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Decompressive craniectomy in a rat model of "malignant" cerebral hemispheric stroke: experimental support for an aggressive therapeutic approach.

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.

Animals↗

Ureteral decompression in advanced nonurologic malignancies.

BACKGROUND: The purpose of this study was to assess the morbidity and determine survival after ureteral decompression in patients with advanced nonurologic malignancies. METHODS: Between June 1988 and June 1993 78 patients were referred to a single surgeon for ureteral decompression. Records were analyzed in relation to primary diagnosis, early and late complications, number of hospitalizations, and survival after decompression. RESULTS: Seventy-two percent of patients initially underwent decompression endoscopically, and 28% required percutaneous nephrostomy placement at initial decompression. Complications occurred in 50% of patients and most commonly included infection (29%), stent obstruction and encrustation (28%), and gross hematuria (9%). The median survival for all patients after the first decompression procedure was 6.8 months (range 0.5-46.1), with an actuarial survival rate at 1 year of 55% and at 3 years of 30%. The eight patients with gastric/pancreatic cancer survived a median of just 1.4 months after decompression (range 0.77-11.8), with a 1-year actuarial survival rate of 12.5% and 3-year actuarial survival of 0%, which was significantly worse when compared with all other groups taken together or individually (p < 0.03). CONCLUSIONS: Ureteral decompression procedures in patients with advanced cancer can be an important component of palliative care but are associated with significant morbidity (50%) in patients whose median survival is < 7 months. The role of ureteral decompression in patients with advanced gastric and pancreatic cancer is limited.

Adult↗

Elective colon and rectal surgery without nasogastric decompression. A prospective, randomized trial.

Nasogastric (NG) decompression after colorectal surgery is practiced commonly. Our aim was to determine whether routine NG decompression benefitted patients undergoing this type of surgery. Five hundred thirty-five patients were randomized prospectively to either NG decompression or no decompression. Stratification was by type of operation and patient age. Excluded were patients who had emergency surgery with peritonitis, extensive fibrous adhesions, enterotomies, previous pelvic irradiation, intra-abdominal infection, pancreatitis, chronic obstruction. prolonged operating times, or difficult endotracheal intubation. Two hundred seventy-four patients received NG decompression (Salem sump, Argyle Co., Division of Sherwood Medical, St. Louis, MO) and two hundred sixty-one did not. There were 33 protocol violations included in the 535 patients. Patients who were not decompressed experienced significantly more abdominal distention, nausea, and vomiting than did those patients who were. Moreover, 13% required subsequent NG decompression as opposed to a reinsertion rate of 5% for patients routinely decompressed. The mean length of hospitalization for both groups was 11 days. There were no significant differences in nasopharyngeal or gastric bleeding, inability to cough effectively, respiratory infections, wound disruptions, reoperation, and wound infection rates (5%) between the two groups. We conclude that even though there is an increase in the rate of minor symptoms of nausea, vomiting, and abdominal distention, routine nasgastric decompression is not warranted after elective colon and rectal surgery.

Adolescent↗

Balanced orbital decompression for Graves' ophthalmopathy.

OBJECTIVE/HYPOTHESIS: Surgical management of Graves' ophthalmopathy is an alternative to medical therapy with corticosteroids or external beam radiotherapy. Orbital decompression has commonly been performed via a transantral approach to the medial orbital wall and floor. Although an endoscopic approach to these walls has been described, a balanced approach (incorporating a lateral decompression by an ophthalmology team) is desirable. STUDY DESIGN: Retrospective review. METHODS: Endoscopic medial decompression and extended lateral decompression were accomplished in 18 orbits (11 patients); inferior decompression was performed in 11 of these. Five additional procedures were performed. RESULTS: Exophthalmos improved by a mean of 4.6 mm. All patients who underwent decompression for vision loss had improved vision after surgery. Exposure keratitis improved in six of six orbits. Two of five patients undergoing orbital decompression for vision loss developed postoperative diplopia, which was successfully treated with strabismus surgery or prism glasses. There were no other significant complications. CONCLUSIONS: The endoscopic approach to the medial orbital wall is an important component of balanced orbital decompression for patients with Graves' ophthalmopathy. Balancing the decompression and preserving the medial orbital strut between the ethmoid cavity and the orbital floor may minimize the risk of diplopia.

