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Transmastoid decompression of the facial nerve in Bell's palsy.

We describe the technique of decompression of the facial nerve from the geniculate ganglion to the stylomastoid foramen. The decompression was made on 51 patients with Bell's palsy, and the results of follow-up study were compared with those of 77 patients in whom the pyramidal and vertical segments were decompressed. The decompressions were indicated when a severe denervation of the nerve was confirmed by electrodiagnostic examinations. Incidences of notable residual palsy and of pronounced sequelae were always lower in the former group of patients regardless of the operational timing. In either group, a more desirable result was obtained by the decompression within 30 days, but a favorable effect of the decompression was recognizable even when the surgery was performed between 31 and 90 days after the onset.

Adolescent

Bilateral transpedicular decompression and Harrington rod stabilization in the management of severe thoracolumbar burst fractures.

Fifty-eight patients with severe thoracolumbar burst fractures were treated with bilateral transpedicular decompression, Harrington rod instrumentation, and spine fusion. Spinal realignment and stabilization was achieved by contoured dual Harrington distraction rods supplemented by segmental sublaminal wiring. Posterior element fractures were noted in 25 patients, 9 of whom had associated dural tears. Computed tomography was performed to assess the cross-sectional area of the spinal canal before surgery and after decompression. Patients at initial evaluation averaged greater than 67% spinal canal compromise. After surgery, successful decompression was accomplished in 57 patients. One patient required staged, anterior thoracoabdominal decompression and fibula strut grafting. At follow-up (average, 43 months; range, 25-70 months), neurologic improvement was found in 77% of the patients who initially presented with neurologic deficits. Thirty-four of 40 patients with incomplete paraplegia improved one or more subgroups on the Frankel scale. A solid fusion was attained in all 58 patients. No patient had a significant residual kyphotic deformity. Single-stage bilateral transpedicular decompression and dual Harrington rod instrumentation reliably provides decompression of the spinal canal and restores spinal alignment. The procedure allows early mobilization and provides an environment for solid fusion and maximum neurologic return.

Adult

Influence of long-term intermittent exposures to hypoxia on decompression-induced pulmonary haemorrhage.

Healthy male rats were acclimatized by being placed in a decompression chamber at a simulated altitude of 18 000 feet (5486 m) for three hours daily for 84 days. The altitude acclimatized rats paired with unacclimatized rats were rapidly decompressed together. The range of decompression was performed from on atmospheric pressure to an ambient pressure of 30 mmHg in 0-2 seconds. It was found that in control rats, 14 of 20 lung (70%) exhibited pulmonary haemorrhage following rapid decompression. In altitude acclimatized rats, however, only 6 of 20 (30%) revealed decompression-induced haemorrhage. The difference was statistically significant. The present findings indicate that long-term intermittent exposures to hypoxia might increase the resistance of pulmonary tissue to rapid decompression, resulting in a decrease in frequency and severity of pulmonary haemorrhage. The possible mechanism of such a phenomenon is discussed.

Acclimatization

Metabolic alterations in obstructive jaundice: effect of duration of jaundice and bile-duct decompression.

We examined the effect of prolonged bile duct obstruction, and subsequent biliary decompression, on biochemical and metabolic parameters, using a reversible jaundice model in male Fischer 344 rats. The animals were studied after biliary obstruction for varying periods (4 days, one week, and two weeks) and following decompression. They were sacrificed one or two weeks following decompression. All the rats were compared to sham operated, pair-fed, controls. Obstructive jaundice rapidly increased bilirubin, liver enzymes, serum free fatty acid, and triglyceride levels. Glucose levels were significantly decreased in the jaundice rats compared to their pair-fed controls. Only after two weeks of jaundice was significant hypoalbuminemia observed. Following decompression, all biochemical and metabolic values gradually returned to normal levels, except for albumin. Hypoalbuminemia was not reversed within the two-week post-decompression period. The rats jaundiced for two weeks had significantly higher mortality, compared to the other groups. We conclude that prolonged jaundice adversely affects the metabolic capacity of the rats, with albumin concentration being markedly decreased, and that biliary decompression could not reverse completely all the alterations seen with cholestasis, especially following two weeks of bile duct obstruction.

Animals

[Indication and prognosis of the transethmoidal decompression of the optical nerve in posttraumatic amaurosis (author's transl)].

