Septic shock and multiple organ failure: treatment with haemofiltration?
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Animals↗
Biomedical subjects
W H Hartl
Publications and source records attributed to W H Hartl.
Pericardial mass mimicking constrictive pericarditis.
Persistent pericardial hematoma due to blunt chest trauma is extremely rare. We report a case of constricted myocardium resulting from a large, partially organized hematoma in the right cardiophrenic angle. The hematoma was assumed to be caused by an occupational accident 17 years before diagnosis. Constriction could only be controlled by complete removal of the fibrous posterior capsule of the hematoma, which covered the epicardium of the right heart.
Aged↗
[Improved survival rate of postoperative renal failure caused by high volume hemofiltration].
Continuous arteriovenous hemofiltration is the treatment of choice for postoperative acute renal failure (ARF). The clinical value of two different treatment modalities (spontaneous vs. pump-driven hemofiltration PDHF) were compared in two groups of patients with postoperative ARF. There were no differences in both groups regarding age, duration of treatment, severity of illness or cause of renal failure. The survival rate of patients treated with PDHF was significantly higher (29.4 vs. 12.5%). PDHF also led to a significantly larger daily ultrafiltrate volume (15.6 +/- 1.9 vs. 7.0 +/- 0.4 l/d, p less than 0.05). The accelerated elimination of toxic mediators through the filtration membrane in high-volume filtration using a pump system (PDHF) may have been responsible for the improved survival rate.
Acute Kidney Injury↗
Relevance of cerebral vasomotor reactivity to prospects for successful endarterectomy.
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Aged↗
Role of prostaglandins in protein turnover in tumor-bearing rats.
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Animals↗
Whole body and plasma protein synthesis in exercise and recovery in human subjects.
The effect of 4 h of exercise at 40% of maximal oxygen consumption (VO2 max) on protein metabolism was assessed in normal volunteers maintained on a diet containing 42 kcal.kg-1.day-1 and either 0.9 or 2.5 g protein.kg-1.day-1. Primed constant infusions of [1,2-13C]-leucine and [15N]glycine enabled the quantitation of whole body protein turnover and also the fractional synthetic rates (FSR) of albumin, fibrinogen, and fibronectin. In subjects who did not exercise, the fractional synthetic rates (%/day) on normal and high-protein intakes, respectively, were as follows: albumin, 10 +/- 1 and 9 +/- 1; fibrinogen, 21 +/- 3 and 18 +/- 1; and fibronectin, 31 +/- 3 and 34 +/- 3. Neither exercise nor recovery had an effect of whole body protein turnover or on albumin FSR, but the FSR of fibronectin was significantly elevated at the end of exercise, and fibrinogen was significantly elevated in recovery. Dietary protein intake had no major effect on the response to exercise. Thus, in response to exercise, there is a stimulation of the synthesis of some acute phase proteins, which may be a mechanism whereby nitrogen resulting from muscle protein breakdown is spared.
Amino Acids↗
Bradykinin attenuates glucagon-induced leucine oxidation in humans.
Trauma and injury are associated with accelerated protein loss. Counterregulatory hormones are possible mediators of this response. In the present study, the effect of glucagon and glucagon plus bradykinin on leucine and urea kinetics was examined in nine normal volunteers during somatostatin infusion and basal insulin replacement. Bradykinin was given because of its prostaglandin-stimulating qualities and the potential anabolic action of prostaglandins. Physiological hyperglucagonemia elicited a small but significant reduction of total leucine flux and rate of urea synthesis. Simultaneously, leucine oxidation increased by 70%. The simultaneous infusion of bradykinin did not alter glucagon-related changes in urea or leucine kinetics. Bradykinin, however, significantly attenuated the stimulation of leucine oxidation by glucagon. These results suggest that glucagon and tissue factors are involved in controlling leucine metabolism in humans.
Adult↗
Effect of exercise and recovery on muscle protein synthesis in human subjects.
Previous studies using indirect means to assess the response of protein metabolism to exercise have led to conflicting conclusions. Therefore, in this study we have measured the rate of muscle protein synthesis in normal volunteers at rest, at the end of 4 h of aerobic exercise (40% maximal O2 consumption), and after 4 h of recovery by determining directly the rate of incorporation of 1,2-[13C]leucine into muscle. The rate of muscle protein breakdown was assessed by 3-methylhistidine (3-MH) excretion, and total urinary nitrogen excretion was also measured. There was an insignificant increase in 3-MH excretion in exercise of 37% and a significant increase (P less than 0.05) of 85% during 4 h of recovery from exercise (0.079 +/- 0.008 vs. 0.147 +/- 0.0338 mumol.kg-1.min-1 for rest and recovery from exercise, respectively). Nonetheless, there was no effect of exercise on total nitrogen excretion. Muscle fractional synthetic rate was not different in the exercise vs. the control group at the end of exercise (0.0417 +/- 0.004 vs. 0.0477 +/- 0.010%/h for exercise vs. control), but there was a significant increase in fractional synthetic rate in the exercise group during the recovery period (0.0821 +/- 0.006 vs. 0.0654 +/- 0.012%/h for exercise vs. control, P less than 0.05). Thus we conclude that although aerobic exercise may stimulate muscle protein breakdown, this does not result in a significant depletion of muscle mass because muscle protein synthesis is stimulated in recovery.
