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Biomedical subjects

K Reinhart

Publications and source records attributed to K Reinhart.

At least 37 records · Page 2Linked to original sources
PubMed2002

[Diagnostic approach to sepsis - state of the art].

Early diagnosis of the different severities of septic inflammation is important for early implementation of specific therapies. Sepsis and severe sepsis are accompanied by clinical and laboratory signs of systemic inflammation. However, patients suffering from non-infectious inflammation may present with similiar signs and symptoms making it difficult to diagnose infection based on clinical findings alone. Bacteriological evidence of sepsis, though definitive and specific, may not be obtainable, is time-consuming and even may not occur concurrently with clinical signs of sepsis. It is therefore important to identify markers, which, by enabling an early diagnosis of sepsis and organ dysfunction, would allow early specific therapeutic interventions. Wheras C-reactive Protein is a more sensitive parameter for the diagnosis of non-systemic infections, Procalcitonin seems to be a useful parameter to improve the diagnosis and monitoring of therapy in patients with severe sepsis and septic shock.

Biomarkers↗
PubMed2002

[New treatment approaches in sepsis].

The treatment of sepsis consists of focus control as well as supportive and adjuvant therapy. Especially the last option has been investigated during the last years. Different approaches showed promising results in animal experiments and phase-I trials but did not prove to be successful in large multicenter studies. The application of TNF-receptors or interleukin-1 receptor antagonists did not lead to an improvement of outcome in patients with sepsis. Most studies with TNF-antibodies also presented negative results. However, a recent large study with a monoclonal antibody against TNFalpha demonstrated a significant survival benefit. The recently published PROWESS study is the first investigation demonstrating the decrease of mortality in patients with sepsis after administration of protein C. Additionally, current data support the low-dose hydrocortisone therapy in patients with vasopressor dependent septic shock.

Animals↗
PubMed2002

[Sepsis].

Explore the source record for details and available documents.

Humans↗
PubMed2001

[Quality management in postoperative pain therapy].

BACKGROUND: Deficits in quality of postoperative pain management are not caused by the complexity of the medical problem or shortage of suitable drugs but by difficulties in organization and hospital structures. Moreover, there is no consensus on how to measure the quality of pain management. Quality management programs consist of strategies to overcome such difficulties and to increase quality continuously. This study reports the implementation of a quality management program to improve postoperative pain management at a university hospital. METHODS: An interdisciplinary task force consisting of nursing staff, anesthesiologists, surgeons, and members of the hospital pharmacy was set up. This task force interviewed patients and performed an analysis of current deficits (phase 1). Then, primary and secondary outcome parameters were defined to measure quality of pain management, and strategies were defined to implement improvements (phase 2). These referred to aspects of organization, standardization, and responsibility. One of the main intentions was the involvement of nursing staff. After implementation (phase 3), a second analysis was performed (phase 4). This was followed by a continuous assessment of parameters indicating quality of procedures and results which were fed back to all participants (phase 5). RESULTS: After implementation of the program (phase 4), significantly more patients reported no or mild (NRS < 4) postoperative pain (40.2% vs 30.1%) compared to phase 1. Also, patients' satisfaction with pain therapy improved significantly. The proportion of patients without pain treatment decreased by one-third. Opioids were given more frequently and more often intravenously. In contrast, the proportion of i.m. injections decreased from 20% to 5%. Continuous assessment of up to now more than 4,900 patients helped to identify possible reasons for problems and to maintain overall quality of pain management. DISCUSSION: Tools of quality management consisting of deficit analysis, definition of outcome parameters, implementation of improving strategies, post-intervention analysis and continuous feed-back may be successfully used to improve postoperative pain therapy. Changes in organization of medical management seem to be more important than medical or technical aspects. Similar strategies might be used to increase quality of other medical procedures.

Analgesics, Opioid↗
PubMed2001

Variability of splanchnic blood flow in patients with sepsis.