In 8 patients with unilateral posttraumatic amaurosis a transethmoidal decompression of the optical nerve was performed. In 4 patients the vision returned completely after operation, 1 patient showed only a partial improvement and in 3 cases the amaurosis remained unchanged. These results agree with those reported by Japanese authors (Sugita et al., 1965; Fukado, 1968) and suggest, that opposite to the neurosurgical transfrontal-intradural resection of the roof of the optical canal the rhinosurgical transethmoidal decompression of the optical nerve may improve the prognosis of the posttraumatic amaurosis, espcially, if the decompression can be done as soon after trauma as possible. Further advantages of this surgical method are the smaller risk, the shorter operation time and the preservation of olfaction. It is emphasized that the rhinologist cannot indicate the decompression of the optical nerve without consulting the ophthalmologist and the neurologist. Contraindications are lesions of the bulbus oculi and the fundus, lesions of the chiasma opticum and a posttraumatic amaurosis caused by a sinus-cavernosus-fistula. Regarding the experiences gained by rhinosurgeons so far the early transethmoidal decompression seems to be indicated, if a unilateral impairment of vision exists right after the trauma or develops within the next 24-48 hrs and if there is no damage to the bulbus and the fundus.

Adult

Inner ear decompression sickness.

With recent increases in commercial, military, and sport diving to deeper depths, inner ear injuries during such exposures have been encountered more frequently and noted during several phases of diving: during compression, at stable deep depths, with excessive noise exposure in diving, and during decompression. The pathophysiology of these injuries differs, depending upon the phase of diving in which the injuries occur. In this report, 23 cases of hearing loss, tinnitus, and/or vertigo occurring during or shortly after decompression are presented. Thirteen of these cases occurred in helium-oxygen dives involving a change to air during the latter stages of decompression. A significant correlation is present between prompt recompression treatment, relief of symptoms, and lack of residual deficits. Current knowledge indicates that the management of otologic decompression sickness should include: 1. prompt recompression to at least 99 feet deeper than the symptom onset depth; 2. recompression using the previous helium-oxygen mixture when the injuries occur during or shortly after a switch from helium-oxygen to air during the latter stages of decompression; 3. the use of parenteral diazepam for symptom relief and cyclic inhalations of oxygen enriched treatment gases; and 4. the avoidance of further diving by divers who exhibit permanent inner ear injuries after the acute symptoms have subsided.

Adult

Intravascular bubble composition in guinea pigs: a possible explanation for differences in decompression risk among different gases.

Differences in risk of decompression sickness (DCS) that have been observed among inert gases may reflect differences in gas solubility or diffusivity or both. A higher risk gas might generate a larger volume of evolved gas during decompression, thereby increasing the probability of DCS. If this hypothesis is correct, the composition of bubbles that develop during decompression should reflect such gas differences. Unanesthetized guinea pigs were compressed to depths ranging from 250 to 350 fsw with air, He-O2 (21% O2) or one of a number of N2-He-O2 or N2-Ar-O2 mixtures (21% O2). Animals were held at depth from 15 to 60 min, then decompressed slowly (60 fsw/min) or rapidly (less than 15 s) to 5 fsw. If severe DCS developed, as judged by changes in physiologic variables, death usually occurred quickly. Gas/blood samples were then immediately withdrawn from the right atrium or the inferior vena cava, and the gas phase analyzed for He, N2, Ar, O2, and CO2 via gas chromatography. Bubbles from all dives contained 5-9% CO2, 1-4% O2, with the balance inert gas. Bubbles after N2-He-O2 dives contained substantially more N2 than He (up to 1.9 times more) compared to the dive mixture; bubbles after N2-Ar-O2 dives contained more Ar than N2 (up to 1.8 times more). For N2-He-O2 dives, the actual inert gas makeup of bubbles was dependent on the time-at-depth and the decompression profile. Results may reflect differences among He, N2, and Ar in tissue solubility/diffusivity and gas exchange rates, and support the rank order of increasing DCS risk (He less than N2 less than Ar) and rate of gas exchange (N2 less than He) observed previously during rat dives.

Animals

Preventive effect of a vasodilator on the occurrence of decompression sickness in rabbits.

