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Although surgical decompression is often advocated for acute spinal cord injury, the timing and efficacy of early treatment have not been clinically proven. Our objectives were to determine the importance of early spinal cord decompression on recovery of evoked potential conduction under precision loading conditions and to determine if regional vascular mechanisms could be linked to electrophysiologic recovery. Twenty-one mature beagles were anesthetized and mechanically ventilated to maintain normal respiratory and acid-base balance. Somatosensory-evoked potentials from the upper and lower extremities were measured at regular intervals. The spinal cord at T-13 was loaded dorsally under precision loading conditions until evoked potential amplitudes had been reduced by 50%. At this functional endpoint, spinal cord displacement was maintained for either 30 (n = 7), 60 (n = 8), or 180 min (n = 6). Spinal cord decompression was followed by a 3-h monitoring period. Regional spinal cord blood flow was measured with fluorescent microspheres at baseline (following laminectomy) immediately after stopping dynamic cord compression, 5, 15, and 180 min after decompression. Within 5 min after stopping dynamic compression, evoked potential signals were absent in all dogs. We observed somatosensory-evoked potential recovery in 6 of 7 dogs in the 30-min compression group, 5 of 8 dogs in the 60-min compression group, and 0 of 6 dogs in the 180-min compression group. Recovery in the 30- and 60-min groups varied significantly from the 180-min group (p < 0.05). Regional spinal cord blood flow at baseline, 21.4+/-2.2 ml/100/g/min (combined group mean +/- SE) decreased to 4.1+/-0.7 ml/100 g/min after stopping dynamic compression. Reperfusion flows after decompression were inversely related to duration of compression. Of the 7 dogs in the 30 min compression group, 5 min after decompression the blood flow was 49.1+/-3.1 ml/100 g/min, which was greater than two times baseline. In the 180-min compression group early post-decompression blood flow, 19.8+/-6.2 ml/100 g/min, was not significantly different than baseline. Of the 8 dogs in the 60-min compression group, 5 who recovered evoked potential conduction revealed a lower spinal cord blood flow sampled immediately after stopping dynamic compression, 2.1+/-0.4 ml/100 g/min, compared to the 3 who did not recover where blood flow was 8.4+/-2.1 ml/100 g/min (p < 0.05). Reperfusion flows measured as the interval change in blood flow between the time dynamic compression was stopped to 5, 15, or 180 min after decompression, were significantly greater in those dogs that recovered evoked potential function (p < 0.05). Three hours after decompression, spinal cord blood flow in the 3 dogs in the 60-min compression group with no recovery, 11.1+/-2.1 ml/100 g/min, was significantly less than the spinal cord blood flow of the recovered group (n = 5), 20.5+/-2.2 ml/100 g/min. These data illustrate the importance of early time-dependent events following precision dynamic spinal cord loading and sustained compression conditions. Spinal cord decompression performed within 1 h of evoked potential loss resulted in significant electrophysiologic recovery after 3 h of monitoring. This study showed that the degree of early reperfusion hyperemia after decompression was inversely proportional to the duration of spinal cord compression and proportional to electrophysiologic recovery. Residual blood flow during the sustained compression period was significantly higher in those dogs that did not recover evoked potential function after decompression suggesting a reperfusion injury. These results indicate that, after precise dynamic spinal cord loading to a point of functional conduction deficit (50% decline in evoked potential amplitude), a critical time period exists where intervention in the form of early spinal cord decompression can lead to effective recovery of electrophysiologic function in the 1- to 3-h post-decompression p
OBJECTIVES: This study was designed to test the hypothesis that active compression-decompression cardiopulmonary resuscitation increases transmitral flow and end-decompression left ventricular volume over levels achieved with standard manual cardiopulmonary resuscitation. BACKGROUND: Recently, cardiopulmonary resuscitation incorporating active compression and decompression of the chest has been demonstrated to improve hemodynamic status in a canine model and in humans after cardiac arrest. METHODS: The active compression-decompression device was applied midsternum in five consecutive patients and results compared sequentially (in random order) with those of standard manual cardiopulmonary resuscitation. Both techniques were performed at 80 compressions/min with a 1.5- to 2-in. (3.8 to 5.1 cm) compression depth and a 50% duty cycle. Transesophageal echocardiographic data obtained in each patient included the velocity-time integral of transmitral pulsed Doppler recordings and two-dimensional images of the left ventricle in the long-axis view. Planimetric volume measurements of the left ventricle were obtained at both end-compression and end-decompression. RESULTS: No difference was observed in end-compression volume between the two techniques (p = 0.81). Increased end-decompression volume (active compression-decompression technique 81.3 +/- 12.5 vs. standard technique 69.4 +/- 10.8, p < 0.05), stroke volume (active compression-decompression technique 32.6 +/- 6.8 vs. standard technique 17.6 +/- 5.2, p < 0.05) and velocity-time integral of transmitral flow (active compression-decompression technique 15.8 +/- 4.3 vs. standard technique 7.8 +/- 2.3, p < 0.05) were found in the active compression-decompression group. The transmitral velocity-time integral was highly correlated with left ventricular stroke volume (r = 0.90). CONCLUSIONS: Improved transmitral flow, end-decompression left ventricular volume and stroke volume are seen with active compression-decompression resuscitation, suggesting a biphasic cardiothoracic cycle of flow. Active decompression of the chest appears to be a beneficial adjunct to standard cardiopulmonary resuscitation.
