in the controls (P < 0.05). The percentage of sections of spinal cord in which the meninges also contained GDEV was assessed. In all except two animals in group 1, the percentage was higher than in the controls, whereas in group 2 the percentage was higher than in the controls. The experiments show that autochthonous bubbles arise as an artifact and that intravascular bubbles arise in situ.

Animals↗
PubMed1976

Transantral-ethmoidal decompression of optic canal fracture.

A case of indirect trauma to the optic nerve was successfully treated with transethmoidal decompression. The literature was reviewed, and reports of poor results from neurosurgical procedures are cited. Improved results from transethmoidal decompression of the optic nerve have been reported by Japanese authors but, in our opinion, without proper selection of cases. Early diagnosis of traumatic compression of the intracanalicular optic nerve as evidenced by delayed and/or progressive vision loss following injury, coupled with prompt transantral-ethmoidal surgical decompression, should yield gratifying results in the treatment of this uncommon condition.

Adult↗
PubMed1975

Retroperitoneal approach for portasystemic decompression.

A left retroperitoneal approach has been developed and used to perform a renal-splenic shunt for portal decompression in seven patients with massive variceal hemorrhage. In each patient, at least one intra-abdominal finding contraindicated a conventional transperitoneal portasystemic shunt. Retroperitoneal approach avoided possible complications and permitted successful portal decompression with cessation of bleeding in each instance. These results support the use of this technique when it is necessary to avoid the peritoneal cavity in a patient requiring portasystemic decompression.

Adult↗
PubMed1979

Pathophysiology of bends and decompression sickness. An overview with emphasis on treatment.

Current concepts in the pathophysiology of decompression sickness are reviewed. Mild, moderate, and severe forms of this syndrome resulting from gaseous and lipid emboli are described. Therapy is aimed at restoring or specifically treating each alteration. Plasma volume deficit is restored by colloidal re-expansion. Decompression sickness is partially treated when recompression alone is used. Blood lipid alterations are managed by use of antilipemic agents. Dextran is mentioned. Divers at depths of 61 m display changes in hematocrit, platelet, and blood lipid profiles. Cord paralysis may occur from bubbles in the vena cava. Retrograde migration blocks the venous circulation of the spinal cord. Ultrasonic devices can detect "silent" bubbles during decompression. Recompression, when available, is a lifesaving treatment for diving accidents involving saturation diving. Air embolism is discussed. Monitoring emboli by EEG and fundoscopy are reported.

Blood Coagulation Factors↗
PubMed1996

Core decompression in avascular necrosis of the hip in sickle-cell disease.

Sickle-cell disease (SCD) is the most common cause of avascular necrosis (AVN) of the hip in childhood. It results in significant physical impairment and chronic pain, and often progresses to require hip replacement. Conservative therapy is ineffective. We evaluated whether core decompression can arrest progression of AVN. We performed 13 coring procedures in 10 patients with SCD and AVN. Patients ranged from age 9-21 years at diagnosis (mean, median age, 15 years); five hips were stage I, six hips were stage II, and two hips were stage III. Mean follow-up on these patients was 3.7 years. Efficacy of the procedure was evaluated by clinical improvement in pain, radiographic progression, and need for further surgery. All 5 stage I patients had substantial improvement in pain, and only one showed X-ray progression. Five of the 6 (83%) stage II patients had improvement in pain, and 2 patients progressed on X-ray. Both stage III patients progressed on X-ray, but one was clinically improved. None of the 10 patients has required further surgery. Our results demonstrate that in early AVN, core decompression was beneficial for almost all patients, even with progression on X-ray. Core decompression should be considered in the management of SCD patients with early AVN.

Adolescent↗
PubMed2006

Catheter-based decompression of the left atrium in patients with hypoplastic left heart syndrome and restrictive atrial septum is safe and effective.

Infants with hypoplastic left heart syndrome (HLHS) and restrictive or intact atrial septum (rAS) present with cyanosis, pulmonary edema, and are critically ill. A previous report from our institution on emergent Norwood for HLHS with rAS showed 10% survival. We hypothesized that transcatheter left atrial (LA) decompression in HLHS with rAS would safely and effectively relieve LA hypertension, improve oxygenation, and improve Norwood survival. Between 1996 and 2004, 30 patients with HLHS and rAS underwent cardiac catheterization for pre-Norwood intervention. Twenty-eight atrial septostomies were performed: 23 static balloon dilations, 4 Rashkind septostomies, and 1 intra-atrial stent. Two procedures were aborted due to perforation (n = 1) or inability to enter the LA (n = 1). Eight total patients required surgical septectomy, for a failure rate of 27%. There were no catheter-related mortalities, although two patients died within 36 hr of the procedure after surgical septectomy. Major complications occurred in three patients (10%)--atrial perforations requiring intervention. Mean atrial septal defect gradient fell from 16.7 +/- 4.9 to 6.3 +/- 3.4 mm Hg (P < 0.001; n = 18). Mean LA pressure dropped from 21.8 +/- 5.5 to 13.1 +/- 6.5 mm Hg (P < 0.001; n = 16). Mean PaO(2) rose from 29.5 +/- 9.1 to 36.5 +/- 5.1 torr (P < 0.001; n = 23). Seventeen of 30 patients (57%) survived to discharge from Norwood. Thirteen have undergone hemi-Fontan and nine Fontan. Sixteen of 22 successful decompressions (73%) survived to discharge. Transcatheter decompression of the LA for patients with HLHS and rAS can be performed safely, reduces the transatrial gradient, and improves oxygenation. Catheter intervention improves survival compared to historical controls undergoing emergent Norwood.