OBJECTIVES: Previous studies on therapeutic interventions in sepsis have assumed stability of the measure of splanchnic blood flow throughout the study. We assessed the variability of splanchnic blood flow during stable global hemodynamics in eight patients with sepsis requiring treatment with dobutamine and/or norepinephrine. DESIGN AND SETTING: Prospective clinical study in an intensive care unit of a university hospital. MEASUREMENTS AND RESULTS: Global and regional hemodynamics were measured at baseline, 2 h later, and 4 h later. Cardiac output was measured by transpulmonary thermodilution, intrathoracic blood volume as an indicator of cardiac preload, and total blood volume by the double indicator (thermo-dye) dilution technique. Total body oxygen consumption was assessed by indirect calorimetry using a metabolic cart. Splanchnic blood flow was measured by the continuous indocyanine green method, and gastric mucosal CO2 tension by gas tonometry. Neither absolute nor fractional splanchnic blood flow (as ratio of cardiac output) revealed significant global tendencies during the study period. However, variance component analysis showed that splanchnic blood flow determinations varied considerably within patients, for repeated measurements at 5-min intervals (standard error 31.1%) as well as for average values at 2-h intervals (25.6%). CONCLUSION: Stable global hemodynamics during a 4-h period in septic patients does not exclude marked changes in splanchnic blood measured by a hepatic venous catheter technique.

Adult↗
PubMed2001

Dysfunction of vasomotor reactivity in severe sepsis and septic shock.

OBJECTIVE: Perfusion abnormalities are an overall phenomenon in severe sepsis and septic shock, leading to organ dysfunction. We investigated whether carbon dioxide (CO2)-induced vasomotor reactivity (VMR) is impaired in septic patients, compared with values obtained outside sepsis. DESIGN: Prospective, clinical study. SETTING: Six-bed neurologic critical care unit of a university hospital. PATIENTS AND PARTICIPANTS: Eight consecutive patients with severe sepsis and septic shock. MEASUREMENTS AND RESULTS: CO2-reactivity was measured during and outside a period of severe sepsis or septic shock according to ACCP/SCCM criteria by means of transcranial Doppler sonography and near-infrared spectroscopy (NIRS). VMR was calculated as the percentage change of cerebral blood flow velocity (normalized CO2-reactivity, NCR) and absolute changes in concentration of oxygenated hemoglobin, deoxygenated hemoglobin, total hemoglobin (HbO2, Hb, HbT) and Hbdiff (difference between HbO2 and Hb) in micromol/l per 1% increase in end-tidal CO2 (CR-HbO2, CR-Hb, CR-HbT, CR-Hbdiff). NCR and NIRS-reactivities were significantly reduced during severe sepsis and septic shock compared with values outside sepsis (mean, SD, Wilcoxon): NCR 11.0 (7.1) versus 30.7 (13.0), p < 0.02; CR-HbO2 0.70 (0.61) versus 2.33 (1.11), p < 0.02; CR-Hb -0.17 (0.74) versus -1.42 (1.28), p < 0.04; CR-HbT 0.53 (0.48) versus 1.05 (0.40), p < 0.03; CR-Hbdiff 0.91 (1.33) versus 3.75 (2.33), p < 0.02. This indicates a severely disturbed VMR. CONCLUSIONS: In the advent of a disturbed cerebral autoregulation, critical drops in blood pressure during sepsis are transferred directly into the vascular bed, leading to cerebral hypoperfusion. This mechanism might contribute to the pathogenesis of septic encephalopathy.

Aged↗
PubMed2001

Immunomorphological sequelae of severe brain injury induced by fluid-percussion in juvenile pigs--effects of mild hypothermia.

Severe traumatic brain injury (TBI) often leads to a bad outcome with considerable neurological deficits. Secondary brain injuries due to a rise of intracranial pressure (ICP) and global hypoxia-ischemia are critical and may be reduced in extent by mild hypothermia. A porcine animal model was used to study the effect of severe TBI, induced by fluid percussion (FP; 3.5+/-0.3 atm) in combination with a secondary insult, i.e., temporary blood loss with hypovolemic hypotension. Six-week-old juvenile pigs were subjected to this kind of severe TBI; one group was then submitted to moderate hypothermia at 32 degrees C for 6 h, starting 1 h after brain injury. Animals were killed after 24 h. TBI and hypothermia-associated alterations in the brains were investigated by immunohistochemistry with antibodies against microtubule-associated protein 2 (MAP-2) and beta-amyloid precursor protein (betaAPP). In addition, DNA fragmentation was investigated by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) method. Seven of the 13 normothermic TBI animals developed a secondary increase in ICP (TBI-NT-ICP) after an interval of several hours. None of the animals in the hypothermic trauma (TBI-HT) group exhibited a secondary ICP increase, indicating a protective effect of the treatment. TBI-HT animals showed significantly higher levels of MAP-2 immunoreactivity, lower levels of betaAPP immunoreactivity and less DNA fragmentation than the TBI-NT-ICP animals. Differences between the TBI-HT group and normothermic animals without an ICP increase (TBI-NT) were less marked. A considerable decrease in MAP-2 outside the site of TBI-FP administration was seen only in the TBI-NT-ICP animals. MAP-2 immunohistochemistry was thus a reliable marker of diffuse brain damage. Axonal injury was present in all TBI groups, indicating its special significance in neurotrauma. Thus, severe TBI caused by FP, combined with temporary blood loss, consistently produced traumatic axonal injury and focal brain damage. Mild hypothermia was able to prevent a secondary increase in ICP and its sequelae of diffuse hypoxic-ischemic brain injury. However, hypothermia did not afford protection from traumatic axonal injury.