1. Bubble formation in the hind limb of anaesthetized guinea-pigs, after decompression from two different saturation exposures to air, 0.69 and 0.83 MPa gauge, has been studied using an ultrasonic pulse--echo imaging technique. 2. A qualitative analysis of the bubble formation, observed over a 30 min period after decompression, showed that profuse, largely stationary bubble formation occurred within 3 min of the decompression from 0.83 MPa gauge but that extensive stationary bubble formation was not observed until 17 min after decompression from 0.69 MPa gauge. Electrocardiogram changes appeared coincidently with the appearance of major bubble formation after the 0.83 MPa decompression but after the 0.69 MPa decompression changes were not observed until the end of the 30 min surveillance period, considerably later than the occurrence of a large number of bubbles. 3. A quantitative analysis of the echo patterns recorded during the 60 sec decompression and for 60 sec after the decompression demonstrated that the increase in severity of the decompression corresponded to an increase of 152% in the number of bubbles observed. The echoes observed during this period have been identified as either transient or persistent and their distribution of size, location and times of appearance and duration have been described. 4. From the quantitative analysis approximate estimates of the contribution by mobile, intravascular gas bubbles to the elimination of the excess gas have been made. These estimates range from 0.01 to 0.9% after the 0.69 MPa decompression and from 0.06 to 6% after the 0.83 MPa decompression. 5. It is concluded that the pulse--echo ultrasonic imaging technique provides a powerful means of analysing the distributions of bubble formation, both qualitatively and quantitatively, after decompression; it has the important attribute of being able to monitor both moving and stationary bubbles simultaneously in a variety of tissue types.
Forty-two neurologically intact adults in whom non-operative treatment of grade-I or grade-II isthmic spondylolisthesis of the most caudad lumbar segment had failed were entered into a prospective study of the results of operative treatment. Twenty patients who smoked were managed with a posterolateral arthrodesis with instrumentation (transpedicular fixation), and twenty-two patients who did not smoke were managed with a posterolateral arthrodesis without instrumentation. Of the patients who were managed with instrumentation, eight were randomized to treatment with a decompressive laminectomy and twelve, to treatment without it; in the group that was managed without instrumentation, the distribution was ten and twelve patients, respectively. The patients were followed clinically for a mean of 4.5 years (range, 3.5 to six years). Of the eighteen patients who had been managed with decompression, four had a pseudarthrosis and six had an unsatisfactory result compared with none and one of the twenty-four who had been managed without decompression (p = 0.02 and p = 0.01, respectively). In the group of twenty patients (smokers) who had been managed with instrumentation, none of the twelve managed without decompression had a pseudarthrosis compared with one of the eight managed with decompression (p = 0.2). In the group of twenty-two patients (non-smokers) who had been managed without instrumentation, none of the twelve managed without decompression had a pseudarthrosis compared with three of the ten managed with decompression (p = 0.04). In the group managed with instrumentation, two of the eight who had had decompression had an unsatisfactory result compared with none of the twelve who had not had decompression. In the group managed without instrumentation, four of the ten who had had decompression had an unsatisfactory result compared with one of the twelve who had not had decompression. The addition of decompression to arthrodesis, performed with or without instrumentation, for the treatment of low-grade isthmic spondylolisthesis in patients who do not have a serious neurological deficit does not appear to improve the result and may significantly increase the rates of pseudarthrosis and unsatisfactory results.