Adult↗
[Pyruvate metabolism using stable isotopes].
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Animals↗
Effects of kinins on glucose metabolism in vivo.
Current concepts of the physiological importance of the kinin/prostaglandin system view these tissue factors as part of a defense system, which protects tissues from potentially noxious factors, such as hypoxia or destructive inflammatory reactions. This kinin-triggered defense reaction includes an improvement in cellular energy metabolism. The latter is brought about in peripheral tissues by an increased availability of glucose for anaerobic and aerobic glycolysis, whereas in liver tissue, energy-consuming reactions such as gluconeogenesis are attenuated. There is evidence that such favorable effects can also be produced in man when kinins are administered systemically. Prostaglandins are most likely the second messengers of kinin-induced metabolic effects. Thus, it may be advantageous to increase the availability of kinins either by exogenous infusion or by inhibiting endogenous degradation during postoperative stress or in diseases such as diabetes mellitus, in which glucose metabolism is severely disturbed.
Blood Glucose↗
Kinin/prostaglandin system: its therapeutic value in surgical stress.
Multiple system organ failure as a consequence of injury or sepsis remains the major reason for death in critically ill patients. One of the treatment concepts that has recently attracted clinical attention is the administration of kinins and prostaglandins (PGs). On the basis of experimental data, there is reason to believe that these compounds may have the potential to manipulate favorably certain processes and mechanisms (such as inflammatory or ischemic reactions) thought to be important in the pathophysiology of surgical stress. However, thus far, information on those effects in humans is still scarce. On the other hand, administration of kinins and PGs is technically possible and can be performed safely, even in intensive care patients. Therefore, different techniques, effects, and side-effects of kinin/PG therapy deserve clinical testing. It remains to be seen whether this concept will be useful in the treatment of critically ill surgical patients.
Animals↗
Protein and amino acid metabolism after injury.
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Alanine↗
Glucagon and hepatic glucose production: modulation by low-dose bradykinin infusion.
The effect of a low-dose bradykinin (BK) infusion (30 ng/kg min) on glucagon-induced hepatic glucose production and glucose cycling was studied in five normal volunteers. Studies were performed during constant insulin concentration as achieved by simultaneous somatostatin infusion and insulin replacement. In the basal period glucagon was infused at a rate of 0.5 ng/kg min. Then, glucagon infusion rate was increased to 3 ng/kg min to test the response to hyperglucagonemia. In a second set of experiments BK was infused concomitantly with the high dose glucagon. Each subject served as his own control. BK infusion did not prevent the glucagon-induced rise in hepatic glucose production and glucose cycling. However, at a later stage BK accelerated the negative feedback mechanisms activated by glucagon (decrease in hepatic glucose production) significantly. These findings suggest that intravenous BK may interact with mechanisms involved in the down-regulation of hepatic glucagon effects.
Adult↗
Ticarcillin/clavulanate in the treatment of severe peritonitis.
A prospective study was performed on 50 consecutive patients with secondary peritonitis. All patients received ticarcillin/clavulanate 5.2 g three times daily as initial antibiotic therapy. In 30 patients a primary perforation was found in the gastro-intestinal tract and 20 had post-operative peritonitis. In two thirds of the patients a diffuse peritonitis was found which affected the whole abdomen. Thirty-six patients underwent one or two laparotomies and 11 patients had more than three laparotomies. Subsequently, 17 patients died. The cause of death was a therapeutic failure as a result of the surgical procedure in ten patients (nine patients with persisting intestinal fistulae, one patient with bleeding), whereas in seven cases antibiotic therapy failed. Micro-organisms found in the latter patients were producers of type 1 beta-lactamase (Pseudomonas aeruginosa, Enterobacter sp., Citrobacter sp., Serratia marcescens) and enterococci. Ticarcillin/clavulanate is characterized by its broad antimicrobial spectrum against anaerobic and aerobic bacteria and seems, therefore, to be well suited for initial chemotherapy in patients with diffuse peritonitis.
Adult↗
Low-dose bradykinin infusion reduces endogenous glucose production in surgical patients.