Age Factors↗
PubMed2001

The plasma elimination rate and urinary secretion of procalcitonin in patients with normal and impaired renal function.

BACKGROUND AND OBJECTIVE: The amount of procalcitonin eliminated in the urine and the plasma disappearance rate of procalcitonin were evaluated in patients with normal and impaired renal function, because patients with sepsis are a main target group for procalcitonin measurement, and these patients often develop renal dysfunction. METHODS: Elimination of procalcitonin in the urine (microgram 12 h-1) was measured in 76 patients. In another 67 patients, the 50% plasma disappearance rate (t1/2, h) was evaluated 48 h after peak concentrations (procalcitonin > 2 micrograms L-1). Renal function was assessed by creatinine clearance. RESULTS: Procalcitonin elimination in the urine was significantly reduced in patients with severe renal dysfunction. However, the plasma disappearance rate correlated only weakly with renal dysfunction (Spearman's rank correlation R = -0.36, P = 0.004, regression t1/2 = 49.87-0.15 creatinine clearance). The 25% quartile and median were 25.2 h and 30.0 h in patients with normal renal function, and 36.3 h and 44.7 h in patients with severely impaired renal function (creatinine clearance < 30 mL min-1). CONCLUSIONS: Renal elimination of procalcitonin is not a major mechanism for procalcitonin removal from the plasma. Although the plasma disappearance rate may be prolonged up to 30-50% in some patients with renal dysfunction, clinical diagnostic decisions may not be severely influenced by this moderate prolongation of procalcitonin elimination. We conclude that procalcitonin can be used diagnostically in patients with renal failure as well as in those with normal renal function.

Area Under Curve↗
PubMed2001

A new endotoxin adsorber: first clinical application.

In an open, uncontrolled pilot study, 5 men and 1 woman with suspected gram-negative sepsis were treated with a new whole-blood endotoxin adsorption system. Lipopolysaccharide (LPS) adsorption was carried out by hemoperfusion over high-affinity polymethacrylate-bound albumin (Fresenius Endotoxin Adsorber EN 500). All patients suffered from endotoxemia (>20 pg/ml LAL) and met at least two systemic inflammatory response syndrome (SIRS) criteria. Four patients suffered from pneumonia due to mechanical ventilation, one from peritonitis, and one from pneumonia and peritonitis. Endotoxin adsorption was very well tolerated, and efficient LPS removal was shown in all patients. Apache II score immediately before immunoadsorption was 23.5 and was 22.3 after the last treatment. All 6 critically ill patients improved substantially and were discharged from the intensive care unit. LPS whole blood immunoadsorption is a promising new method. No side effects have been observed thus far. A large controlled study to prove clinical efficacy in patients with severe sepsis is under way.

APACHE↗
PubMed2001

Does the optimization of cardiac output by fluid loading increase splanchnic blood flow?

