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J A Sturm

Publications and source records attributed to J A Sturm.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Can post-traumatic renal failure be modified therapeutically?].

Acute renal failure in the late phase after severe trauma is particularly dangerous, since it is resistant to therapy and contributes to the development of post-traumatic multiple organ failure. We have studied different treatment regimes in order to establish whether late renal failure can be prevented (study A: colloidal and crystalloid solutions; study B greater than: crystalloid solutions and dopamine; continuous infusion 3 micrograms/kg body weight). Renal function was assessed by means of the score by Goris as well as by creatinine clearance over a period of 14 days. Haemodynamics and cardiac function were determined on a daily basis. The demographic parameters were comparable in both groups. In group A 37 of 61 patients died (60.6%), and in group B 17 of 38 patients (44.7%) (P less than 0.05). The incidence of impairment of renal function was comparable; in group A there was significantly more severe damage (18%) compared to group B (2.6%). This coincided with significantly higher mortality in group A (group A: 60.65%; group B: 44.7%). In group A a lesser volume was given during the preclinical and clinical course, even after correcting for the volume-saving effect of colloidal solutions. In addition, cardiac index was higher in group B (day 9: 5.9 +/- 0.61 l/min) than in group A (day 9: 4.4 +/- 0.5 l/min) and pulmonary capillary wedge pressure (PCWP) was lower and systemic vascular resistance (SVR) higher over the whole period. Also, the arterio-venous oxygen difference (AvDO2) was higher following day 9 in patients in group A, but creatinine clearance was better in group B patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1992

Phagocytic cell function in recurrent endotoxemia in sheep.

Sepsis syndrome in severely traumatized patients is supposedly due to a blockade of the phagocytic cell system--for example, the reticulo endothelial system (RES) and polymorph nuclear leukocytes (PMNL), which cause insufficient elimination of bacterial substances (e.g., endotoxin). In contrast we found in a previous study using a model of acute endotoxemia that RES clearance is enhanced, while PMNL function gave evidence for decompensation. In order to clarify whether or not our results were just a matter of single dose endotoxemia, we have investigated RES and PMNL function in a sheep model with recurrent endotoxemia. A sheep receiving endotoxin at a dose of 1 microgram/kg body weight every 12 hours was monitored over a 5-day period. RES clearance was calculated by the half-life of Tc99 phytate each day. The PMNL function was determined by measuring chemiluminescence (CL) of isolated PMNL and total blood. The half-life of Tc99 phytate decreased from 56 min to 44 min with endotoxin (P less than or equal to 0.01) the second day and further to 42 min (P less than or equal to 0.002) on the third day. Values then returned to baseline until the end of study. Zymosan induced and luminol enhanced CL response indicated an acute cellular exhaustion after the first endotoxin dose. Under subsequent endotoxin administration, a daily attenuation of the acute response was noted in combination with baseline opsonin capacity. Our results give evidence that also in recurrent endotoxemia RES function is characterized by a sufficient clearance, whereas the PMNL function remains decreased and therefore possibly is responsible for the well-known clinical post-traumatic septic complications.

Animals↗
PubMed1991

[Does lung contusion and general injury severity have an effect on the lung following intramedullary femoral nailing? An animal model].

We evaluated changes in lung function after closed intramedullary femoral nailing (IMN) in sheep. The effects of isolated IMN were compared with those of nailing after lung contusion and hemorrhagic shock. In adult female merino sheep a chronic lung lymph fistula was prepared according to the method described by Staub. At day 1, group 1 received right-sided lung contusion and hemorrhagic shock to a mean blood pressure of 50 mmHg for 2 h. Group 2 was the control group. At day 3 both groups were submitted to IMN, followed by a 2-h observation period. IMN caused a transient significant increase in pulmonary artery pressure and central venous triglycerides in both groups. Chemiluminescence of isolated polymorphonuclear leukocytes (PMNL) decreased in group 1 from 2.699 +/- 0.344 to 2.460 +/- 0.187 x 10(6) cpm/25000 PMNL and increased in group 2 from 2.757 +/- 0.127 to 3.824 +/- 0.439 x 10(6) cpm/25000 PMNL. Lymph flow in group 1 increased 1.5-fold while microvascular pressure decreased. In group 2 lymph flow increased less, while MVP increased. The filtration coefficient in group 1 was 5 times (7.533 +/- 0.044) that in the control group (1.45 +/- 0.133). Calculations of permeability indicated a 2-fold increase (0.044 group 1 vs 0.026 group 2). In the presence of previous lung contusion and hemorrhagic shock there is definite lung damage from IMN. This is probably mediated by stimulation of PMNL.

Animals↗
PubMed1991

[Multiple organ failure. Reflection of generalized cell damage of all organs following severe trauma].

