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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin and terlipressin are increasingly used as alternative non-adrenergic vasopressors for hemodynamic support of septic patients with arterial hypotension. Despite excellent vasopressive effects, vasopressin analogues may potentially impair macro-hemodynamics, oxygen transport and microvascular blood flow. Due to those unwanted side-effects, vasopressin and terlipressin may potentially compromise organ function and possibly foster the development of multiple organ failure. This review article discusses the results of clinical and experimental studies to judge the effects of vasopressin and terlipressin on microcirculation, oxygen supply, metabolism and organ function in patients with sepsis or systemic inflammatory response syndrome (SIRS). Although vasopressin analogues are emerging as promising alternatives to treat catecholamine-refractory hypotension, there is no evidence that vasopressin receptor agonists improve outcome. To date, vasopressin and terlipressin can, therefore, not be recommended for routine clinical use.
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PMID:[Vasopressin and terlipressin in sepsis and systemic inflammatory response syndrome. Effects on microcirculation, oxygen transport, metabolism and organ function]. 1562 98

This manuscript gives a review about important studies addressing problems in intensive care medicine that have been published in journals focussing on critical care medicine and surgery in 2004. Only clinical studies are included in this review, mostly metaanalyses, randomized controlled trials and a few important or interesting observational studies. In addition to describing major results a critical appraisal of each study is undertaken, which, however, is neither comprehensive nor complete. It is merely intentioned to address some important aspects for the reader that should be accounted for while interpreting the results. It is important to note that among the large number of excellent studies there is a substantial proportion of trials with negative results that significantly add to our knowledge. Some of the topics addressed in this manuscript include vasopressin as an alternative to epinephrine during cardiopulmonary resuscitation, a specification concerning the use of activated protein C in patients with sepsis, the role of steroids in the treatment of sepsis and traumatic brain injury, the epidemiology of ALI and ARDS, the role of sedation protocols, weaning protocols and the timing of tracheostomy for the duration of mechanical ventilation, the potential benefit of catheters with antimicrobial coating to reduce catheter-related sepsis, and the benefit of enteral nutrition as compared to the parenteral application.
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PMID:[Intensive care medicine -- update 2004]. 1596 70

Sepsis causes microvascular dysfunction. Increased heterogeneity of capillary blood flow results in local tissue hypoxia, which can cause local tissue inflammation, impaired oxygen extraction, and, ultimately, organ dysfunction. Microvascular dysfunction is clinically relevant because it is a marker for mortality: it improves rapidly in survivors of sepsis but fails to improve in nonsurvivors. This, along with the fact that resuscitation of mean arterial pressure and cardiac output alone fails to improve microvascular function, means that microvascular resuscitation is therefore a therapeutic goal. In animal studies of sepsis, volume resuscitation improves microvascular permeability and tissue oxygenation, and leads to improved organ function, including a reduction in myocardial dysfunction. Microvascular resuscitation strategies include hemodynamic resuscitation using the linked combination of volume resuscitation, judicious vasopressor use, and inotropes and vasodilators. Alternative vasoactive agents, such as vasopressin, may improve microcirculatory function to a greater degree than conventional vasopressors. Successful modulation of inflammation has a positive impact on endothelial function. Finally, targeted treatment of the endothelium, using activated protein C, also improves microvascular function and ultimately increases survival. Thus, attention must be paid to the microcirculation in patients with sepsis, and therapeutic strategies should be employed to resuscitate the microcirculation in order to avoid organ dysfunction and to reduce mortality.
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PMID:Microvascular resuscitation as a therapeutic goal in severe sepsis. 1616 71

To evaluate if low plasma vasopressin and high norepinephrine concentrations predict grave prognosis of sepsis, a prospective sample of consecutive patients visiting the emergency department of a university teaching hospital who met the American College of Chest Physicians criteria of sepsis or severe sepsis was enrolled. Besides septic workup, we measured serum vasopressin and norepinephrine concentrations to correlate the impending outcome. One hundred eighty-two patients aged 27 to 99 years met the inclusive criteria and were classified as those with septic shock (n = 72), severe sepsis (n = 56), and those with sepsis only (n = 54) according to the outcome within 6 hours. Thirty healthy subjects were included as control. The plasma vasopressin level at baseline was significantly lower for those who finally developed septic shock (septic shock group, 3.6 +/- 2.5 pg/mL; 95% confidence interval [CI], 3.0-4.2 pg/mL; severe sepsis group, 21.8 +/- 4.1 pg/mL, 95% CI, 20.7-22.9 pg/mL; sepsis group, 10.6 +/- 6.5 pg/mL, 95% CI, 8.8-12.4 pg/mL, P < .001), whereas the norepinephrine level was highest for the same group (septic shock group, 3650 +/- 980 pg/mL, 95% CI, 3420-3880 pg/mL; severe sepsis group, 3600 +/- 1000 pg/mL, 95% CI, 3330-3870 pg/mL; sepsis group, 1720 +/- 320 pg/mL, 95% CI, 1630-1810 pg/mL). The vasopressin/norepinephrine ratio was significantly lower for the patients with final diagnosis of septic shock (P < .001). The mean interval between the time of samples drawn and the time of the most severe occurring sequelae was 2.4 +/- 0.8 hours. Receiver operating characteristic analysis revealed that the vasopressin/norepinephrine ratio 1 x 10(-3) had a sensitivity of 97% (95% CI, 90%-99%) and a specificity of 85% (95% CI, 78%-91%) for detecting impending septic shock. Low serum vasopressin/norepinephrine ratio can predict impending septic shock.
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PMID:Low plasma vasopressin/norepinephrine ratio predicts septic shock. 1618 77