The effect of terbutaline on the occurrence of decompression sickness was studied in seven rabbits. Terbutaline is a vasodilator, a sympathomimetic beta2-receptor stimulator. The rabbits were given a hyperbaric exposition at 2 ATA followed by oxygen breathing at 1 ATA and a hypobaric exposition at 0.2 ATA. Each rabbit got a hyperbaric exposition long enough for symptoms of decompression sickness to occur at the hypobaric exposition. With a time interval of at least 1 week, each rabbit received an identical pressure exposition, except that terbutaline was injected intravenously at the beginning of the denitrogenation period at 1 ATA. Of the seven experiments with the drug, only one case of decompression sickness occurred and with a delayed appearance. This may be compared to rapid-appearing decompression sickness in all cases in the control series. The results may be of importance in diving routines and, possibly, in the treatment of decompression sickness.

Animals

Changes in blood enzyme activity and hematology of rats with decompression sickness.

Plasma activities of lactic dehydrogenase (LDH), creatine phosphokinase (CPK), glutamic pyruvic transaminase (GPT), and alkaline phosphatase (ALP) were studied, along with hematological changes, in rats suffering from various degrees of experimental decompression sickness (DS). By 1 h after decompression, LDH and CPK activities were elevated in moderate and severe DS whereas GOT and GPT were elevated only in severe DS. ALP was reduced in all decompressed rats. Hematological changes indicated hemoconcentration, the degree of which paralleled the severity of DS. By 24 h after decompression, all enzyme activities were approaching control levels with the exception of GOT, which was further elevated from the 1-h value. The observed lung damage in rats with severe DS in conjunction with the hematologic and enzyme data suggested that hypoxemic-hypoxia, incident to bubble embolization of pulmonary vasculature, was a major factor in altering the blood enzyme pattern in DS. Serum enzyme data from two inadequately decompressed divers are also reported.

Alanine Transaminase

Ogilvie's syndrome: colonoscopic decompression and analysis of predisposing factors.

Forty-eight cases of Ogilvie's syndrome, colonic pseudo-obstruction, presenting between 1983 and 1989 were retrospectively reviewed to assess the results of colonoscopic decompression and to identify potential etiologic factors. Three patients had spontaneous resolution with medical treatment. Forty-five patients required 60 colonoscopic decompressions: 38 (84 percent) were successfully treated using colonoscopy; five (11 percent) required an operation; and two died within 48 hours of colonoscopy from medical causes. No complications or deaths were the result of colonoscopy. Twenty-nine patients (64 percent) were successfully treated with a single colonoscopy. One-third of patients required serial decompressions. Average cecal diameter in patients with successful colonoscopic decompression was 12.4 cm but was larger for patients requiring more than one colonoscopy (13.3 cm) and for those who failed colonoscopic therapy (13.4 cm). The spine or retroperitoneum had been traumatized or manipulated in 52 percent of patients. Patients with Ogilvie's syndrome were being treated with narcotics (56 percent), H-2 blockers (52 percent), phenothiazines (42 percent), calcium-channel blockers (27 percent), steroids (23 percent), tricyclic antidepressants (15 percent), and epidural analgesics (6 percent) at diagnosis. Electrolyte abnormalities included hypocalcemia (63 percent), hyponatremia (38 percent), hypokalemia (29 percent), hypomagnesemia (21 percent), and hypophosphatemia (19 percent). Colonoscopic decompression in Ogilvie's syndrome is safe and effective management. Multiple pharmacologic and metabolic factors, as well as spinal and retroperitoneal trauma, appear to alter autonomic regulation of colonic function, resulting in colonic pseudo-obstruction.

Adult

Gliosis and ganglion cell death in the developing cat retina during hydrocephalus and after decompression.

Even after surgical decompression, infantile hydrocephalus often results in permanent neurological symptoms, including visual deficits. However, little is known about the cellular changes that may be responsible for these effects. The present study was designed to analyze the retinae of normal, mildly hydrocephalic, severely hydrocephalic and surgically decompressed kittens to determine if changes occur in the density and size of retinal ganglion cells. Hydrocephalus was induced in 10 day old kittens by intra-cisternal injection of kaolin. Kittens were allowed to survive from 7 to 28 days after injection. Animals that were decompressed received ventriculoperitoneal shunts 10-15 days after the induction of hydrocephalus and were sacrificed 10-14 days after shunt placement. The density and area of neuronal and glial cells were determined within a sample area in peripheral nasal retina. Total cell density was significantly increased in mildly and severely hydrocephalic animals but returned to normal following decompression. This change represents a significant increase in the glial population. In addition, there was a significant loss of ganglion cells in both the severely hydrocephalic and the shunted groups. Based on these findings, we conclude that gliosis occurs as a result of cell death in the retina following severe hydrocephalus, and decompression is unable to reverse these effects. Furthermore, gliosis occurs in mild cases of hydrocephalus, and may be an early indication that cellular degeneration will follow.

