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Orbital decompression for Graves' disease. Exposure through lateral canthal and inferior fornix incision.

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.

Adult

Nitrogen partial pressures in man after decompression from simulated scuba dives at rest and during exercise.

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.

Adult

Endoscopic decompression for acute colonic pseudo-obstruction.

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.

Acute Disease

Current trends in orbital decompression.

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.

Combined Modality Therapy

Decompression of the spinal cord improves recovery after acute experimental spinal cord compression injury.

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.

Animals

Effects of various degrees of compression and active decompression on haemodynamics, end-tidal CO2, and ventilation during cardiopulmonary resuscitation of pigs.

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.

Animals

Cardiopulmonary changes with moderate decompression in rats.

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.

Animals

Nitrogen partial pressures in man after decompression from simulated scuba dives.

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.

Arteries

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

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

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

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