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PubMed1989

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↗
PubMed1995

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↗
PubMed1979

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↗
PubMed1975

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↗
PubMed1987

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↗
PubMed1975

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↗
PubMed1975

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↗
PubMed1989

[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↗
PubMed1978

Relationship between CO2 levels and decompression sickness: implications for disease prevention.

Extensive data concerning the incidence of decompression sickness among workers participating in the deepest caisson operation in Japan to date have been collected and analyzed for the period April through August, 1976. When the bottom pressure was between 3.0 and 3.2 ATA, the incidence of decompression sickness was 3.05%; subsequently, the incidence was only 0.96% between 3.2 and 3.4 ATA. The man lock (i.e., decompression chamber) had never been ventilated during the former group of decompressions and the level of CO2 had ranged between 1.8 and 2.3% (v/v); in the latter group of decompressions, the CO2 level ranged between 0.3 and 0.8% with ventilation. All other conditions, including the decompression table used, were the same. Moreover, based upon the nature of the muscular activity required of the caisson workers just prior to decompression, their most common site of affliction was found to lie within the body region where the highest tissue tensions of CO2 would be expected during decompression.

Adult↗
PubMed1982

Evaluation of different decompression schedules by an agarose gel bubble technique.

It is well known that diving decompression schedules vary according to country and that Navy schedules are often different from civilian ones. Furthermore, it is difficult to compare them effectively, because the bends incidence for each schedule is rarely known accurately. We have evaluated various decompression schedules by an agarose gel bubble technique in which the appearance of bubbles in a dry chamber at a controlled temperature was used, and we report this as a useful method of evaluating decompression tables. It is generally accepted that decompression sickness symptoms are due to bubble formation and the body's subsequent physiological reaction. Individual differences and physical conditions are also influential factors. However, bubble formation appears to be the most important factor in initiating symptoms. As the number of bubbles is influenced by the physical decompression ratio, it can be estimated which decompression schedule is more likely to minimize the number of bubbles. Nine decompression schedules were studied in this experiment: U.S. Navy Table, French Navy Table, Japanese Standard Decompression Schedule Numbers 1 and 2, Royal Naval Physiological Laboratory Table, French Ministry of Labor Table, Model 1 Table by Mano et al., Washington State Table, and Blackpool Table.

Decompression↗
PubMed1995

Cardiovascular pressures with venous gas embolism and decompression.

Venous gas embolism (VGE) is reported with decompression to a decreased ambient pressure. With severe decompression, or in cases where an intracardiac septal defect (patent foramen ovale) exists, the venous bubbles can become arterialized and cause neurological decompression illness. Incidence rates of patent foramen ovale in the general population range from 25-34% and yet aviators, astronauts, and deepsea divers who have decompression-induced venous bubbles do not demonstrate neurological symptoms at these high rates. This apparent disparity may be attributable to the normal pressure gradient across the atria of the heart that must be reversed for there to be flow patency. We evaluated the effects of: a) venous gas embolism (0.025, 0.05 and 0.15 ml.kg-1.min-1 for 180 min.); b) hyperbaric decompression; and c) hypobaric decompression on the pressure gradient across the left and right atria in anesthetized dogs with intact atrial septa. Left ventricular end-diastolic pressure was used as a measure of left atrial pressure. In a total of 92 experimental evaluations in 22 dogs, there were no reported reversals in the mean pressure gradient across the atria; a total of 3 transient reversals occurred during the peak pressure gradient changes. The reasons that decompression-induced venous bubbles do not consistently cause serious symptoms of decompression illness may be that the amount of venous gas does not always cause sufficient pressure reversal across a patent foramen ovale to cause arterialization of the venous bubbles.

Altitude↗
PubMed1990

Endoscopic transnasal orbital decompression.

Orbital decompression for dysthyroid orbitopathy has traditionally been performed through either an external or a transantral approach. The advent of intranasal endoscopes allowed for the development of a transnasal approach for medial and inferior orbital wall decompression. Using this approach, orbital decompressions were performed on 13 orbits in eight patients with severe complicated dysthyroid orbitopathy. Simultaneous bilateral lateral orbitotomies were performed on five patients. Walsh-Ogura decompressions and lateral orbitotomies were performed on two orbits. When combined with lateral orbitotomy, Hertel measurements improved an average of 5.7 mm in orbits decompressed transnasally and 4.5 mm in orbits decompressed with a Walsh-Ogura approach. Transnasal decompression alone improved Hertel measurements an average of 4.7 mm. Visual acuity improved in three of four patients with optic neuropathy, and in all patients with exposure keratopathy. We conclude that the endoscopic transnasal approach provides comparable decompression to traditional methods while avoiding the morbidity of an external ethmoidectomy or Caldwell-Luc antrotomy.

