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Biomedical subjects

R J Goris

Publications and source records attributed to R J Goris.

At least 55 records · Page 3Linked to original sources
PubMed1996

Increasing cytotoxic activity and production of reactive oxygen and nitrogen intermediates by peritoneal macrophages during the development of multiple organ dysfunction syndrome in mice.

A major problem in the intensive care unit nowadays is the development of multiple organ dysfunction syndrome (MODS), a cumulative sequence of progressive deterioration of organ functions. While the pathogenic pathways of MODS remain to be elucidated, it is assumed that cells of the host defence system, especially the macrophages, are altered in their function. During the development of MODS it is assumed that macrophages are overactivated and that an exaggerated inflammatory response may contribute to its pathogenesis. In order to gain insight into the alterations of the functional status of the macrophage during the development of MODS, a series of macrophage functions was measured in the subsequent phases of zymosan induced generalized inflammation in mice. Male C57BL/6 mice received a single dose of zymosan intraperitoneally and groups of animals were killed after 2, 5, 8, and 12 days. Peritoneal macrophages were collected for in vitro assessment of the ADCC, the production of superoxide (O2-) and nitric oxide (NO), and complement mediated phagocytosis and intracellular killing of Staphylococcus aureus. A single intraperitoneal injection with zymosan resulted in a three-phase illness. During the third phase the animals developed MODS-like symptoms. Peritoneal cells from control animals produced very low to non-detectable amounts of O2- and NO, and the cytotoxic activity was also low. During the development of MODS, from day 7 onwards, the ability to produce O2- and NO2- became strongly elevated, as did the cytotoxic activity. These findings are in parallel with the development of MODS whereas the phagocytic and killing capacity remained essentially unaltered. The changes found could be detrimental for the organism, thus possibly contributing to the onset and development of MODS.

Animals↗
PubMed1996

Inflammatory cytokines in an experimental model for the multiple organ dysfunction syndrome.

OBJECTIVE: To investigate the alterations in circulating pro-inflammatory cytokines and cytokine production by peritoneal macrophages during the development of multiple organ dysfunction syndrome. DESIGN: Prospective, controlled laboratory study on zymosan-induced generalized inflammation in mice. Single intraperitoneal administration of zymosan induces, over a 12-day period, a triphasic illness in mice; the third phase, from day 6 onward, resembles multiple organ dysfunction syndrome. SETTING: Animal research laboratory. SUBJECTS: C57BL/6CRW mice received a single intraperitoneal dose of zymosan on day 0, and standard numbers of animals were killed at different time points up until day 12. MEASUREMENTS AND MAIN RESULTS: Plasma concentrations of interleukin (IL)-1 alpha and IL-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha were measured from 3 hrs to 12 days after administration of zymosan. At the same time points, both lipopolysaccharide-stimulated and unstimulated production of these cytokines by peritoneal macrophages were measured in vitro. Plasma TNF and IL-6 concentrations transiently increased during the first 24 hrs after administration of zymosan. After 8 days, a prominent peak of biologically inactive TNF was observed. Both unstimulated and lipopolysaccharide-stimulated cytokine production by peritoneal cells showed profound changes during the experimental period. CONCLUSIONS: These findings seem to confirm our hypothesis that the macrophages are in a continuously activated state and altered in their function, when the animals develop multiple organ dysfunction syndrome. Further studies are needed to elucidate what happens with these cytokines at the tissue level, to better understand the pathophysiology of multiple organ dysfunction syndrome.

Animals↗
PubMed1996

Infection, the gut and the development of the multiple organ dysfunction syndrome.