Analysis of Variance

Percutaneous endoscopic gastrostomy for decompression of the stomach and small bowel.

Percutaneous endoscopic gastrostomies are used most commonly for enteral feeding. We report the use of such gastrostomies for decompression of the obstructed gastrointestinal tract. Percutaneous endoscopic gastrostomies were performed on 53 patients over a 2-year period for gastrointestinal decompression because of gastric or small bowel obstruction. Forty-six patients had malignant obstruction from a primary abdominal or metastatic carcinoma and 7 patients had non-malignant obstruction or stasis. Gastrostomy for decompression was successful in 41 of 46 (89%) cases of malignant obstruction and in all 7 of the non-malignant cases. Tube utilization for decompression averaged 60 +/- 91 days. A 28 F tube with a 4-inch perforated intragastric portion was fashioned to maximize drainage. This efficient decompression tube allowed oral intake of liquids and soft foods in 88% of patients. Complications, which occurred in 4%, included one case of fatal peritonitis and one case of cellulitis.

Digestive System Neoplasms

Neurologic recovery associated with anterior decompression of spine fractures at the thoracolumbar junction (T12-L1).

Between 1981 and 1990, twenty-two patients with incomplete neurologic deficits after thoracolumbar junction fractures were treated by anterior decompression and stabilization. Two patients were unavailable for follow-up examination, eleven underwent spinal canal decompression within 48 hours of injury (Group A); and nine patients underwent surgical decompression in an average of 61 days after injury (Group B). Neurologic recovery was analyzed by a modified Frankel grading system, the ASIA motor point scale and conus medullaris function. Patients were followed for an average of 3.5 years (range, 6-92 months). No patients had any deterioration in neurologic function after surgery. Patients in Group A had a modified Frankel grade improvement with a median of two grades and a mean American Spine Injury Association motor point improvement of 21.1 +/- 4.1. Four of nine patients with conus medullaris deficits demonstrated complete functional bladder and bowel return postoperatively. Those patients in Group B had a modified Frankel grade improvement with a median of one grade and a mean ASIA motor point improvement of 7.6 +/- 1.7. None of the six patients with conus medullaris injuries showed complete improvement in bladder or bowel function postoperatively. The modified Frankel grade and ASIA motor point score improvements were significant when the two groups were compared (P less than 0.04 and P less than 0.01, respectively). In this series of patients, early anterior decompression for traumatic injuries at the thoracolumbar junction was associated with improved rates of neurologic recovery when compared to late decompression.

Adolescent

Comparison of the effects of surgical decompression and resection of local edema in the therapy of experimental brain trauma. Investigation of ICP, EEG and cerebral metabolism in cats.

The effect of decompressive trepanation was compared to that of surgical resection of the traumatized tissue in the course of traumatic brain edema in standardized experimental brain trauma. Following a right parietal cold injury, the following parameters were monitored continuously in 12 cats: ventricular pressure, epidural pressure over both hemispheres, arterial and central venous pressure and heart rate. The EEG was evaluated continuously, using a computer (power spectra). After catheterization of the superior sagittal sinus, cerebral arteriovenous differences of glucose, lactate, O2 and CO2 were calculated. 6 animals were treated surgically when showing elevated intracranial pressure ICP and markedly altered EEG. In 3 animals, the right hemisphere was decompressed by extensive resection of bone and dura. In 3 further animals, the softened brain tissue of the cold lesion was resected and the skull defect closed. 6 untreated animals were used in controls. A decompression by skull hemiresection for ablation of the injured cortex abolished the high intracranial pressure, but only the latter method seemed to prevent further damage. This could be demonstrated by the EEG registration, and by the normalization of arteriovenous metabolite differences. Only animals treated with edema resection had a normal arousal reaction and survived the trauma. The results indicate, that only an ablation of the local injury will prevent further damage to the brain. After decompressive trepanation alone, the progression of tissue edema is not interrupted. As can be seen from the literature, the poor results obtained even from extensive decompressive operations in traumatic brain edema, indicate that the further development of edema is independent of the intracranial pressure, whereas the favorable results of resection of lobar contusions show an interruption of the spread of dysbolism.

Animals

Enhancement of experimental cerebral edema after decompressive craniectomy: implications for the management of severe head injuries.