Multiple organ failure (MOF) is presently recognized as the most severe, and often lethal, complication after multiple trauma. Causal factors and pathomechanisms remain unclear, however. Generalized inflammatory cell tissue injury with a subsequent increase in permeability in all organs has been suggested. For this reason, 38 polytraumatized patients were examined in a prospective study. Organ function was analyzed, and specific clinical and histological studies were performed to check for generalized cell tissue damage and increased respiratory permeability. In all organs we found signs of tissue damage immediately after trauma. Disturbances of organ function were seen consistently, starting precisely from day 4. It was not possible to confirm an influence of blunt organ trauma on organ function during follow-up. The severity of injury (especially intrathoracic and intraabdominal) and massive bleeding increases the risk of MOF. MOF was not always associated with the onset of sepsis, and no temporal dependence could be shown. Histological studies demonstrated an inflammatory change in organ tissues, which is probably the result of toxic substances (endotoxin, TNF, oxygen radicals, proteases and eicanosoids) released into the blood circulation after trauma. Insufficient neutralization of these toxic metabolites leads to generalized permeability damage and consequently to progressive organ failure. Therefore, even with optimized initial treatment of multiple trauma patients, MOV and mortality can only be reduced with a causal approach to therapy.

Adolescent↗
PubMed1991

[Heart contusion as an unusual cause of shock in severe polytrauma].

The reported incidence of myocardial contusion after blunt chest trauma is 7-17%. Only one third of these patients present with significant morbidity. The polytrauma is generally dominated by hypovolemic and traumatic shock. Other causes of hypotension are less common, and may thus be ignored. The standard algorithm of care in multiple trauma care, however, leads to the diagnosis even in these cases, as illustrated by a case of prolonged shock induced by blunt myocardial trauma.

Adult↗
PubMed1991

[Liver failure as part of multiple organ failure following polytrauma].

In the last few years there has been increasing evidence that adult respiratory distress syndrome is only part of a much more complex syndrome called multiorgan failure (MOF). Since renal and lung failure have become rare because of our increased understanding of the pathomechanisms involved and the treatment changes, liver dysfunction has been noted more often. In a clinical trial with 38 patients with severe trauma, we investigated liver function using ordinary parameters like the transaminases, bilirubin, etc. To define one group with MOF and one without we used the Goris MOF Score. In both groups glutamate dehydrogenase (GLDH) was increased initially up to 14 U/l, indicating hypoxia of the liver cells right after trauma. From day 6 on, a second increase up to 12 U/l of GLDH in the MOF group was evidence of liver cell dysfunction. The glutamine oxalacetic transaminase (GOT) level remained normal in both groups after an initial increase of up to 60 U/l in both groups. As 30% of serum GOT is released by muscle cells, the initial peak values could be due to direct muscle trauma, because an initial increase was noted even in the creatinine kinase. A decrease in clotting factor V down to 30% on day 8 in the MOF group indicated that the metabolic synthesis activity of the liver was lower. Bilirubin increased in the MOF group from day 5 on up to 240 mumol/l on the day 14. As this increase was not parallel to the gamma glutamyl transferase (Gamma BT) level, the reason for the bilirubin increase may be dysfunction of the liver cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Bronchoscopy in severe blunt chest trauma.

Extended lesions of the lung parenchyma are often seen in association with blunt chest trauma. Blood aspiration, atelectasis and the formation of bronchopleural fistulae can lead to early respiratory deterioration and the development of severe post-traumatic complications (pneumonia, acute respiratory distress syndrome). Diagnostic and therapeutic bronchoscopy is essential on admission. This procedure helps to estimate the severity and extent of parenchymal lesions even before chest X-ray signs are noted. Bronchoalveolar lavage is needed for removal of aspirates. In our study bronchoalveolar lavage on admission reduced bacterial contamination and pneumonia in comparison to patients not lavaged. A new method for closure of bronchopleural fistulae is described. Fibrin instillation after balloon catheter occlusion leads to a significant reduction of tidal volume loss (greater than 50% in average).

Adult↗
PubMed1990

Complement activation and the prognostic value of C3a in patients at risk of adult respiratory distress syndrome.

In vivo and in vitro studies have shown that complement activation plays an important role in the pathogenesis of the adult respiratory distress syndrome (ARDS). In a prospective study of polytrauma patients at risk of ARDS (n = 38) complement parameters were determined over a period of 14 days in serial plasma samples (obtained every 6 h during the first 48 h). Polytrauma induced a rapid and remarkable complement activation. Low levels of the complement proteins C3, C4, C1 inhibitor (C1 INH) factor I and factor H during the first 48 h indicated complement consumption in all patients. Elevated C3a levels in the first few hours after injury were associated with the later development of ARDS. A more sensitive indicator than C3a alone was the calculated C3a:C3 ratio discriminating ARDS and non-ARDS patients. A second rise of C3a levels and C3a:C3 ratio from day 4 on paralleled the course of extravascular lung water. To assess the mode of complement activation, the activation-specific protein complexes C1rC1s-C1 INH and C3b(Bb)P were measured in some of the patients. We demonstrate that in the first 48 h complement activation occurred via the alternative pathway only and was later followed by an additional activation via the classical pathway. Our observations suggest that monitoring of C3a and C3 in plasma can identify polytrauma patients at high risk for ARDS at an early stage of the disease.

