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Biomedical subjects

R J Goris

Publications and source records attributed to R J Goris.

At least 127 records · Page 7Linked to original sources

Are toxic oxygen radicals involved in the pathogenesis of reflex sympathetic dystrophy?

A crossover study was performed for patients with RSD to evaluate the therapeutic efficacy of the hydroxyl radical scavenger DMSO. All patients were given DMSO locally 5 times a day during one week, and a placebo during one week. Before and after each treatment, subjective evaluation was performed by both the patient and the examinor as to clinical activity of RSD, and measurement was performed of the range of motion (ROM) of all joints in the affected extremity. DMSO was the most effective treatment as to improvement of ROM (p = 0.035) and as to overall improvement (p = 0.001). The efficacy of the hydroxyl radical scavenger DMSO indicates that RSD primarily involves an inflammatory process rather than a sympathetic reflex. As during the last 20 years no single report was published studying RSD in terms of inflammation, it is suggested that such studies are urgently needed to elucidate the real nature of RSD.

Adult↗

Emergency management of lower urinary tract injuries.

Trauma to the bladder and (or) urethra mostly occurs in multiple trauma patients and their emergency management often poses problems to both the general surgeon and the urologist. Fourteen cases of bladder rupture and 16 cases of urethral laceration were retrospectively studied, with regard to etiology, trauma mechanism, diagnosis and therapeutic possibilities. Immediate diagnosis and surgical repair are important to reduce mortality and morbidity in cases of bladder rupture. The emergency treatment of urethral injuries is more controversial. The different factors influencing the therapeutic approach are discussed and rational guidelines are suggested to decrease the high complication rate of these injuries.

Adolescent↗

Whole body inflammation in trauma patients; an autopsy study.

The autopsy reports of 35 trauma patients were reviewed. We found signs of generalized inflammation and tissue damage with increases in organ weights. Organs not primarily injured by trauma were also affected. These abnormalities were found in patients who died within 24 hours after trauma, as well as in patients who died of mere brain injury. The most pronounced signs of inflammation and increases in organ weights were found especially when the "Adult Respiratory Distress Syndrome" (ARDS), hypovolemic shock or "Multiple Organ Failure" (MOF) were the causes of death. Our findings are similar to those found in the lungs of humans suffering from ARDS and in several organs of rabbits after 4 hours of complement activation in combination with 20 minutes of hypoxia. Therefore, the autopsy findings in this series of trauma patients might represent the morphologic features of ARDS and MOF in an early-even preclinical-stage. We interpret these syndromes as the clinical expression of an uncontrolled inflammatory response to trauma, mediated by massive activation of the complement system.

Adolescent↗

Multiple-organ failure and sepsis without bacteria. An experimental model.

Multiple-organ failure is generally attributed to bacterial infection, although a correlation with positive blood cultures is not consistently found. Consequently, we studied the effects of a local nonbacterial inflammatory stimulus on distant organ functions and metabolism. Wistar rats were inoculated intraperitoneally with zymosan. Heart and ventilatory rates, oxygen consumption, and body temperature were measured. Survivors were killed at day 12 for blood analysis, weighing of organs, and microscopy. Intraperitoneal zymosan resulted in an early hyperdynamic "septic" response with a 35% mortality. After a few days, oxygen consumption decreased, serum lactate levels increased, and the function of multiple organs deteriorated, while blood cultures remained sterile. The experiment was repeated in germ-free rats with similar results but a lower mortality. We concluded that a severe inflammatory response in itself is capable of inducing multiple-organ failure with "sepsis."

Animals↗

Spinal cord injury following surgery for acute traumatic rupture of the thoracic aorta.

From 1970 to 1985, 49 patients were operated for traumatic aortic rupture (TAR) in 2 university hospitals. Protection of distal ischemia was performed 31 times with a left heart bypass (LHB), 5 times with a heparin coated shunt and, 13 times using simple aortic cross-clamping combined with pharmacological vasodilatation. Total mortality was 17 out of 49, 5 during and 12 after the operation, 2 of them being directly related to systemic heparinization during LHB. In the LHB and shunt groups there was one postoperative paraplegia out of 35 patients, while 4 from the 13 patients operated without a shunt developed paraplegia. If risk factors such as long cross-clamping time, hypotension, extensive laceration of the inner curvature of the aorta, or cross-clamping of the aortic arch at a high level are anticipated, LHB or the shunt technique must be considered to avoid paraplegia. A repair without a shunting procedure should be limited to those cases in which the individual surgeon believes that he can do the operation within 30 minutes aortic cross-clamping time.