It has been hypothesised that failure of the gut is an important pathophysiological phenomenon of the generalised inflammatory response that leads to the multiple organ dysfunction syndrome (MODS). Abnormal colonisation, infections of gut origin, bacterial translocation are all signs of gut failure that have been implicated in the pathogenesis of MODS. We have concluded after summarising published experimental and clinical studies that have tried to correlate the occurrence or prevention (by selective decontamination of the digestive tract) of these phenomena with the development of MODS, it seems that in some patients it is clear that loss of intestinal barrier function or the onset of infection precedes the development of MODS. In other patients, however, this relationship is not so clear and it seems that these phenomena may reflect a failure of the host's immune and mechanical defence systems and are epiphenoma of critical illness. The causal relation between those phenomena and the development of MODS are complex and need further clarification.

Animals↗
PubMed1996

SIRS, MODS and tertiary peritonitis.

Some patients with peritonitis develop a septic response without a detectable infective focus. It is suggested that an immunological dysfunction is responsible for this so called tertiary peritonitis. The role of the gastrointestinal tract in the development of multiple organ dysfunction syndrome (MODS) is discussed. In patients with tertiary peritonitis treatment should be directed towards restoration of the immunological balance, which is probably more important than the elimination of microorganisms with antibiotics.

Anti-Bacterial Agents↗
PubMed1996

The relationship between gut-derived bacteria and the development of the multiple organ dysfunction syndrome.

Abnormal colonisation, infections of gut origin and bacterial translocation are all signs of gut failure that have been hypothesised as being implicated in the pathogenesis of the multiple organ dysfunction syndrome (MODS). We have summarised published experimental and clinical studies that have tried to correlate the occurrence or prevention of these phenomena with the development of MODS. We conclude that in some patients loss of intestinal barrier function or the onset of infection precedes the development of MODS. In other patients, however, this relationship is not so clear and it seems that these are epiphenoma of critical illness and may reflect a failure of the host's immune and mechanical defence systems. The causal relationship between these phenomena and the development of MODS is complex and needs further clarification.

Animals↗
PubMed1995

Shoulder complaints in patients with reflex sympathetic dystrophy of the upper extremity.

Five hundred forty-one patients with reflex sympathetic dystrophy (RSD) of the upper extremity were prospectively studied. One hundred fifteen patients complained of pain and/or limited range of motion in the shoulder. Shoulder complaints more often occurred in women (p = .01); age and etiology were not different from patients with RSD without shoulder complaints. Physical examination showed a tendinitis of one or both tendons of the biceps muscle in 109 patients. Seventy one patients were treated with local injection of bupivacaine followed by methylprednisolone. This resulted in permanent relief of complaints in 34 patients, temporary or moderate relief in 31, no difference in 3, increase of complaints in 1 patient, and in 2 patients results were not documented. We conclude that shoulder complaints in RSD occur in a minority of patients and more often in female patients. There are no predisposing factors. The pathophysiologic mechanism for developing shoulder complaints remains unknown. In most cases complaints can be attributed to a bicipital tendinitis for which local injection of bupivacaine followed by prednisolone are both diagnostic and therapeutic.

Adolescent↗
PubMed1995

Inflammatory mediators in relation to the development of multiple organ failure in patients after severe blunt trauma.

OBJECTIVE: To evaluate the posttraumatic course of several inflammatory mediators or markers (complement components C3, C3a, terminal complement complex, thromboxane B2, C-reactive protein, elastase, and neopterin) in relation to the development of multiple organ failure and mortality. DESIGN: Prospective study of a selected patient group. SETTING: Surgical intensive care units in three European trauma hospitals. PATIENTS: Patients (n = 56) with severe blunt trauma (Injury Severity Score of > or = 33). INTERVENTIONS: Arterial blood samples were sequentially obtained. MEASUREMENTS AND MAIN RESULTS: Nonsurvivors (n = 8) had significantly higher circulating C3a and elastase concentrations on the first postinjury day, compared with survivors (n = 48). No differences between these groups were found for terminal complement complex, thromboxane B2, C-reactive protein, and the neopterin/creatinine ratio. Five patients died before day 5. Eighteen patients developed multiple organ failure, which was diagnosed from day 5 onward, leaving 33 patients without multiple organ failure. The patients with subsequent multiple organ failure showed significantly higher mean circulating concentrations of C3a (914 +/- 190 [SEM] ng/mL), terminal complement complex (57 +/- 17 U/mL), and thromboxane B2 (275 +/- 37 pg/mL) at the first postinjury day than the patients without multiple organ failure (566 +/- 110 ng/mL, 27 +/- 2 U/mL, and 169 +/- 14 pg/mL, respectively). In patients with multiple organ failure, elastase concentrations were significantly higher on days 2, 3, 4, and 5 postinjury. Neopterin/creatinine ratios, on the other hand, were significantly higher in patients with multiple organ failure when the multiple organ failure had already become established (on days 8 and 10). CONCLUSION: In multiple trauma patients, excessive triggering of the inflammatory cascade-as expressed by complement activation and stimulation of neutrophils producing elastase--plays an important and early role in the development of multiple organ failure.