Adult↗
PubMed1993

Orbital fat removal. Decompression for Graves orbitopathy.

BACKGROUND: Orbital decompression has been used to describe surgical procedures that remove some portion of the orbital walls to reduce pressure on the orbital contents. Substantial morbidity associated with these procedures includes infraorbital anesthesia, worsened extraocular motility, globe displacement, and blindness. The authors believe that orbital contents also may be decompressed by removing orbital fat. METHODS: Eighty-one patients with nonactive Graves orbitopathy were selected for orbital fat decompression based on the presence of proptosis and associated signs and symptoms to avoid bone removal. Soft-tissue analysis by computed tomography (CT) scan showed distended pockets of fat extending into the intraconal space, which were removed through medial-upper and lateral-lower anterior orbitotomies. Decompression with bone removal was reserved for those few patients with compressive optic neuropathy unresponsive to medical treatment and those patients with residual deforming exophthalmos after fat removal. RESULTS: One hundred fifty-eight fat decompressions were performed on 81 patients over 9 years. The authors measured an average reduction in proptosis of 1.8 mm (range, 0-6.0 mm). The greatest average reduction in proptosis (3.3 mm) was produced in patients with preoperative Hertel measurements of greater than 25.0 mm. Morbidity was limited to temporary motility impairment of the inferior oblique in two patients. CONCLUSION: The concept of orbital decompression can include removal of orbital fat to reduce proptosis, eliminate symptoms, and improve appearance with far less morbidity than when bone decompression is used as the primary decompressive procedure.

Adipose Tissue↗
PubMed1993

A comparison of active compression-decompression cardiopulmonary resuscitation with standard cardiopulmonary resuscitation for cardiac arrests occurring in the hospital.

BACKGROUND: Recent studies have demonstrated improved cardiopulmonary circulation during cardiac arrest with the use of a hand-held suction device (Ambu CardioPump) to perform active compression-decompression cardiopulmonary resuscitation (CPR). The purpose of this study was to compare active compression-decompression with standard CPR during cardiac arrests in hospitalized patients. METHODS: All patients over the age of 18 years who had a witnessed cardiac arrest while hospitalized at our center were enrolled in this trial; they were randomly assigned according to their medical-record numbers to receive either active compression-decompression or standard CPR. The study end points were the rates of initial resuscitation, survival at 24 hours, hospital discharge, and neurologic outcome. Compressions were performed according to the recommendations of the American Heart Association (80 to 100 compressions per minute; depth of compression, 3.8 to 5.1 cm [1.5 to 2 in.]; and 50 percent of the cycle spent in compression). RESULTS: Sixty-two patients (45 men and 17 women) with a mean age (+/- SE) of 68 +/- 2 years were entered into the trial. Sixty-two percent of the patients who underwent active compression-decompression were initially resuscitated, as compared with 30 percent of the patients who received standard CPR (P < 0.03); 45 percent of the patients who underwent active compression-decompression survived for at least 24 hours, as compared with 9 percent of patients who underwent standard CPR (P < 0.004). Two of the 62 study patients survived to hospital discharge; both were randomly assigned to receive active compression-decompression. Neurologic outcome, as measured by the Glasgow coma score, was better with active compression-decompression (8.0 +/- 1.3) than with standard CPR (3.5 +/- 0.3; P < 0.02). CONCLUSIONS: In this preliminary study, we found that, as compared with standard CPR, active compression-decompression CPR improved the rate of initial resuscitation, survival at 24 hours, and neurologic outcome after in-hospital cardiac arrest. Larger trials will be required to assess the potential benefit in terms of long-term survival.

Aged↗
PubMed1995

A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy.