Adult↗

Decompressive craniectomy for cerebral infarction. An experimental study in rats.

BACKGROUND AND PURPOSE: Acute ischemia in the territory of the carotid artery can lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Thus far, only anecdotal experience with supratentorial ischemia treated by decompressive craniectomy has been reported; and there are no published experimental data dealing with this kind of therapy in acute supratentorial stroke. In this study, we present our results on the effect of decompressive craniectomy in an endovascular model of cerebral infarction in rats. METHODS: Focal cerebral ischemia was induced in 50 rats using an endovascular occlusion technique of the middle cerebral artery. Decompressive craniectomy was performed in 30 animals: in 15 animals after 1 hour and in the remaining 15 animals 24 hours after vessel occlusion. Twenty animals were not treated by decompressive craniectomy (control group). RESULTS: Mortality in the nontreated group was 35%, whereas none of the animals treated by decompressive craniectomy died. Neurological behavior, weight loss, and infarction size were all significantly better in the animals treated by decompressive craniectomy, regardless of whether they had been treated after 1 or 24 hours (P < .01). CONCLUSIONS: Our results suggest that decompressive craniectomy for cerebral ischemia not only reduces mortality but also significantly improves outcome and reduces infarction size, probably because of increased perfusion pressure through leptomeningeal collaterals. This experimental study suggests that a controlled study of decompressive craniectomy in patients with acute internal carotid or middle cerebral artery occlusion would be worthwhile. By performing decompressive craniectomy in a small, selected group of patients, neurosurgeons may play an important role in the management of these patients.

Acute Disease↗

Species differences in decompression.

In an effort to bring together the diverse laboratory-animal decompression studies, a literature review and statistical evaluation were undertaken. Although 22 different species that had been used in decompression studies were identified, systematic data were available for only 7 of these species: man, goat, dog, guinea-pig, rat, hamster, and mouse. Mathematical functions using physiological data on these seven species were developed to estimate 1) saturation time (the time for the body to equilibrate after an increase in hydrostatic pressure), and 2) no-decompression saturation-exposure limits (the maximum saturation-exposure pressure from which an abrupt return to 1 ATA can be tolerated). Data from man, rat, and mouse were used to develop physiological relationships for two additional decompression variables: change in pressure-reduction limits associated with increased exposure pressure and time to onset of decompression symptoms. Finally, data on rats for two other decompression variables, gas elimination time and optimum decompression stop time, are discussed in the hope that this will stimulate additional animal laboratory research in other mammalians. The general functional relationships developed in this paper provide a preliminary and rough means for extrapolating among species the decompression results obtained during animal laboratory experiments.

Animals↗

Analysis of dural configuration for evaluation of posterior decompression in cervical myelopathy.

OBJECTIVE: The goal of this study was to establish the criteria for sufficient decompression of the cervical spinal cord in laminoplastic surgery. METHODS: Radiological examinations and neurological evaluations were conducted for 63 patients with cervical spondylotic myelopathy (CSM) and 31 patients with ossification of the posterior longitudinal ligament (OPLL) of the cervical spine who underwent suspension laminotomy. RESULTS: The dural configuration in computed tomographic myelograms was evaluated in comparison with the critical value for the dural configuration established from 36 control subjects. Seventy-six of 94 patients were judged to have achieved full decompression. The neurological improvement of patients with full decompression was significantly better than that of patients with insufficient decompression (P<0.01). The postoperative sagittal diameter of the spinal canal was more than 14 mm in most of the sufficiently decompressed cases of CSM and more than 17 mm in OPLL cases. The laminotomy width was more than 70% of the transverse diameter of the spinal canal in both CSM and OPLL cases. There were four OPLL cases with insufficiently decompressed dura mater in the well-enlarged spinal canal after surgery. In these cases, the ossified posterior longitudinal ligament continuously occupied more than 25% of the preoperative spinal canal area over three or more segments. CONCLUSION: The following conditions were considered critical for sufficient decompression of the spinal cord in laminoplastic operations: postoperative sagittal diameter of the spinal canal of more than 14 mm in CSM cases and more than 17 mm in OPLL cases and laminotomy width of more than 70% of the transverse diameter of the spinal canal in both CSM and OPLL cases. However, in cases of extensive OPLL, sufficient decompression could not be obtained through posterior enlargement of the spinal canal.