In a serial analysis of splanchnic hemodynamics, we compared partial with total portal decompression in 16 alcoholic cirrhotic patients who underwent portacaval shunts for variceal hemorrhage. Partial decompression was achieved with 8 or 10 mm polytetrafluorethylene portacaval H grafts and aggressive collateral ligation. Total decompression was achieved with larger diameter H grafts (12 or 14 mm). Early and follow-up (mean interval, 18 months) postoperative studies of portal hemodynamics included: direct measurement of shunt gradients, scintigraphic quantitation of portal and mesenteric flow distribution to the liver, and a portal and splenic collateral scoring system developed from standardized splenic venography. Partial portal decompression reduced portal pressure by 43% +/- 8% compared with 81% +/- 5% after total decompression (p less than 0.01). Scintigraphy demonstrated that partial decompression provided a greater fraction of portal flow to the liver than did total decompression (57% +/- 9% versus 2% +/- 1% intrahepatic radioactivity) and mesenteric flow distribution (14.5% +/- 5.4% versus 1.2% +/- 0.7%). Only one patient with partial decompression had a significant loss of portal perfusion during the interval studies. Significantly more residual collaterals were visualized in patients with partial decompression than in those with total decompression, and interval studies showed no significant changes from early studies. We conclude that partial decompression maintains higher portal pressures, more residual collaterals, and a greater fraction of portal and mesenteric flow to the liver than does total decompression. A modest but uniform reduction of portal pressure minimizes stimulus for new collateral formation and further shunting of portal flow.
A surgical procedure is described to perform orbital decompression in patients suffering from orbitopathy in Graves' Disease. The decompression technique employs exposure of the orbit through a lateral incision and an inferior fornix incision. These combined incisions with exposure can be used to perform an antral-ethmoidal decompression (two-wall decompression) or an antral-ethmoidal-lateral wall decompression (three-wall decompression). This present series contains 34 patients who underwent decompression through a 2 1/2-year period ending October 1980. The results of decompression were quantitated by measuring the retroplacement of the globe and in patients with compressive optic neuropathy by improvement in vision. The retroplacement of the globe with the antral-ethmoidal (two-wall decompression) was 4 to 7 mm (average 6 mm), and the retroplacement was 6 to 8 mm in four patients who underwent antral-ethmoidal-lateral decompression (three-wall decompression). All patients with compressive optic neuropathy improved to a final visual acuity of 20/40 or better. Five of 11 patients, with compressive optic neuropathy required postoperative super-voltage irradiation to reach this acuity. Fifty percent of the patients undergoing antral-ethmoidal decompression for proptosis required additional eyelid surgery with recession of upper lid retractors.
In 5 subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure to air at 6 bar for 30 min corresponding to a depth of 50 m. Afterward the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6, and 1.3 bar with a total decompression time of 67 min. In 3 of the subjects the measurements were repeated after they had exercised (workload 75 W) during bottom time. Immediately after decompression and every 40 min until Minute 240 arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min after decompression, indicating still incomplete nitrogen washout for at least 2 h after decompression had been accomplished. We did not find any difference in PN2 values after decompression from dives at rest and after exercise. Applying a computer program based on a wide range of theoretical tissue half-times nitrogen elimination proved to be consistent with Haldanian theories when using our decompression profile. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest and after exercise.
BACKGROUND: Acute colonic pseudo-obstruction is often treated by colonoscopic decompression. Efficacy, safety, and outcome of endoscopic decompression was assessed. METHODS: Colonoscopic decompressions from 1988 to 1994 were reviewed. Resolution without further endoscopic intervention was defined as clinical success. RESULTS: Acute colonic pseudo-obstruction was diagnosed in 50 patients. Thirty-three cases followed surgery or trauma and 17 developed during severe medical illness. Orthopedic joint surgery was most common. Nineteen of 50 patients (38%) had severe underlying medical disease. Forty-one patients (82%) had one colonoscopic decompression with clinical success in 39 (95%). Nine patients (18%) required multiple (2 to 4) colonoscopic decompressions with clinical success in 5 (56%). A decompression tube positioned in the right colon (57%) and in the transverse colon (33%) had similar clinical success. In 8 procedures a decompression tube was not placed, with poor clinical success (25%). The overall clinical success of colonoscopic decompression was 88% (44 of 50). An endoscopic perforation occurred in 1 patient (2%). Overall hospital mortality was 30%. CONCLUSIONS: Colonoscopic decompression is effective and safe for acute colonic pseudo-obstruction that does not respond to conservative therapy. Most patients will respond to one colonoscopic decompression with decompression tube placement. Complete colonoscopy and cecal tube placement is unnecessary.