The systemic effect of low-dose bradykinin infusion on total body glucose production and arterial substrate concentrations was examined during D5W infusion (1.0 mg/kg/min) in five normal-weight postsurgical subjects and compared to the response in four saline infused control patients, well matched for age, weight, and degree of postoperative stress. The primed-constant infusion of 6,6-d2-glucose was used to determine the rate of endogenous glucose production. After a basal period of 90 minutes, subjects in the study group were infused with bradykinin at increasing rates of 2.0 and 4.0 micrograms/kg/h, each infusion rate lasting for 90 minutes, whereas in controls corresponding amounts of saline were given. After 75 minutes of bradykinin, endogenous glucose production was significantly reduced as compared to basal values (1.63 +/- 0.21 mg/kg/min, P less than .0125 v 2.20 +/- 0.35 basal). This was accompanied by a significant reduction in arterial concentrations of glucose, lactate, pyruvate, and alanine. Corresponding concentrations of insulin, glucagon, glycerol, free fatty acids, and ketone bodies, as well as mean arterial blood pressure and heart rate was not affected by bradykinin. In the control group no significant changes in substrate and hormone concentrations, or the rate of glucose production were observed. The higher bradykinin infusion rate did not further affect substrate metabolism or systemic hemodynamics. These results demonstrate the inhibitory effect of low-dose bradykinin on glucose production in surgically stressed patients. The stimulation of hepatic prostaglandin synthesis by bradykinin may explain the results since prostaglandins are known to exert an inhibitory effect on hormone stimulated gluconeogenesis and glycogenolysis in liver tissue.
Adult↗
Minor role of ketone bodies in energy metabolism by skeletal muscle tissue during the postoperative course.
To evaluate changes of peripheral ketone body (KB) metabolism after operation, muscle metabolism in postsurgical patients was studied at 3 hours (SI) and 24 hours (SII) after surgery by the forearm catheter technique. Data were compared to those of equivalent fasted controls (CI, CII). In a manner consistent with enhanced mobilization of endogenous substrate stores, arterial concentrations of free fatty acids (FFA), 3-hydroxybutyrate (3-HOB), and acetoacetate (AcAc) were markedly elevated immediately after surgery. This increase was accompanied by a rise in muscular utilization of AcAc (SI: 0.21 +/- 0.05 mumol/100 g/min; CI: 0.08 +/- 0.05, p less than 0.05) and 3-HOB (SI: 0.24 +/- 0.06 mumol/100 g/min; CI: 0.11 +/- 0.01, p less than 0.05). Surprisingly, on the first postoperative day, concentrations of AcAc and 3-HOB fell below those of fasting controls. Concomitantly, the utilization rate of AcAc by muscle (SII: 0.07 +/- 0.03 mumol/100 g/min; CII: 0.27 +/- 0.04, p less than 0.05) was significantly lower in patients than in controls. Reduction of the fractional extraction rate of AcAc (SI: 38.4 +/- 3.8%; SII: 24.0 +/- 6.1%, p less than 0.05), as well as a net production of 3-HOB by muscle (SII: -0.08 +/- 0.05 mumol/100 g/min; CII: 0.49 +/- 0.13, p less than 0.05) 24 hours after surgery indicated a reduced peripheral capacity for KB removal. Since this finding was related to a significantly higher rate of muscular glycerol production (SII: -0.13 +/- 0.03 mumol/100 g/min; CII: -0.06 +/- 0.02, p less than 0.05), one may suggest that increased intramuscular availability of FFA from triglyceride hydrolysis was responsible for the impairment of peripheral KB utilization. These results indicate that KBs contribute little to energy metabolism in skeletal muscle tissue in the late postoperative phase.
3-Hydroxybutyric Acid↗
Gunshot and blast injuries to the extremities. Management of soft tissue wounds by a modified technique of delayed wound closure.
Thirty-three soft tissue wounds to the extremities from high-energy missiles were treated in 26 patients by using a modified technique of delayed wound closure. The modifications included planned re-examination and, if indicated, re-debridement of the wound every 48 hours after the initial treatment, and temporary wound coverage with synthetic skin substitutes. With this approach we observed only one wound infection postoperatively. This finding demonstrates that these modifications may be helpful in the management of this type of injury, that is otherwise associated with a high complication rate, including wound infection.
Adolescent↗
Reactive hyperemia in patients with septic conditions.
In a prospective study microvascular reactivity was examined in 12 patients with septic conditions by means of the provocation of reactive hyperemia (RH) for evaluation of microcirculatory function. Data were compared with data from 10 nonseptic, postsurgical patients. At the time of the initial measurement, an adequate hyperemic response could be produced in all patients. In the further course of the disease, in nine of the 12 patients severe multiple organ failure developed. In spite of sufficient values for arterial blood pressure, oxygenation, and the clotting system, RH was absent in these patients (8 +/- 2 days after the initial measurement). Subsequently, seven of these nine patients died (4 +/- 2 days after the onset of microvascular nonreactivity). Until death, RH was absent in each patient, and at this time therapy-resistant hypoxemia, hypotension, and severe disturbances of the clotting system were present. In the two surviving patients RH was restored completely. These results indicate that (1) the septic state per se is not necessarily combined with impaired microvascular reactivity (rather, the absence of RH may be a sign of generally poor clinical conditions); (2) the absence of RH is not related to therapy-resistant hypotension, hypoxia, and severe clotting disorders but precedes these changes; and (3) provocation of RH may be of clinical use for early detection of microcirculatory malfunction in high-risk patients.
Age Factors↗