We studied the effects of increasing cardiac output by fluid loading on splanchnic blood flow in patients with haemodynamically stabilized septic shock. Eight patients (five female, 39-86 yr) were assessed using a transpulmonary thermo-dye-dilution technique for the measurement of cardiac index (CI) intrathoracic blood volume (ITBV) as a marker of cardiac preload and total blood volume (TBV). Splanchnic blood flow was measured by the steady state indocyanine-green technique using a hepatic venous catheter. Gastric mucosal blood flow was estimated by regional carbon dioxide tension (PRCO2). Hydroxyethyl starch was infused to increase cardiac output while mean arterial pressure was kept constant. In parallel, mean norepinephrine dosage could be reduced from 0.59 to 0.33 microg kg(-1) min(-1). Mean (SD) TBV index increased from 2549 (365) to 3125 (447) ml m(-2), as did ITBV index from 888 (167) to 1075 (266) ml m(-2) and CI from 3.6 (1.0) to 4.6 (1.0) litre min(-1) m(-2). Despite marked individual differences, splanchnic blood flow did not change significantly neither absolutely (from 1.09 (0.96) to 1.19 (0.91) litre min(-1) m(-2)) nor fractionally as part of CI (from 28.4 (19.5) to 24.9 (16.3)%). Gastric mucosal PRCO2 increased from 7.7 (2.6) to 8.3 (3.1) kPa. The PCO2-gap, the difference between regional and end-tidal PCO2, increased slightly from 3.2 (2.7) to 3.4 (3.1) kPa. Thus, an increase in cardiac output as a result of fluid loading is not necessarily associated with an increase in splanchnic blood flow in patients with stabilized septic shock.

Adult↗
PubMed2001

Randomized, placebo-controlled trial of the anti-tumor necrosis factor antibody fragment afelimomab in hyperinflammatory response during severe sepsis: The RAMSES Study.

OBJECTIVE: This study investigated whether treatment with the anti-tumor necrosis factor-alpha monoclonal antibody afelimomab would improve survival in septic patients with serum interleukin (IL)-6 concentrations of >1000 pg/mL. DESIGN: Multicenter, double-blind, randomized, placebo-controlled study. SETTING: Eighty-four intensive care units in academic medical centers in Europe and Israel. PATIENTS: A total of 944 septic patients were screened and stratified by the results of a rapid qualitative immunostrip test for serum IL-6 concentrations. Patients with a positive test kit result indicating IL-6 concentrations of >1000 pg/mL were randomized to receive either afelimomab (n = 224) or placebo (n = 222). Patients with a negative IL-6 test (n = 498) were not randomized and were followed up for 28 days. INTERVENTIONS: Treatment consisted of 15-min infusions of 1 mg/kg afelimomab or matching placebo every 8 hrs for 3 days. Standard surgical and intensive care therapy was otherwise delivered. MEASUREMENTS AND MAIN RESULTS: The study was terminated prematurely after an interim analysis estimated that the primary efficacy end points would not be met. The 28-day mortality rate in the nonrandomized patients (39.6%, 197 of 498) was significantly lower (p <.001) than that found in the randomized patients (55.8%, 249 of 446). The mortality rates in the IL-6 test kit positive patients randomized to afelimomab and placebo were similar, 54.0% (121 of 224) vs. 57.7% (128 of 222), respectively. Treatment with afelimomab was not associated with any particular adverse events. CONCLUSIONS: The IL-6 immunostrip test identified two distinct sepsis populations with significantly different mortality rates. A small (3.7%) absolute reduction in mortality rate was found in the afelimomab-treated patients. The treatment difference did not reach statistical significance.

APACHE↗
PubMed2001

Anti-tumor necrosis factor therapy in sepsis: update on clinical trials and lessons learned.

OBJECTIVE: Tumor necrosis factor (TNF) is an important mediator involved in the pathogenesis of sepsis. We review clinical studies investigating the efficacy of anti-TNF therapy in decreasing mortality rates in septic patients. DATA SOURCES: We conducted a computerized bibliographic search of randomized, clinical, multicenter trials studying the effects of anti-TNF therapy in the treatment of sepsis. We included all primary studies, reviewed all published meta-analyses, and contacted primary investigators of multicenter trials where necessary. DATA SYNTHESIS: Almost all randomized studies targeting TNF during sepsis show a small, albeit nonsignificant, benefit in decreasing mortality. Strategies using monoclonal antibodies are more effective than are strategies using TNF receptor proteins. Analysis of randomized multicenter trials shows a small but significant benefit with anti-TNF therapeutic strategies. Furthermore, a recent study in 2634 septic patients using a murine anti-TNF antibody shows a 3.6% significant benefit in reducing mortality. CONCLUSIONS: Anti-TNF strategies are only partially effective in patients with sepsis. Although individual studies show small, nonsignificant benefits, analysis of all trial data as well as data from a recent trial in a large population of septic patients show that anti-TNF strategies may confer a small survival benefit. Better characterization of patients and a more multimodal approach by concomitantly targeting other mediators involved in sepsis may be helpful in enlarging the clinical benefit of anti-TNF therapy.