Cardiac Catheterization↗
PubMed1978

The ultrastructural effects of acute decompression on the lung of rats: the influence of frusemide.

Rats were placed in a decompression chamber and the chamber and the pressure reduced to 265 mm Hg over a period of 1 hr. Other rats were subjected to the same treatment after having been given an injection of frusemide. An ultrastructural study of the lungs of these rats showed that acute decompression of this magnitude can cause swelling and disintegration of type I alveolar epithelial cells. Although capillary endothelial cells showed only minor cytoplasmic damage many capillaries were ruptured with diapedesis of red cells. This is believed to be caused by gross capillary dilatation associated with pulmonary congestion. Pretreatment with frusemide prevented capillary rupture and reduced the degree of epithelial degeneration. However, frusemide induced swelling of capillary endothelial cells which was unassociated with acute decompression.

Acute Disease↗
PubMed2006

Fetoscopic and ultrasound-guided decompression of the fetal trachea in a human fetus with Fraser syndrome and congenital high airway obstruction syndrome (CHAOS) from laryngeal atresia.

Congenital high airway obstruction syndrome (CHAOS) from laryngeal atresia bears a poor prognosis for hydropic fetuses owing to cardiac failure. We attempted percutaneous fetoscopic and ultrasound-guided tracheal decompression in a hydropic human fetus with CHAOS associated with Fraser syndrome. Percutaneous fetoscopic and ultrasound-guided tracheal decompression was performed using three trocars under general materno-fetal anesthesia at 19 + 5 weeks of gestation. Abnormal fetoplacental blood flow normalized within hours as a result of the intervention. Furthermore, a normalization of lung : heart size and lung echogenicity was observed within days. Resolution of hydrops was complete within 3 weeks. Premature rupture of membranes and premature contractions prompted emergency delivery of the fetus by ex-utero intrapartum treatment (EXIT) at 28 + 2 weeks of gestation. Following delivery, the lungs could be ventilated at low pressures and ambient oxygen concentration. Weaning from ventilation was achieved at 18 days of postnatal life. Our experience indicated that percutaneous fetoscopic and ultrasound-guided decompression of the fetal trachea is feasible and may permit normalization of hemodynamics in hydropic human fetuses with CHAOS from laryngeal atresia. The procedure may also result in normalization of heart : lung size and provide the time needed to regain the function of the overstretched diaphragm in this grave fetal condition.

Airway Obstruction↗
PubMed1995

Role of ischemia in rats with spinal cord injury induced by decompression sickness.

The microsphere technique was used to determine whether blood flow to the central nervous system and various organs is impaired in rats with spinal cord injury induced by decompression sickness. For this purpose cannulas were placed in the left ventricle of the rats for the injection of microspheres and in the tail artery as the reference site for withdrawal of blood for the calculation of cardiac output (CO) and blood flow (BF) and for measurement of blood pressure (BP) and heart rate (HR). The rats were then subjected to a simulated dive that by electrophysiologic criteria rapidly (within 60 min after diving) induces severe neurologic deficits in the cord. Microspheres were used to determine CO and BF before and at 10, 60, and 180 min after diving. CO, BP, and HR were not affected by diving. BF to various regions of the brain, heart, bone, and fat was also not affected by diving. BF decreased in the lung (40%) and skeletal muscle (50%) and increased in spinal cord (20%) at 10 min after diving. At 60 and 180 min after diving the only alterations seen were increases in hepatic arterial and portal BF. Analysis of the distribution of cardiac output showed that diving induced changes that essentially paralleled the BF changes described above. We conclude that perfusion in the central nervous system is maintained in rats with spinal cord injury induced by decompression sickness. These results indicate that ischemia does not play a role in the pathophysiology of neuronal injury in this model of decompression sickness.

Animals↗
PubMed2005

Improvement of brain tissue oxygen and intracranial pressure during and after surgical decompression for diffuse brain oedema and space occupying infarction.