A questionnaire was sent to members of the American Society of Ophthalmic Plastic and Reconstructive Surgery (ASOPRS) and the Orbital Society in regard to indications, surgical techniques and results of orbital decompression for Graves' disease. It was found that more than 60% of orbital decompressions were performed for mild to severe exophthalmos to correct corneal exposure or disfigurement. A total of 3.9% of these procedures were performed to relieve visual loss in compressive neuropathy. The large majority of decompressions were performed using antral-ethmoidal decompression via a translid or fornix approach. The amount of retrodisplacement was greatest with Kennerdell-Maroon or four-wall decompression and the least with lateral wall decompression. The antral-ethmoidal and three-wall decompression techniques gave an average of 4 to 6 mm of retrodisplacement. It was determined from the survey that antral-ethmoidal decompressions performed through the transantral approach were more likely to relieve the pressure in compressive neuropathy and also more likely to induce a worsening of muscle balance. In contrast, antral-ethmoidal decompressions performed via the translid approach were not as effective in relieving compressive neuropathy but had a much lower incidence of worsened muscle balance, and in fact, resulted in a higher incidence of improved muscle balance. The same trends were confirmed in the author's surgical practice, and an anatomic explanation is offered. The importance of creating nasoantral windows following decompression is emphasized. The risks of cerebrospinal fluid leakage and changes in eyelid positioning following decompression are described.
STUDY DESIGN: Ten fresh, cadaveric, two-vertebrae, functional spinal units were used to study the pathoanatomy, intervertebral foraminal area, and flexibility changes after posterior and transforaminal decompression. OBJECTIVES: To determine the feasibility of an endoscopic transforaminal approach as an alternative to conventional approaches, to establish the adequacy of transforaminal decompression without destabilizing the spine, and to study the structural changes in the spine after decompressions. SUMMARY OF THE BACKGROUND DATA: Posterior decompression entails major dissection and excision of bone and ligaments to access the spinal canal. Posterior decompression may be complicated by acute or chronic spinal instability, and the adequacy of lateral decompression is highly subjective. METHODS: The functional spinal units were mounted in quick-setting epoxy blocks. Pre- and postoperative computed tomography scans were taken to study changes in the foraminal area. Pre- and postoperative flexibility and anatomic studies were performed to compare the results. RESULTS: A 45.5% increase in the intervertebral foraminal area was possible, there was no flexibility change, and minimal anatomic damage to the spine was noted after transforaminal decompression. A 34.2% increase in the intervertebral foraminal area and a significant increase in extension and axial rotation flexibility were noted after the posterior decompression. CONCLUSION: Transforaminal decompression produced a significantly larger increase in the intervertebral foraminal area than posterior decompression, without increasing the range of motion or neutral zone in any direction. Because there was no violation of the anatomic integrity of the spine in the transforaminal approach, the risk of surgically induced instability was minimized. Endoscopic transforaminal decompression is a feasible alternative to current approaches.
The value of decompression after spinal cord injury in patients is still an unresolved issue. It has previously been shown in our laboratory that functional recovery in rats after cord compression varied with both the force and time until decompression. However, the longest duration studied was only 15 minutes, which is far less than that usually encountered in clinical practice, and therefore, the present study was undertaken to determine the value of decompression after more prolonged periods of compression. A factorially designed experiment with five rats per cell was used with the clip compression injury model. Forces of 2.3, 16.9 or 53.0 gms were applied at C7-T1 until decompression was performed after 15, 60, 120, or 240 minutes of compression. Functional recovery was assessed weekly for 8 weeks using the inclined plane technique. Maximum and minimum performance limits were established in normal rats and rats with cord transection, respectively. Univariate analysis and multiple comparison tests were used to analyse the data. The major determinant of recovery was the force of the injury. For example, the animals injured by the 2.3 gm clip performed significantly better than those injured at higher forces for all times until decompression (p less than 0.0001), and there was a significant difference in recovery between the groups injured by the 16.9 and 53.0 gm clips, although only for the 15 minutes until decompression group (p less than 0.05). The time until decompression also affected recovery, but only for the lighter compression forces (2.3 and 16.9 gm). For example, animals decompressed after 60 minutes of 2.3 gm compression recovered significantly better than those decompressed after 240 minutes (p less than 0.05). Thus, if the initial injury force is small, decompression is beneficial even after prolonged injury.