OBJECTIVE: A meta-analysis of all published clinical trials comparing selective versus routine nasogastric decompression was performed in an attempt to evaluate the need for nasogastric decompression after elective laparotomy. BACKGROUND: Many studies have suggested that routine nasogastric decompression is unnecessary after elective laparotomy and may be associated with an increased incidence of complications. Despite these reports, many surgeons continue to practice routine nasogastric decompression, believing that its use significantly decreases the risk of postoperative nausea, vomiting, aspiration, wound dehiscence, and anastomotic leak. METHODS: A comprehensive search of the English language medical literature was performed to identify all published clinical trials evaluating nasogastric decompression. Twenty-six trials (3964 patients) met inclusion criteria. The outcome data extracted from each trial were subsequently "pooled" and analyzed for significant differences using the Mantel-Haenszel estimation of combined relative risk. RESULTS: Fever, atelectasis, and pneumonia were significantly less common and days to first oral intake were significantly fewer in patients managed without nasogastric tubes. Meta-analysis based on study quality revealed significantly fewer pulmonary complications, but significantly greater abdominal distension and vomiting in patients managed without nasogastric tubes. Routine nasogastric decompression did not decrease the incidence of any other complication. CONCLUSIONS: Although patients may develop abdominal distension or vomiting without a nasogastric tube, this is not associated with an increase in complications or length of stay. For every patient requiring insertion of a nasogastric tube in the postoperative period, at least 20 patients will not require nasogastric decompression. Routine nasogastric decompression is not supported by meta-analysis of the literature.

Elective Surgical Procedures↗
PubMed1993

Effects of decompressive craniectomy on regional cerebral blood flow in severe head trauma patients.

The effect of decompressive craniectomy on regional cerebral blood flow (rCBF) was investigated in five patients with severe head trauma who underwent decompressive craniectomy. Repeated rCBF studies using single photon emission computed tomography with 99mtechnetium-hexamethylpropyleneamine oxime observed that a hyperperfusion area (focal CBF increase) occurred in the decompressed brain within 24 hours after decompressive craniectomy. The hyperperfusion area in the decompressed brain enlarged and increased in severity by 1 week after surgery. However, it attenuated and disappeared by 1 month after surgery. The chronology of the hyperperfusion area corresponded to the change in the swelling of decompressed brain observed by x-ray computed tomography. Patient consciousness showed a significant and progressive improvement in the postoperative 1 month period. Decompressive craniectomy may cause a focal CBF increase in the decompressed brain related to the beneficial effect in patients with acute severe head trauma.

Adolescent↗
PubMed1993

The effect of surgical decompression on neurologic outcome after lumbar fractures.

From 1980 until 1989, 69 patients with lumbar fractures resulting in incomplete paraparesis were admitted to the authors' medical center for treatment. Thirty had anterior vertebrectomy, including 18 who had posterior instrumentation and four who had anterior instrumentation. Twenty-two patients were treated with a posterolateral decompression and fusion, including four who also required an anterior decompression. Nineteen of the remaining 21 patients required posterior spine instrumentation and fusion only. The American Spinal Injury Association (ASIA) motor index score was determined for each patient pre- and postoperatively and used to compare these three treatment groups. Average follow-up period for the patients was 19 months. The improvement in ASIA motor score for all patients treated with decompression averaged 10 and similar improvement was obtained in those who were treated with posterior decompression (10.2 points). The average improvement in those who had vertebrectomy was 9.9 points. For those who had fusion without decompression, average improvement was 4.2 points. Comparing those patients who were surgically decompressed, either anteriorly or posteriorly, with those patients who only underwent fusion, the difference in neurologic improvement was statistically significant. Neurologic outcome after lumbar fractures is improved by surgical decompression. The neurologic outcome results were similar after anterior and posterior decompression.

Follow-Up Studies↗
PubMed1991

Decompression comparison of N2 and O2 in rats.

We have previously reported that O2 in the breathing gas mixture contributed significantly to the risk of decompression sickness (DCS) in rats after rapid (less than 10 s) decompression to the surface from depth. The rate of O2 uptake was extremely fast (less than 1 min estimated for equilibrium after a pressure change) compared to much slower rates for He and N2. To further define the role that O2 plays in diving, the present investigation examined decompression outcome in unanesthetized male albino rats after 60-min N2-O2 dives (1-3 atm abs O2, depth 6.26 or 7.26 atm abs). Slower decompression profiles were used to determine the elimination rates of N2 and O2 as pressure was reduced and included "stops" of up to 20 min. The probability of DCS was modeled using the maximum likelihood technique. O2 again contributed significantly to the risk of DCS, although O2 was eliminated very rapidly during decompression; the washout of N2 was considerably longer. These findings support the view that O2 can add significantly to decompression risk. However, this phenomenon may not normally be encountered during human diving operations where relatively slower decompression and lower PO2's are used.

Animals↗