BACKGROUND: We evaluated the perioperative and intraoperative changes of intracranial pressure (ICP) and partial pressure of brain tissue oxygen (PtiO2) after decompressive craniectomy in patients with diffuse brain oedema and space occupying infarction. METHODS: Ten patients suffering from medically intractable raised intracranial pressure (ICP) were included. The underlying diseases and causes for elevated ICP were diffuse brain oedema after subarachnoid haemorrhage (n = 3) and head injury (n = 3), or space occupying infarction of the middle cerebral artery territory due to vasospasm after SAH (n = 4). Continuous perioperative and intraoperative monitoring of PtiO2 and ICP was performed at the side of decompression. FINDINGS: ICP and PtiO2 improved significantly in a uniform pattern during bone flap removal and dura opening, irrespective of the underlying disease (mean ICP from 52 mmHg to 8 mmHg, mean PtiO2 from 9 mmHg to 25 mmHg). ICP, PtiO2, and cerebral perfusion pressure were further improved in the subsequent 12 hours after surgery, as compared to the preoperative 12 hours. CONCLUSIONS: Decompressive craniectomy seems to be a successful option in the treatment of intractable intracranial hypertension with associated cerebral hypoxia. These positive effects may last for several hours after the procedure irrespective of the underlying disease.

Brain↗
PubMed1997

Surgical decompression: a life-saving procedure for an extensive spinal epidural abscess.

Extensive spinal epidural abscesses (SEAs) carry a high mortality rate. Traditionally they are treated non-operatively with long-term antibiotics and/or surgical decompression, but there is a continuing debate as to whether they should be managed by emergency surgical decompression. However, such decisions are made in the light of the clinical setting. We report the successful management of a female patient who presented with features of upper cervical cord compression and later developed septic shock and multisystem failure. Surgical decompression of the cervical spine and irrigation of the epidural space with a paediatric catheter was performed followed by tricortical strut grafting and plating. At review, 36 weeks after surgery, the patient remained asymptomatic, having made full neurological recovery. The purpose of this report is to highlight the importance of emergency surgical intervention for extensive SEA in the presence of progressive neurological loss associated with multisystem failure.

Abscess↗
PubMed1997

Unilateral laminotomy for bilateral decompression of lumbar spinal stenosis. Part II: Clinical experiences.

The surgical aim in the treatment of symptomatic lumbar spinal stenosis is the relief of the patient's complaints by an adequate neural decompression. Unilateral laminotomy and bilateral spinal canal decompression represents such a safe, effective and minimally invasive surgical method. This technique has been successfully used in the operative treatment of 29 patients with symptomatic mono- or multisegmental lumbar stenosis. There was no surgically induced neurological deterioration. In one patient, an inadvertent dural tear occurred, and due to unchanged symptoms another patient with a multisegmental stenosis had to be re-operated on at an additional level. Postoperatively, 25 of the 27 patients with neurogenic claudication (93%) demonstrated a marked improvement of the walking distance. The follow-up of 25 patients (mean follow-up time was 18 months) demonstrated an excellent result without pain in 7 patients (28%); a good outcome with mild residual pain, but a normal working capacity in 15 patients (60%); and a fair outcome with unchanged postoperative low-back pain but markedly improved working capacity and walking distance in 3 patients (12%). Postoperative morphometric evaluation as well as the clinical improvement of the patient's symptoms clearly demonstrated that bilateral ligamentectomy and recess decompression were adequately and successfully achieved via unilateral approach.

Adult↗
PubMed1997

[Value of intraluminal intestinal decompression by endoscopic placement of a Dennis tube in therapy of ileus. Retrospective clinical study of 174 patients].

For determination of the efficacy of intraluminal bowel decompression by an endoscopically placed Dennis tube, 174 patients with paralytic ileus or different kinds of partial small bowel obstruction were reviewed retrospectively. There were 66 cases (37.9%) of early postoperative ileus (A), 27 (15.5%) of late postoperative ileus (B), 38 (21.8%) of paralytic ileus (C), 31 (17.8%) with obstruction due to advanced intraabdominal tumors (D), and 12 (6.8%) of obstructive ileus caused by inflammatory stenosis of the small bowel in Crohn's disease (E). Successful endoscopic placement of the intestinal tube was achieved in 97.2% of patients. Placement of the tube was impossible in 5 cases. A total of 95 patients (54.6%) were successfully managed by long intestinal tube decompression. Success rates for the individual groups were 71.2% (A), 18.5% (B), 86.8% (C), 16.1% (D), and 41.7% (E). Some 75 patients (43.1%) had to be operated on because of insufficient conservative therapy. Four patients with advanced intraabdominal tumors died during the treatment with the intestinal tube; 13 patients died postoperatively. There was no tube-related mortality, but tube-related complications occurred in 6.9%. We conclude that intraluminal intestinal tube decompression after endoscopic placement provides a therapeutic tool with a concomitant low complication and high success rate in paralytic and early postoperative ileus.

Adolescent↗