Adult↗

Management of severe traumatic brain injury by decompressive craniectomy.

OBJECTIVE: The beneficial effect of decompressive craniectomy in the treatment of head trauma patients is controversial. The aim of our study was to assess the value of unilateral decompressive craniectomy in patients with severe traumatic brain injury. METHODS: We retrospectively investigated 49 patients who underwent decompressive craniectomy. Intracranial pressure, cerebral perfusion pressure, therapy intensity level, and cranial computed tomographic scan features (midline shift, visibility of ventricles, gyral pattern, and mesencephalic cisterns) were evaluated before and after craniectomy. The gain of intracranial space was calculated from cranial computed tomographic scans. Patient outcome was graded using the Glasgow Outcome Scale. RESULTS: Thirty-one patients (63.3%) underwent rapid surgical decompression within 4.5 +/- 3.8 hours after trauma; in 18 patients (36.7%), delayed surgical decompression was performed 56.2 +/- 57.0 hours after injury. Patients younger than 50 years or patients who underwent rapid surgical decompression had a significantly better outcome than older patients or patients who underwent delayed surgical decompression. Craniectomy significantly decreased midline shift and improved visibility of the mesencephalic cisterns. The state of the mesencephalic cisterns correlated with the distance of the lower border of the craniectomy to the temporal cranial base. Alterations in intracranial pressure, cerebral perfusion pressure, and therapy intensity level were not significant. The overall mortality of the patients corresponded to the reports of the Traumatic Coma Data Bank (1991). CONCLUSION: Although there was a significant decrease in midline shift after craniectomy, this did not translate into decompressive craniectomy demonstrating a beneficial effect on patient outcome.

Adolescent↗

Endoscopically assisted decompression for metastatic thoracic neoplasms.

STUDY DESIGN: The author describes a technique for complete vertebrectomy and anterior decompression followed by a formal anterior column reconstruction, using readily available endoscopic instruments. This procedure is indicated in patients with radioresistant metastasis of the thoracic spine, particularly those involving the upper thoracic segments where a thoracotomy is difficult and causes a high rate of morbidity. This is also a suitable technique for patients with pulmonary disease who cannot tolerate a standard thoracotomy. OBJECTIVES: To demonstrate the feasibility and potential benefits of endoscopically controlled decompression through an extrapleural, posterolateral approach. SUMMARY OF BACKGROUND DATA: Posterolateral decompression of the thoracic spine offers potential advantages in comparison with traditional anterior-posterior procedures combining thoracotomy and posterior instrumentation, including decreased operative time, decreased morbidity, and reduced hospital stay. Results of previous studies have not demonstrated the same benefit for posterolateral decompression as for anterior vertebrectomy and decompression. Drawbacks to the traditional posterolateral decompressions have included poor visualization of the spinal cord and anterior tumor, poor access to tumor on the side contralateral to the approach, and the need to manipulate the spinal cord to completely remove adjacent tumor and tumor adherent to the dura. METHODS: Surgical indications, rationale, and technique are provided, and initial clinical results are described. RESULTS: Transpedicular decompression using endoscopy is described in five patients. The mean operative time for the combined procedure was 7.25 hours, with a mean blood loss of 1800 mL. Neurologic recovery and maintenance were excellent. Inpatient days averaged 7.5, and intensive care days averaged 2. One patient died of disease 8 months after surgery, and four were living, with disease, 3-24 months after surgery. CONCLUSIONS: Endoscopically assisted decompression can reduce morbidity, hospital stay, and treatment costs while matching the efficacy of traditional combined procedures. Endoscopy provides a readily available and easily applied tool that dramatically improves the surgeon's vision, providing light, magnification, and a direct view of remote structures.