Adolescent↗
PubMed1995

Deficiency of complement factor C5 reduces early mortality but does not prevent organ damage in an animal model of multiple organ dysfunction syndrome.

OBJECTIVE: To evaluate the role of complement factor C5 in a model of zymosan-induced multiple organ dysfunction syndrome. DESIGN: Experimental animal study. SETTING: Central animal laboratory of a university hospital. SUBJECTS: Twenty-five C5-deficient B2D10/Old and 25 C5-sufficient B2D10/New mice. INTERVENTIONS: On day 0, all mice received an intraperitoneal injection with zymosan suspended in paraffin in a dose of 1 mg/g body weight. MEASUREMENTS AND MAIN RESULTS: Between days 0 and 12, biological parameters (temperature, body weight, and clinical condition) were measured daily and mortality was monitored. Clinical condition was assessed as a symptom score by blindly grading the degree of lethargy, conjunctivitis, diarrhea, and ruffled fur of each mouse on a 2-point scale (maximum score of 4). On day 12, all surviving mice were killed and relative organ weights of lungs, liver, spleen, and kidneys were calculated. Relative organ weight was defined as (organ weight/body weight) x 100%. Zymosan administration induced a typical triphasic illness. Deterioration of the clinical condition, as indicated by the symptom score, and the decrease in temperature and body weight in the acute phase were all significantly less severe in C5-deficient mice (p < .005). In the late phase, no differences could be noticed in the courses of these biological parameters. Overall mortality was 2 (8%) of 25 in C5-deficient mice and 8 (32%) of 25 in C5-sufficient mice (p = .049), a difference that was mainly due to a difference in the acute phase. Organ damage, assessed as the relative organ weights, did not show any statistical differences for any organ between both strains. CONCLUSIONS: Complement factor C5 appears to play an important role in the acute hyperdynamic septic response in this model. However, deficiency of C5 could not prevent organ damage in the late multiple organ dysfunction syndrome phase. This finding suggests that other factors must be more important in the development of the inflammatory response leading to multiple organ dysfunction syndrome.

Aging↗
PubMed1995

Amputation for reflex sympathetic dystrophy.

We have reviewed 28 patients with reflex sympathetic dystrophy (RSD) who had 34 amputations in 31 limbs. The amputations had been performed for untenable pain (5), recurrent infection (14) or to improve residual function (15). Only two patients were relieved of pain by amputation, and this could not be predicted. Ten of 14 patients were cured of infection and 9 of 15 patients had improvement of residual function. In 28 of the amputations, RSD recurred in the stump, especially after amputation at a level which was not free from symptoms. Because of recurrence of RSD in the stump or severe hyperpathia only two patients wear a prosthesis. Despite this 24 patients were satisfied with the results.

Activities of Daily Living↗
PubMed1995

Surgery on extremities with reflex sympathetic dystrophy.