Sepsis remains a significant problem and cause of morbidity and mortality in intensive care. Vasopressin infusions are currently used as rescue therapy for the treatment of vasodilatory, catecholamine-resistant septic shock. At present, there are no large randomised, controlled trials in the literature investigating vasopressin in this role, although two such studies are currently ongoing in Canada. This review outlines the pathophysiology of sepsis and that of vasopressin in sepsis and reviews the available evidence for the use of vasopressin in sepsis and septic shock. A review of the safety data for vasopressin in this indication is included. Recommendations for the use of vasopressin in septic shock, along with suggestions for the direction of further work in the field are presented.
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PMID:The safety and efficacy of the use of vasopressin in sepsis and septic shock. 1625 62

An estimated 700,000 cases of sepsis occur each year in the United States alone, over half of which will develop renal failure. Of those that develop renal failure, 70% will die. This article will examine how the use of vasopressin in sepsis may improve some aspects of renal function. The effects of vasopressin on the renal system in vasodilatory shock.
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PMID:The effects of vasopressin on the renal system in vasodilatory shock. 1650 61

Since the prognosis for all forms of shock essentially depends on immediate and effective therapy, early diagnosis and determination of the underlying cause are of central importance to the disease course. Except for cardiogenic shock, all forms of shock require early and adequate fluid substitution. It has previously been shown that septic shock treatment guided by central venous oxygen saturation may lead to a reduction in mortality in patients with septic shock. Similar therapeutic strategies are currently being developed for the more invasive monitoring procedures used in intensive care, but their effectiveness has to yet to be proven. Novel therapeutic approaches for the treatment of septic shock include improved adjunctive sepsis therapy and the use of vasopressin. However, the effectiveness of the latter treatment option cannot yet be conclusively assessed.
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PMID:[Targeted cardiovascular therapy: shock treatment in ambulance, emergency room and intensive care unit]. 1655 92

Septic shock is a major cause of death following trauma and a persistent problem in surgical patients. It is a challenge to the critical care medicine specialist and carries an unacceptably high mortality rate, despite adequate antibiotic and vasopressor therapy. The prevalent hypothesis regarding its mechanism is that the syndrome is caused by an excessive defensive and inflammatory response. During the acute phase some signalling mechanisms are activated, particularly hormone release, which function to restore the host homeostasis that has been disturbed by the infection. Since the neuroendocrine and immune systems are functionally related, so the exposure to antigens induces a synchronized response, which allows the organism to successfully endure immunology changes. An important characteristic of this communication includes the appearance of proteins released into the circulation by activated immune cells. These proteins, called cytokines can enter the circulation and reach neuroendocrine organs, where they act either themselves or through the release of intermediates such as prostaglandin, catecholamines and nitric oxide. The synthesis of nitric oxide may be induced in brain as a consequence of infection and may alter the function of the hypothalamic-pituitary axis. In this review we discuss the physiologic roles of the nitric oxide in central nervous system controlling the regulation of vasopressin and oxytocin during the pathophysiology of sepsis.
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PMID:Neuro-immune-endocrine mechanisms during septic shock: role for nitric oxide in vasopressin and oxytocin release. 1678 87

Vasopressin, a neurohypophyseal peptide hormone, is the endogenous agonist at V1a, V1b and V2 receptors. The most important physiological function of vasopressin is the maintenance of water homeostasis through interaction with V2 receptors in the kidney. Vasopressin and related compounds are used in various clinical settings such as acute variceal bleeding associated with portal hypertension, septic shock, diabetes insipidus and coagulation disorders. The effect in the former two indications relates to the V1a receptor, and in the two latter indications the effect relates to the V2 receptor. Vasopressin and related compounds have demonstrated activity in animal models of portal hypertension, sepsis and septic shock, diabetes insipidus and coagulation disorders. The use of the compounds in animal models is reviewed. Generally, the effect of vasopressin and related compounds in animal models reflect the activity in the clinical setting, but in some cases important species differences exist.
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PMID:The effect of vasopressin and related compounds at V1a and V2 receptors in animal models relevant to human disease. 1691 9

Vasopressin, synthesized in the hypothalamus, is released by increased plasma osmolality, decreased arterial pressure, and reductions in cardiac volume. Three subtypes of vasopressin receptors, V1, V2, and V3, have been identified, mediating vasoconstriction, water reabsorption, and central nervous system effects, respectively. Vasopressin and its analogs have been studied intensively for the treatment of states of "relative vasopressin deficiency," such as sepsis, vasodilatory shock, intraoperative hypotension, and cardiopulmonary resuscitation. Infusion of vasopressin (0.01-0.04 U/min) decreases catecholamine requirements in patients with sepsis and other types of vasodilatory shock. Bolus application of 1 mg terlipressin, the V1 agonist, reverses refractory hypotension in anesthetized patients and has been studied in patients with septic shock and chronic liver failure. During cardiopulmonary resuscitation, a 40-U bolus dose of vasopressin may be considered to replace the first or second bolus of epinephrine regardless of the initial rhythm. The side effects of vasopressin and its analogs must be further characterized.
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PMID:The vasopressin system: physiology and clinical strategies. 1741 42


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