Bone Nails↗

Staged spinal cord decompression through posterior approach for thoracic myelopathy caused by ossification of posterior longitudinal ligament.

STUDY DESIGN: Prospective clinical study of the effect of staged elimination of anatomic factors inhibiting posterior shift of the thoracic spinal cord on the degree of posterior shift of the thoracic spinal cord and its significance in augmenting the safety of ossification of posterior longitudinal ligament (OPLL) manipulation in thoracic OPLL myelopathy. OBJECTIVES: To develop a comprehensive method that enables safe and sufficient decompression of the spinal cord for thoracic OPLL myelopathy. SUMMARY OF BACKGROUND DATA: Decompression of the spinal cord by direct manipulations of thoracic OPLLs, via either anterior or posterior approach, caused some iatrogenic catastrophic spinal cord injuries, and methods to prevent such injuries during surgery have not yet been developed. METHODS: Procedures of elimination of anatomic factors inhibiting posterior shift of the thoracic spinal cord were performed in stages at intervals of between 1 month and 11 years depending on patients' neurologic status. The first stage operation consisted of extensive cervicothoracic laminoplastic decompression with or without posterior longitudinal durotomy, and if the decompression were insufficient, measures for OPLL-spinal cord separation with or without OPLL manipulation were added. RESULTS: All 17 patients with thoracic OPLL myelopathy showed improvements of neurology comparable with those with successful anterior approaches after decompression. The mean follow-up period was 42 months (range 6-101 months). Neurologic improvements persisted for the entire follow-up period in all patients except one patient who developed arachnoid cyst compressing the dorsum of the once-decompressed spinal cord 30 months after surgery. CONCLUSIONS: Staged posterior decompression to eliminate anatomic factors inhibiting posterior shift of the thoracic spinal cord is the safest and the most reliable method of spinal cord decompression to treat thoracic OPLL myelopathy, so far. However, long-term results are required before the methods can be established.

Adult↗

Blood flow during 2-Torr exposures at different decompression rates.

Central and peripheral blood flow of denitrogenated dogs, measured in the femoral artery and aorta, declined rapidly and ceased within mean times of 28, 35, 70, or 90 s after 1-, 10-, 30-, or 60-s decompressions from 258 Torr to 2 Torr, respectively. Neither arterial nor venous hypoxemia was seen after 1-s decompressions since the hypoxic blood did not reach the aorta. In contrast, arterial and venous O2 saturation levels dropped as low as 12 or 6% following 10- to 60-s decompressions since circulation continued. A severe and transient decerebratelike rigidity and subsequent temporary flaccid paralysis of the hind legs was seen during recovery from decompressions slower than 1 s, whereas only a mild temporary flaccid paralysis was frequently present after 1-s decompression. The more severe responses following 10- to 60-s decompressions are associated with the greater hypoxemia after slow decompressions, indicating tissue hypoxia is more severe when decompression rate is slow.

Animals↗

Consumption of platelets in decompression sickness of rabbits.