UNLABELLED: The effects of various degrees of compression and active decompression during cardiopulmonary resuscitation were tested in a randomized cross-over-design during ventricular fibrillation in eight pigs using an automatic hydraulic chest compression device. Compared with 4/0 (compression/decompression in cm), mean carotid arterial blood flow rose by 60% with 5/0, by 90% with 4/2 and 4/3, and 105% with 5/2. Two cm active decompression increased mean brain and myocardial blood flow by 53% and 37%, respectively, as compared with 4/0. Increasing standard compression from 4 to 5 cm caused no further increase in brain or heart tissue blood flow whether or not combined with active decompression. Tissue blood flow remained unchanged or decreased when active decompression (4/3) caused that 50% of the pigs were lifted from the table due to the force required. Myocardial blood flow was reduced with 5/0 vs. 4/0 despite no reduction in end decompression coronary perfusion pressure ((aortic-right atrial pressure) (CPP), (7 +/- 8 mmHg with 4/0, 14 +/- 11 mmHg with 5/0)(NS)). End decompression CPP increased by 186% with 4/2 vs. 4/0, by 200% with 4/3, and by 300% with 5/2. Endo-tracheal partial pressure of CO2 was significantly increased during the compression phase of active decompression CPR compared with standard CPR. Active decompression CPR generated an significantly increased ventilation compared with standard CPR. CONCLUSION: Carotid and tissue blood flow, ventilation, and CPP increase with 2 cm of active decompression. An attempt to further increase the level of active decompression or increasing the compression depth from 4 to 5 cm did not improve organ blood flow.
STUDY DESIGN: An evaluation of whether the immediate operative results can be improved in anterior cervical surgery in patients in whom disc fragments could remain hidden behind a vertebral body or far laterally in the foramen or in canal stenosis that involved a significant amount of a vertebral body. OBJECTIVES: To determine whether intraoperative ultrasonography can provide immediate evaluation of the decompression. SUMMARY OF BACKGROUND DATA: The anterior cervical approach has anatomic limitations that prevent good visualization of deep structures. Sequestered disc fragments can be hidden behind the bone of the vertebral body. Even careful preoperative measurements cannot ensure adequate length and width of decompression for stenotic lesions. METHODS: Three groups of patients were studied. Group 1 contained seven patients with soft disc herniations that were either behind the vertebral body or extended laterally into the neural foramen. Group 2 consisted of five patients with canal stenosis involving at least one third of the length of a vertebral body and causing myelopathic signs and symptoms. Group 3 consisted of four patients with radicular and cord symptoms. All were studied with either magnetic resonance imaging or computed tomography myelography or both. The size of the desired decompression was measured from these studies. A standard anterior decompression using magnification was performed that satisfied the surgeon's visual and tactile evaluation. The operative site was imaged ultrasonically and the decompression extended until preset imaging criteria were met. These criteria were clear root visualization for radiculopathy and good dural pulsations for stenotic lesions. RESULTS: Twelve of the 16 patients did not meet the set criteria on initial imaging, and 11 had their decompression extended. A hidden lateral disc fragment was found in one. In this selected group of 16 patients with complicated cervical pathology, 14 improved neurologically after the use of ultrasonic guidance intraoperatively. One error of interpretation was made. One patient who did not meet the ultrasonic decompression criteria and did not have the decompression extended did not improve after surgery. CONCLUSIONS: In complicated anterior cervical decompressions, intraoperative ultrasonic imaging provides immediate evaluation of the extent of the decompressive procedure and may improve the operative result.