Adolescent↗
PubMed1990

Alveolar cell pattern and chemiluminescence response of blood neutrophils and alveolar macrophages in sheep after endotoxin injection.

In order to study the pathomechanisms of the Adult Respiratory Distress Syndrome in an acute animal model, we monitored the alveolar cell pattern and the stimulatory chemiluminescence responses of blood neutrophils and alveolar macrophages in sheep after Escherichia coli endotoxin injection (2 micrograms/kg of body weight). Using appropriate bronchoalveolar lavage techniques, thereby avoiding local inflammation, it was demonstrated that endotoxin injection did not cause any recruitment of neutrophils into the alveoli for a period of up to 24 hours. Following endotoxin injection, blood neutrophils showed a maximal stimulatory response after 5 minutes, and alveolar macrophages after 4 hours. It is concluded that if neutrophils are responsible for initiating the increase in microvascular permeability, then this action must be purely intravascular.

Anesthesia↗
PubMed1990

[Fluid balance and postoperative lung function].

Postoperative volume therapy: 1. Replacement of fluid loss. 2. Therapy of intravasal hypovolaemia in case of permeability damage or intracellular fluid shift. Monitoring: 1. Circulation (HR, CVP, art. pressure). 2. Homeostasis (Na, K). 3. Metabolic changes (BE, pH). 4. Kidney function. In complications like sepsis or ARDS with pulmonary problems and increase of pulmonary vascular resistance the use of a pulmonary artery catheter is necessary. Differential treatment has to be based on additional measurement of cardiac output and pulmonary capillary pressure. Volume treatment in postoperative complications is essential because of intravasal hypovolaemia. Kidney and cardiac failure have to be ruled out.

Acid-Base Equilibrium↗
PubMed1989

[Humoral and cellular changes of non-specific immune response following severe trauma].

The influence of trauma and hemorrhagic shock on the non-specific immune system has been pointed out in various experimental studies. Other investigations have also been able to find a relationship between these changes and a higher incidence of post-traumatic complications in the form of organ failure. Our aim was to demonstrate the potential changes in the cellular defense system in a clinical study on multiple trauma patients. The polymorphonuclear leukocytes (PMNL) are the main representative of the mobile, non-specific immune system. Our study revealed a significant deterioration of PMNL function after trauma. The metabolic activity and phagocytic function were mainly affected by a decrease in the concentration of so-called "opsonins." The opsonins are important for the identification and engulfment of debris (necrosis, fat emboli and thrombi) and bacterial substances (endotoxin). Next to the opsonin level, a change in the receptor configuration is important for phagocytosis. However, we could not find any substantial evidence of surface receptor alteration. The reticuloendothelial cells (RES), a stationary phagocytic system, also showed a significant reduction in clearance function in these polytraumatized patients. Similar to PMNL, these disturbances were based on the reduction of the opsonine concentration. We were able to demonstrate a significant disturbance in immune function in multiple trauma patients with post-traumatic complications compared to patients with a normal clinical course after injury. Disturbances in the PMNL function (seen after 4 days) were found to appear after the RES disturbances. Systemic interaction between these two phagocytic systems cannot be excluded and further investigation is therefore required.

Adolescent↗
PubMed1988

[Significance of lung contusion in mortality following polytrauma. Possibilities for therapeutic influence].

Multiple trauma is often associated with blunt thoracic injuries. Especially lung contusion can result in respiratory insufficiency and therefore a higher mortality rate. In our prospective study comparing 8 multiple trauma patients with and without associated lung contusion, we found that respiratory function was already significantly disturbed (decrease of paO2/FiO2 and increase of AaDO2, a rise in extravascular lung water (EVLW) both early after trauma and also with a second peak following the 4th day. This group (LK) developed significantly more cases of respiratory distress (ARDS). The disturbance of respiratory function seen initially was interpreted as a consequence of the direct mechanical impact, leading to the formation of interstitial fluid and hematoma. The frequent development of ARDS in the LK-group probably results from a pronounced activation of cellular and humoral mechanisms and therefore an enforced injury of the pulmonary capillary bed. A significant increase of pulmonary infections or the development of sepsis was not seen in the LK-group and is probably not responsible for the higher ARDS-rate in this group.

Adolescent↗
PubMed1987

[Prognostic significance of early management as exemplified by the accident patient].

Progress in the therapeutic management of multiple trauma patients has led to a decline in mortality (now 20%). The main cause for death is still the multiple organ failure (MOF), which is initiated in an early phase after trauma by shock and tissue damage, and manifests in a late phase during posttraumatic sepsis. Humoral and cellular changes accelerate the capillary damage, which provokes the failure of the organ systems. For this reason all therapeutic efforts should aim to minimize these influences. Next to infusion and ventilation therapy, early definite reduction of bleeding and tissue damage (debridement) and early osteosynthesis in multiple trauma patients seems reasonable.

Combined Modality Therapy↗