Platelet behavior was studied in rabbit decompression sickness which was brought about by the exposure to 6 ATA for 40 min (bottom time) followed by rapid decompression. Platelet counts significantly decreased after the decompression. Kinetic studies with 111In-oxine-labeled platelets revealed shortened survivals of circulating platelets, and audioradiograms indicated the accumulation of radioactivity in the lungs after the decompression. Although there was no change in the mode volume of platelets after the decompression, the transient appearance of circulating smaller or fragmented platelets suggested a random overdestruction of platelets. Whole and releasable adenine nucleotide contents of platelets were decreased significantly after the decompression. There were no significant changes in cytoplasmic adenine nucleotide contents. Therefore, in decompression sickness, the circulating platelets behaved similarly to those in acquired storage pool disease. Platelet thrombi were found in the pulmonary arteries, compatible with the accumulation of 111In-oxine-labeled platelets. These findings suggest that circulating air bubbles interact with platelets, causing the platelet release reaction, and these activated platelets participate in the formation of thrombi in experimental decompression sickness.

Adenine Nucleotides↗

Effect of oxygen tension and rate of pressure reduction during decompression on central gas bubbles.

Reduction in ascent speed and an increase in the O2 tension in the inspired air have been used to reduce the risk for decompression sickness. It has previously been reported that decompression speed and O2 partial pressure are linearly related for human decompressions from saturation hyperbaric exposures. The constant of proportionality K (K = rate/partial pressure of inspired O2) indicates the incidence of decompression sickness. The present study investigated the relationship among decompression rate, partial pressure of inspired O2, and the number of central gas bubbles after a 3-h dive to 500 kPa while breathing nitrox with an O2 content of 35 kPa. We used transesophageal ultrasonic scanning to determine the number of bubbles in the pulmonary artery of pigs. The results show that, for a given level of decompression stress, decompression rate and O2 tension in the inspired air can be traded off against each other by using pulmonary artery bubbles as an end point. The results also seem to confirm that decompressions that have a high K value are more stressful.

Animals↗

Recovery of nerve conduction following microvascular decompression for trigeminal neuralgia.

OBJECTIVE: To assess the function of trigeminal nerve before and after microvascular decompression for trigeminal neuralgia. BACKGROUND: To date there is no direct evidence that microvascular decompression of the trigeminal root restores normal conduction in the nerve. METHODS: The authors examined 10 patients with trigeminal neuralgia in whom preoperative MRI and MR angiography demonstrated neurovascular contact. During microvascular decompression, the trigeminal nerve was monitored by recording early scalp trigeminal evoked potentials immediately before, during, and after decompression. Direct recordings from the root entry zone were also performed. RESULTS: In all patients preoperative scalp evoked potentials showed impaired conduction of the trigeminal root. Microvascular decompression was associated with immediate recovery of conduction in seven patients, demonstrated by both scalp evoked potentials and direct root recordings. All 10 patients were pain free postoperatively. CONCLUSIONS: Improvement in trigeminal neuralgia following microvascular decompression is often associated with normalization of neurophysiologic data, suggesting recovery of nerve function. Rapid electrophysiologic recovery and pain relief following microvascular decompression argue that neither phenomenon is linked to remyelination. It is possible that the trigeminal evoked potentials might predict an effective microvascular decompression.

Decompression, Surgical↗

Relationship between the clinical features of neurological decompression illness and its causes.

There is dispute as to whether paradoxical gas embolism is an important aetiological factor in neurological decompression illness, particularly when the spinal cord is affected. We performed a blind case-controlled study to determine the relationship between manifestations of neurological decompression illness and causes in 100 consecutive divers with neurological decompression illness and 123 unaffected historical control divers. The clinical effects of neurological decompression illness (including the sites of lesions and latency of onset) were correlated with the presence of right-to-left shunts, lung disease and a provocative dive profile. The prevalence and size of shunts determined by contrast echocardiography were compared in affected divers and controls. Right-to-left shunts, particularly those which were large and present without a Valsalva manoeuvre, were significantly more common in divers who had neurological decompression illness than in controls (P<0.001). Shunts graded as large or medium in size were present in 52% of affected divers and 12.2% of controls (P<0.001). Spinal decompression illness occurred in 26 out of 52 divers with large or medium shunts and in 12 out of 48 without (P<0.02). The distribution of latencies of symptoms differed markedly in the 52 divers with a large or medium shunt and in the 30 divers who had lung disease or a provocative dive profile. In most cases of neurological decompression illness the cause can be determined by taking a history of the dive profile and latency of onset, and by performing investigations to detect a right-to-left shunt and lung disease. Using this information it is possible to advise divers on the risk of returning to diving and on ways of reducing the risk if diving is resumed. Most cases of spinal decompression illness are associated with a right-to-left shunt.