Antibodies, Monoclonal↗
PubMed2001

Tissue factor pathway inhibitor activity in severe sepsis.

OBJECTIVE: To review the preclinical and clinical evidence that provides the therapeutic rationale for recombinant human tissue factor pathway inhibitor (rTFPI) as a novel treatment for human sepsis. DATA SOURCES: A summary of published English-language literature regarding preclinical studies and limited information published about three phase II clinical studies for the evaluation of rTFPI safety in sepsis patients. DATA SUMMARY: Tissue factor pathway inhibitor, the physiologic inhibitor of the tissue factor pathway, interrupts activation of coagulation at multiple steps, including tissue factor VIIa activity, Xa activity, prothrombinase complex, and thrombin generation. Recombinant human TFPI exhibits anticoagulant and anti-inflammatory activities in animal models and humans with sepsis. These activities appear to have an important therapeutic role in protecting the microvasculature from injury and preventing multiple organ failure in sepsis. CONCLUSIONS: Tissue factor pathway inhibitor is a potent inhibitor of clotting in the microvasculature, which is thought to protect organs from injury. Recombinant TFPI improved survival of septic animals in multiple models. Recent phase II results suggest that rTFPI is well tolerated, and they show a trend toward reduction in 28-day all-cause mortality in rTFPI-treated patients; in addition, rTFPI demonstrated significant reduction in thrombin generation. These results suggest that a powered study is indicated to further evaluate rTFPI utility for the adjunctive management of severe sepsis.

Animals↗
PubMed2001

Assessment of the safety of recombinant tissue factor pathway inhibitor in patients with severe sepsis: a multicenter, randomized, placebo-controlled, single-blind, dose escalation study.

OBJECTIVE: To identify a safe and potentially effective recombinant tissue factor pathway inhibitor (rTFPI) dose for further clinical evaluation in patients with severe sepsis. DESIGN: Prospective, randomized, single-blind, placebo-controlled, dose escalation, multicenter, multinational phase II clinical trial. SETTING: Thirty-eight intensive care units in the United States and Europe. PATIENTS: Two hundred and ten subjects with severe sepsis who received standard supportive care and antimicrobial therapy. INTERVENTIONS: Subjects received a continuous intravenous infusion of placebo or rTFPI at 0.025 or 0.05 mg/kg/hr for 4 days (96 hrs). MEASUREMENTS AND MAIN RESULTS: There were no significant imbalances in demographics, severity of illness, or source of infection in patients randomized to placebo or either dose of rTFPI. A 20% relative reduction in 28-day all-cause mortality was observed when all rTFPI-treated patients were compared with all placebo patients. An improvement in pulmonary organ dysfunction score and in a composite intensive care unit score (pulmonary, cardiovascular, and coagulation) were also noted in the rTFPI-treated patients. Logistic regression modeling indicated a substantial treatment by baseline laboratory international normalized ratio (INR) interaction effect when only treatment and INR were in the model (p =.037) and when baseline Acute Physiology and Chronic Health Evaluation (APACHE II) and log10 interleukin 6 were adjusted for (p =.026). This interaction effect indicates that higher baseline INR is associated with a more pronounced beneficial rTFPI effect. There was no increase in mortality in subjects treated with either dose of rTFPI compared with placebo. Biological activity, as detected by a statistically significant reduction in thrombin-antithrombin complexes (TATc), was noted in the all rTFPI-treated patients compared with those receiving placebo. There were no major imbalances across all treatment groups with respect to safety. The frequency of adverse events (AEs) and severe adverse events (SAEs) was similar among the treatment groups, with a slight increase in SAEs and SAEs involving bleeding in the 0.05 mg/kg/hr rTFPI group. The overall incidence of AEs involving bleeding was 28% of patients in the all placebo group and 23% of patients in the all rTFPI-treated group; a slight but statistically insignificant increase in incidence of SAEs involving bleeding was observed in the all rTFPI group (9%) as compared with the all placebo group (6%; p =.39). CONCLUSIONS: Although the trial was not powered to show efficacy, a trend toward reduction in 28-day all-cause mortality was observed in the all rTFPI group compared with all placebo. This study demonstrates that rTFPI doses of 0.025 and 0.05 mg/kg/hr could be safely administered to severe sepsis patients. Additionally, rTFPI demonstrated bioactivity, as shown by reduction in TATc complexes and interleukin-6 levels. These findings warrant further evaluation of rTFPI in an adequately powered, placebo controlled, randomized trial for the treatment of severe sepsis.