Adult↗

Acute generalized microvascular injury by activated complement and hypoxia: the basis of the adult respiratory distress syndrome and multiple organ failure?

It has been suggested that generalized endothelial damage and permeability changes, induced by prolonged activation of the complement system and ensuing release of lysosomal enzymes, prostaglandins and toxic oxygen products, underlie the genesis of the Adult Respiratory Distress Syndrome (ARDS) and Multiple Organ Failure (MOF). The effects in New Zealand white rabbits were investigated of a 4 h infusion of activated complement and its combination with a short hypoxic episode on respiratory function, leukocyte count, platelet count and morphology of the lungs, heart, liver, kidney and spleen. Prolonged activation of the complement system induced hyperventilation with respiratory alkalosis and hypocapnia, depletion of granulocytes (PMN), and a variable accumulation PMN in the capillaries of all organs examined, in combination with interstitial, and, in the liver, cellular oedema. Electron microscopy of the lungs revealed degranulation of PMN, endothelial swelling and widening of the alveolar septa. The combination of hypoxia and systemic complement activation appeared to aggravate this microvascular injury with the occurrence of protein rich alveolar oedema and haemorrhage in the lungs and accumulation of PMN debris containing macrophages in the spleen. The alterations in respiratory function and pulmonary morphology in these rabbits, imitate the clinical and morphological characteristics of the early phase of ARDS. The inflammatory reaction, found in all other organs examined, might represent the early phase of MOF. If so, ARDS and MOF -- clinically closely interconnected syndromes -- might be interpreted as manifestations of the same syndrome and as the clinical expression of an uncontrolled whole body inflammation.

Animals↗

Acute acalculous cholecystitis.

Retrospective study of acute acalculous cholecystitis from 1973 to 1983. Twenty-one cases were found, while in this period 1211 cholecystectomies were performed (incidence 1.7%). Only nine patients developed acute acalculous cholecystitis in conjunction with a life-threatening situation, while in 12 others no acute illness was present predisposing to this type of cholecystitis. In all cases cultured, positive bile cultures were found. As necrosis of the gallbladder wall was present in a high percentage of cases, cholecystectomy is advised when possible. The pathogenesis, prevention and diagnosis of acute acalculous cholecystitis are discussed.

Acute Disease↗

Multiple-organ failure. Generalized autodestructive inflammation?

As multiple-organ failure (MOF) has been generally associated with sepsis, the importance of bacterial sepsis was evaluated retrospectively in 55 trauma and 37 intra-abdominal-sepsis patients with MOF. The severity of MOF was graded, and an analysis was made of day of onset, incidence, severity, sequence, and mortality of organ failures. No difference was found between groups in sequence, severity, or mortality of organ failures. In contrast, bacterial sepsis was found in 65% of intra-abdominal-sepsis patients but only in 33% of trauma patients. It is concluded that sepsis is probably not the essential cause of MOF. Instead, an alternative hypothesis is presented involving massive activation of inflammatory mediators by severe tissue trauma or intra-abdominal sepsis, resulting in systemic damage to vascular endothelia, permeability edema, and impaired oxygen availability to the mitochondria despite adequate arterial oxygen transport.

Adolescent↗

Pathophysiology of the adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF)--a hypothesis.

A review of the recent literature concerning the Adult Respiratory Distress Syndrome (ARDS) and Multiple Organ Failure (MOF) is presented. We hypothesize that the two syndromes probably have a common pathophysiology, with ARDS as the first occurring organ failure. The clinical situations that may cause ARDS and MOF are characterized by massive and prolonged activation of the complement system. This results in activation of granulocytes with ensuing release of lysosomal enzymes, toxic oxygen products and prostaglandins, which collectively cause endothelial damage and permeability changes. In the lungs interstitial and alveolar edema develops, with an impaired alveolo-capillary gas exchange. Oxygen diffusion in the peripheral tissues is impeded by the same mechanism, ultimately resulting in organ failure. Hypoxia may cause additional microvascular lesions, as toxic oxygen radicals are produced during reoxygenation. The implications of this hypothesis for the prevention and therapy of ARDS and MOF are discussed.

Complement Activation↗