Case-Control Studies↗

Factors in 171 navy diving decompression accidents occurring between 1960-1969.

Comparisons were made between the incidence of specific factors in U.S. Navy decompression accidents and the incidence of these factors in routine (nonexperimental) U.S. Navy operational dives. It was found that decompression accidents are disproportionately high among a) air dives less than 140 ft which have bottom times of 30 min or less and air dives greater than 140 ft which have bottom times of more than 15 min, b) Divers First Class, c) older divers, and d) dives which do not involve work or divers which require heavy work. Repetitive dives have a lower decompression accident rate than expected. Decompression accidents were not disproportionately high for any category of body build. These results indicate that the present U.S. Navy decompression tables are extremely safe (5 decompression accidents/10,000 dives), and do not appear to require modification. Future decompression research may be directed toward analyzing the relationship of work and aging to physiological processes involved in decompression. In addition, the present findings should be cross-validated using more recent accident and operational diving data.

Accidents↗

Changes in hemostatic parameters in fish following rapid decompression.

The effect of rapid decompression on the stress-accelerated blood coagulation system of male and fingerling coho salmon (Oncorhynchus kisutch) was examined after simulated 100- and 200-fsw dives. Blood samples taken either through a dorsal aorta cannula or from a severed caudal peduncle were analyzed for total plasma protein and fibrinogen concentrations, prothrombin times (PT), and partial thromboplastin times (PTT). The effect of mild decompression (100-fsw) on the hemostatic mechanism of both adult and fingerling coho salmon indicated an alternating fibrinogen concentration, declining from normal levels 1 min after decompression, followed by an increase 10 to 15 min later with an eventual loss of fibrinogen to one half the original level an hour after decompression. Partial thromboplastin times were found to increase 10 to 15 min after decompression occurred. Prothrombin times showed an increase 1 hour after decompression in adult salmon, whereas in fingerlings, prothrombin times increased almost immediately from normal levels. The effect of severe decompression (200-fsw) showed similar trends, but at an accelerated rate. It was concluded that both mild and severe decompression activates the hemostatic mechanism of fish which may eventually result in consumption coagulopathy at a greater rate than reported for experimental mammals.

Age Factors↗

[Decompression of deep divers].

For industrial saturation dives over 50 m, Heliox (He-O2) is now used routinely as respiratory gas mix. The decompression after such dives has been investigated thoroughly as well on the animal (minipig, monkeys) as on humans. Results show that for a given ascending speed, the number of bubbles detectable by the Doppler method in the bloodstream rises according to the maximal depth. The incidence of decompression accidents follows the same trend. This finding prompted us to adopt since 1979 slower decompression speeds. Moreover we modified the ascension profile, using henceforth a linear decompression in maintaining a constant speed for a given partial oxygen pressure. For our research program Hydra, we replaced in part Helium by Hydrogen in the respiratory gas mix. We were thus able to do the first hydrogen saturation decompression between 450 and 200 meters, during our Hydra V (1985) experiment. During our following diving research program Hydra VI (1986), 8 divers were decompressed under Hydreliox (H2-He-O2) mix from 500 to 300 m by eliminating hydrogen by chemical means. We used for this purpose a dehydrogenation apparatus developed by our engineering team. These decompressions took place without any difficulty and only a low number of bubbles detected. It is therefore possible to use decompression speeds for hydrogen and helium which are very similar. A confirmatory experiment on mice, where we exposed them to a 2000 m depth dive under Hydreliox (H2-He-O2), gave good results. This gives us the possibility, to perform gas exchange studies on small animals and to extrapolate the results to humans.

Animals↗