Decompressive craniectomy has been advocated as a treatment for the cerebral edema associated with massive head injury. Although craniectomy has been successful in lowering intracranial pressure after head injury, a comparison of computerized tomographic scans of comparable patients with traumatic brain edema treated by medical means or decompressive craniectomy showed that bony decompression resulted in apparent exacerbation of edema. To investigate the possibility of enhancement of brain edema by craniectomy, we produced standardized cold lesions in the brains of 10 dogs. Five animals served as controls. In the other 5 animals we performed large decompressive craniectomies after lesioning. Physiological parameters were comparable in both groups. The dogs were killed 8 hours after lesioning. After fixation, their brains were cut into 1-mm-thick slices. We used an image analysis facility built around a PDP 11/105 computer to measure the volume of edema as outlined by Evans blue staining. The mean volume of the brain edema in the control animals was 0.27 +/- 0.19 ml. Mean edema volume was over 7 times greater in craniectomized animals (1.96 +/- 1.89 ml). This difference is statistically significant (p less than 0.05). The driving force for the formation of edema fluid is the difference between intravascular and interstitial presssure. Decompression of the brain by bone removal probably results in a reduction of interstitial fluid pressure and edema enhancement. The clinical literature contains no evidence that craniectomy decreases the morbidity or mortality of human head injury. In view of our experimental findings, this is not surprising. Indeed, pathological evidence indicates that severe edema (such as that accentuated by craniectomy) may produce permanent changes in the neuropil.

Animals

Influence of hypothalamic hyperphagia on tolerance of lung to explosive decompression.

A study was made of the effect of hypothalamic hyperphagia on the tolerance of lung to explosive decompression in male Long-Evans rats. The control and hypothalamic hyperphagic rats were explosively decompressed together from 1 atm to an ambient pressure of 30 min Hg in 0.04s. The hypothalamic-lesiones rats gained from 252 g average weight to 460 g, a 82% gain. The respective figures for the controls. were from 248 g to 336 g and 36%. It was also observed that a considerable amount of fat was accumulated between pleura and lungs in experimental animals. The average accumulation of fat between pleura and lungs in experimental rats was 3.23 g, while the value of the control group was only 0.42 g. The difference was statistically significant. Such an increase of fat accumulation in the thoracic cage could decrease the tidal volume. The severity of decompression-induced pulmonary hemorrages might thus be decreased. On the other hand, it also seems possible that the soft fat cushion between pleura and lungs might damp the bruising of the pulmonary tissue against the resistant thoracic wall to a certain extent, thus resulting in a decreased susceptibility to decompression-induced lung damage. Besides , the mortality in obese rats undergoing explosive decompression was also significantly lower than that of the controls

Adaptation, Physiological

Ethmoidectomy decompression for the treatment of Graves' optic neuropathy.

When orbital decompression becomes necessary in Graves' optic neuropathy, medial wall decompression is a necessary component of the decompression procedure. The ethmoidectomy approach allows more direct visualization of the posterior ethmoids and sphenoids to effect maximum decompression. This is particularly important in cases in which computed tomography shows the medial rectus muscle to be enlarged posteriorly in the orbit. The procedure provides excellent visualization of the medial rectus. As with any medial wall decompression procedure, postoperative restriction of horizontal motility is a frequent complication, often necessitating more than one subsequent operation. The authors describe their experience with the procedure in 25 patients with Graves' optic neuropathy.

Adult

A prospective randomized trial of routine postoperative nasogastric decompression in patients with bowel anastomosis.

Until relatively recently, the nasogastric (NG) tube has been used routinely for decompression in the patient with small- or large-bowel anastomosis. To determine if routine postoperative NG decompression benefited such patients, 102 patients were randomized prospectively to either NG decompression or no-NG tube. Excluded were patients with chronic bowel obstruction, peritonitis, gross fecal contamination or spillage, and previous abdominal or pelvic irradiation. There were 52 patients in the no-NG group and 50 in the NG group. Patients in the no-NG group had earlier bowel sounds, return of flatus, oral intake and first bowel movement. Four patients (8%) in the no-NG group, compared with one patient (2%) in the NG group, required subsequent decompression. Length of hospital stay was significantly (p < 0.001) shorter in the no-NG group. There were no significant differences in the presence of atelectasis, postoperative fever, wound infections and anastomotic leaks between the two groups. The authors conclude that routine nasogastric decompression is not warranted after elective surgery involving small- or large-bowel anastomosis.

Adolescent