APACHE↗
PubMed2001

Plasma concentrations and clearance of procalcitonin during continuous veno-venous hemofiltration in septic patients.

We determined the elimination characteristics of procalcitonin (PCT) during continuous veno-venous hemofiltration (CVVHF) and the resulting effect on PCT plasma levels. A prospective study was conducted in patients with sepsis and acute oliguric renal failure, treated with CVVHF using a polysulfone membrane (Baxter Renaflo II PSHF 1200). Patients had sepsis and PCT plasma levels > 4 ng ml(-1) (n = 26). PCT was measured in the pre- and post-filter plasma and the ultrafiltrate at 0, 5, 10, and 15 min and 1, 2, 4, 6, 12, and 24 h after setup of CVVHF. PCT sieving coefficient was 0.24. Elimination of PCT, however, depended on the duration of filtration, because filter adsorption was the main mechanism of PCT clearance during the first hour of hemofiltration, finally increasing to a clearance of PCT into the ultrafiltrate of 2.8-5.5 mL/min after 2 h. PCT plasma levels were not significantly altered during CVVHF (96% of the initial concentration after 24 h, P = 0.72). Similar to what has been observed with cytokines and other proteins of a comparable molecular weight, PCT is removed from the plasma during CVVHF, but plasma PCT levels are unchanged. Thus, PCT can be used as a diagnostic parameter even in patients with acute renal failure undergoing CVVHF.

Aged↗
PubMed2001

Procalcitonin and CGRP-1 mrna expression in various human tissues.

Procalcitonin (PCT) is a highly sensitive and specific marker of systemic bacterial infection and sepsis. In contrast to its diagnostic significance, the cellular sources of plasma procalcitonin remain to be clarified. Two forms of PCT mRNAs originate from calcitonin/calcitonin gene-related peptide gene (CALC-I gene) along with mRNA for calcitonin gene-related peptide-I (CGRP-I). Reverse transcription polymerase chain reaction with newly designed primers detecting different PCT mRNAs and CGRP-I mRNA was used to identify tissues that might contribute to PCT production. Our study indicates that a variety of human tissues (13 of the 16 analyzed overall) express PCT-I, PCT-II, and/or CGRP-I mRNAs, with the highest levels detected for liver, testis, lung, prostate, kidney, and small intestine. Various tissues differ in the proportions of PCT-I, PCT-II, and CGRP-I mRNA expression levels. Thus we demonstrate the complexity of tissue-specific regulation of CALC-I gene expression and suppose a variety of tissues as a potential source of CALC-I-encoded peptides.

Calcitonin↗
PubMed2001

Therapeutic options for the treatment of impaired gut function.

Tissue hypoxia, especially in the splanchnic area, is still considered to be an important cofactor in the pathogenesis of multiple organ failure. Therefore, the specific effects of the various therapeutic interventions on splanchnic perfusion and oxygenation are of particular interest. Restoring and maintaining oxygen transport and tissue oxygenation is the most important step in the supportive treatment of patients with sepsis and impaired gut perfusion. Therefore, supportive treatment should be focused on an adequate volume resuscitation and appropriate use of vasoactive drugs. Adequate volume loading may be the most important step in the treatment of patients with septic shock. An elevated oxygen delivery may be beneficial in some patients, but the increase of oxygen delivery should be guided by the measurement of parameters assessing global and regional oxygenation. Forcing an elevation in oxygen delivery by the use of very high dosages of catecholamines can be harmful. Vasopressors should be used for achieving an adequate perfusion pressure. For norepinephrine, no negative effects on gut perfusion have been demonstrated. Epinephrine and dopamine should be avoided because they seem to redistribute blood flow away from the splanchnic region. There are no convincing data yet to support the routine use of low-dose dopamine or dopexamine to improve an impaired gut perfusion. There is even evidence that low-dose dopamine may reduce the mucosal perfusion in the gut in some patients. It has been suggested that dopexamine can improve splanchnic perfusion, but because these effects remain somewhat controversial, a general recommendation for dopexamine to improve gut perfusion is not justified.

Bacterial Infections↗