Surgery on extremities suffering from reflex sympathetic dystrophy (RSD) is generally avoided because it is presumed that RSD will recur or worsen. In order to study this problem we analyzed our patients. The affected limb of 47 patients suffering from RSD was operated on for various reasons. If possible, the operation was postponed until the signs and symptoms of RSD decreased at rest and perfusion of the affected limb was optimized; tourniquet haemostasis was avoided, and perioperative intravenous infusion of mannitol was administered. Recurrence of RSD was seen in 6 patients (13%). This recurrence was mild and temporary in 5 patients, but serious and permanent in 1 patient. Surgery on limbs suffering from RSD is not as dangerous as widely believed, but one should be aware of the risk of recurrence of RSD when surgery is being considered.

Adolescent↗
PubMed1994

Serum lipofuscin as a prognostic indicator of adult respiratory distress syndrome and multiple organ failure.

Toxic oxygen free radical damage is thought to play an important role in events such as trauma and sepsis, in which adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF) are the major causes of late death. Serum lipofuscin concentration has been proposed as an indicator of lipid peroxidation caused by toxic oxygen free radicals. Serum lipofuscin level was measured in 75 healthy controls and sequentially in 66 patients in the intensive care unit; the latter included 18 patients who had undergone elective major vascular surgery, 20 after repair of ruptured abdominal aortic aneurysm and 28 with severe blunt trauma. Fifteen of the 66 patients died within 2 days. Ten of the remaining 51 patients developed ARDS and/or MOF and 41 had an uncomplicated postoperative course. Serum lipofuscin concentration in controls showed a positive correlation with age. Compared with controls, all three patient groups had significantly increased lipofuscin concentrations during the first day after major vascular surgery, trauma or shock. In addition, the ten patients who subsequently developed ARDS and/or MOF showed significantly increased lipofuscin levels on day 1, compared with those in the 41 who had an uncomplicated clinical course. The concentration of serum lipofuscin, which may act as a simple and valuable measure of grading oxidative stress, is positively related to the incidence of subsequent ARDS and/or MOF in patients at risk of these syndromes.

Aged↗
PubMed1994

Gastric tonometry in multiple trauma patients.

Splanchnic ischemia, leading to intestinal mucosal damage, is thought to be common in patients after severe trauma. The adequacy of mucosal oxygenation can indirectly be determined by gastric intramucosal pH (pHi) measurement. We prospectively examined the posttraumatic gastric pHi values in 15 multiple trauma patients. In all patients gastric pHi was measured using a tonometer via the nasogastric route. A pHi value < or = 7.32 was used to differentiate between normal and low gastric pHi. Six hours after the injury four patients showed abnormally low pHi levels. Four other patients with normal initial pHi values exhibited low pHi values during one or more of the next measuring periods. Three of these eight patients developed major complications (two, ARDS) and two of them subsequently died. The seven remaining patients never had abnormal pHi levels and all patients had an uncomplicated recovery. Although intestinal ischemia was expected to be a common condition in multiple trauma patients, no consistent pattern of abnormal pHi measurements in the direct posttraumatic course could be discovered. No correlation was found between initial pHi values (at 6 hours) and ISS, shock, and lactic acidosis or APACHE II scores on admission. It is concluded that monitoring gastric pHi is useful in severely injured patients admitted to the ICU.

Adolescent↗
PubMed1994

Is early osteosynthesis safe in multiple trauma patients with severe thoracic trauma and pulmonary contusion?

The timing of osteosynthesis of major fractures in patients with multiple injuries is still disputed. Recently questions have been raised as to the possible detrimental effects of this treatment on pulmonary function in patients who have additional thoracic trauma. In this study the charts of 57 consecutive patients with multiple injuries including thoracic trauma were analyzed. Thirty patients without major fractures were compared with 27 patients with major fractures treated by early osteosynthesis. Despite a significantly higher Injury Severity Score (ISS) in in the group with major fractures, there was no significant difference in pulmonary function between the two groups. We conclude that the presence of thoracic trauma should not be regarded as a contraindication for early surgical stabilization of major fractures.

Adolescent↗