Sprague-Dawley rats were compressed to 616 kPa (a) for 120 min then decompressed at 38 kPa/min to assess the cardiovascular and pulmonary responses to moderate decompression stress. In one series of experiments the rats were chronically instrumented with Doppler ultrasonic probes for simultaneous measurement of blood pressure, cardiac output, heart rate, left and right ventricular wall thickening fraction, and venous bubble detection. Data were collected at baseline, throughout the compression/decompression protocol, and for 120 min post decompression. In a second series of experiments the pulmonary responses to the decompression protocol were evaluated in non-instrumented rats. Analyses included blood gases, pleural and bronchoalveolar lavage (BAL) protein and hemoglobin concentration, pulmonary edema, BAL and lung tissue phospholipids, lung compliance, and cell counts. Venous bubbles were directly observed in 90% of the rats where immediate post-decompression autopsy was performed and in 37% using implanted Doppler monitors. Cardiac output, stroke volume, and right ventricular wall thickening fractions were significantly decreased post decompression, whereas systemic vascular resistance was increased suggesting a decrease in venous return. BAL Hb and total protein levels were increased 0 and 60 min post decompression; pleural and plasma levels were unchanged. BAL white blood cells and neutrophil percentages were increased 0 and 60 min post decompression and pulmonary edema was detected. Venous bubbles produced with moderate decompression profiles give detectable cardiovascular and pulmonary responses in the rat.
OBJECTIVE AND IMPORTANCE: We describe three cases in which ventrally situated cervical arachnoid cysts led to spinal cord or cervicomedullary compression after repeat craniocervical decompression for Chiari II malformations. CLINICAL PRESENTATION: All three patients underwent craniocervical decompression when their Chiari malformations became symptomatic. The first patient developed chronic vertiginous spells and headache and was treated with repeated craniocervical decompression procedures during several years. Seven months after undergoing her third decompression procedure, she developed severe dizzy spells, which were determined to be of brain stem origin. The second patient had a small, asymptomatic arachnoid cyst anterior to the brain stem discovered at age 6 years. After undergoing repeat craniocervical decompression for headaches 8 years after undergoing his first procedure, the patient developed severe neck pain and acute quadraparesis. A third patient underwent repeat craniocervical decompression at age 14 years for cranial nerve dysfunction. Postoperatively, he acutely developed paresis of extraocular movements and incoordination of the upper extremities. All three patients were found to have anteriorly situated arachnoid cysts compressing the brain stem and/or cervical spinal cord. INTERVENTION AND TECHNIQUE: Fenestration of the arachnoid cyst or drainage with cystoperitoneal shunting adequately treated acute brain stem or cervical spinal cord compression. All three patients had achieved satisfactory relief from their acute symptoms of neural compression at their follow-up examinations. CONCLUSION: An association between spinal arachnoid cysts and neural tube defects has previously been reported. However, the development of previously undetected spinal arachnoid cysts after craniocervical decompression was unexpected. We hypothesize that extensive craniocervical decompression may alter the cerebrospinal fluid pressure dynamics in such a way that the anterior subarachnoid space, previously compressed, may dilate. Occasionally, because of perimedullary arachnoiditis, the cerebrospinal fluid may become loculated and act as a mass. Direct fenestration or shunting may successfully treat this problem, and less extensive craniocervical decompression may avoid it.
In five subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure at rest to air at 6 bar for 30 min. corresponding to a depth of 50 m. Afterwards the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6 and 1.3 bar with a total decompression time of 73 min. Immediately after decompression and every 40 min. until the 240th min. arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min. after decompression indicating still incomplete nitrogen wash-out at least two hours after decompression had been accomplished. Bubble formation is discussed as a cause for prolonged nitrogen elimination. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest.
Acute ischemia in the complete territory of the carotid artery may lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Although clinical data suggest that patients benefit from undergoing decompressive surgery for acute ischemia, little data about the effect of this procedure on experimental ischemia are available. In this article the authors present results of an experimental study on the effects of decompressive craniectomy performed at various time points after endovascular middle cerebral artery (MCA) occlusion in rats. Focal cerebral ischemia was induced in 68 rats using an endovascular occlusion technique focused on the MCA. Decompressive craniectomy was performed in 48 animals (in groups of 12 rats each) 4, 12, 24, or 36 hours after vessel occlusion. Twenty animals (control group) were not treated by decompressive craniectomy. The authors used the infarct volume and neurological performance at Day 7 as study endpoints. Although the mortality rate in the untreated group was 35%, none of the animals treated by decompressive craniectomy died (mortality 0%). Neurological behavior was significantly better in all animals treated by decompressive craniectomy, regardless of whether they were treated early or late. Neurological behavior and infarction size were significantly better in animals treated very early by decompressive craniectomy (4 hours) after endovascular MCA occlusion (p < 0.01); surgery performed at later time points did not significantly reduce infarction size. The results suggest that use of decompressive craniectomy in treating cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. By performing decompressive craniectomy neurosurgeons will play a major role in the management of stroke patients.