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

Both undetected and clinically evident venous thrombosis and venous thromboembolism (VTE) can seriously impact the prognosis of acutely and/or critically ill patients. Pulmonary embolism (PE) is harder to diagnose in the acutely and/or critically ill, many of whom also have developed respiratory failure for other reasons. Deep vein thrombosis (DVT) of the upper and lower extremities can subsequently complicate insertion of central venous catheters, leading to PE, sepsis and septic shock. Recovery from the original critical illness (e.g. weaning from mechanical ventilation) can be adversely affected by these complications. There are recent data suggesting that, for prophylaxis, low-molecular-weight heparin (LMWH) is more effective than unfractionated heparin (UFH) in critically ill trauma patients, and that high-dose LMWH is more effective than placebo or low-dose LMWH in seriously ill medical patients. In both populations, LMWH appeared safe. While LMWH appears superior to UFH in acute stroke patients to prevent venographically-proven lower-extremity DVT, whether it provides a superior long-term outcome after acute stroke is uncertain. One study found that a high dosage of the LMWH dalteparin was more effective than placebo in preventing left ventricular thrombi after acute myocardial infarction, but there was a significant safety cost. Current questions surrounding prophylaxis of VTE and the use of LMWH in acutely and/or critically ill patients include whether monitoring levels and dosage adjustment in some of these patients would improve outcome, and whether the diagnosis of VTE can be improved so that treatment can be instituted when prophylaxis has failed.
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PMID:Risk assessment and prophylaxis of venous thromboembolism in acutely and/or critically ill patients. 1125 46

In a review of the literature on the perioperative complications of Burch colposuspension we found only sparse data associated with this problem. We describe our own experience (> 1800 procedures) and the literature, discussing bleeding/hematoma, injury to the bladder, kinking/injury to the ureters, voiding dysfunction, infection, and rare complications such as deep venous thrombosis, pulmonary embolism, ileus, sepsis, external iliac vein injury and mortality rate. Knowledge of the possible risks and complications of Burch colposuspension may minimize the intraoperative complications and increase postoperative surgical success and patient satisfaction.
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PMID:Perioperative complications of Burch colposuspension. 1137 16

The most serious and fatal complication of deep venous thrombosis (DVT) is still accepted as pulmonary embolism (PE). One of the methods used for PE prophylaxis is inferior vena cava filter(VCF). Between 1999 and 2000, VCF is used in 12 patients (8 male, 4 female) who were hospitalized in Trauma and Surgical Emergency Service of Istanbul Medical Faculty. 10 of the VCF used were permanent and 2 of them were temporary filters. 8 permanent filter were applied to patients with life-long paraplegia or quadriplegia due to spinal cord injury. Two patients to whom permanent filters were applied had malignancy. Patient who had the diagnosis of late stage cervical carcinoma, had DVT. In this patient, because of the high bleeding risk, we applied permanent filter. In the other patient, who had the diagnosis bladder carcinoma, had DVT despite the usage of low molecular weight heparin. In two patients who needed short term PE prophylaxis, had temporary VCF. In one of these patients, primary diagnosis was subarachnoidal hemorrhage due to head trauma. In the 8th day of hospitalization, DVT occurred. Because of high risk of intracranial bleeding, VCF was performed. The second patient had the diagnosis of subdural hematoma and subarachnoidal hemorrhage due to head trauma and multiple lower extremity fractures. VCF were applied in Istanbul Medical Faculty, Department of Radiology. For cannulation line of permanent VCF (LGM Venatech-B. Braun) right femoral vein was used. For temporary filters (Proliser Cordis-Johnson and Johnson Company), right internal jugular vein was the preferred way. Two multitrauma patients who had permanent filters died due to sepsis and multiorgan failure. In the follow up of other patients during the average period of 7.6 months, any problem due VCF application or by related complication and PE did not occur. Although larger patient groups with follow up period are necessary to evaluate better, we think that in PE prophylaxis, VCF is safe and effective modality.
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PMID:[Applications of the inferior vena cava filter for the prevention of the risk for pulmonary emboli]. 1170 71

Key elements of the current approach to treating sepsis are reviewed, and examples are given to illustrate the difficulty of designing and evaluating trials in sepsis. A patient with sepsis is likely to have symptoms characteristic of the systemic inflammatory response syndrome. Initially, ruling out noninfective causes, locating the site of infection, and obtaining cultures before beginning antimicrobial therapy are critical. Aggressive fluid resuscitation and hemodynamic support are used to restore tissue perfusion and normalize cellular metabolism. Vasopressor therapy with dopamine or norepinephrine is needed in patients unresponsive to fluid resuscitation. Dobutamine should be administered in patients whose cardiac output is inadequate despite optimization of fluids and pressors. Supportive care includes deep vein thrombosis prophylaxis, nutrition support, stress ulcer prophylaxis, and management of acute lung injury. Attempts to modify the sepsis response and improve the outcome in these patients have yielded limited benefits. Recent small studies have shown benefits with low-dose hydrocortisone in patients with refractory sepsis. One challenge in study design is that a therapy may target a subset of patients that cannot be identified at the outset. Management of patients with suspected or documented sepsis focuses on hemodynamic support, appropriate antimicrobial therapy, and other supportive care.
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PMID:Current strategies for managing the patient with sepsis. 1188 13

Deep vein thrombosis (DVT) is uncommon in children but can occur given certain circumstances. The authors describe four children in whom DVT developed in association with musculoskeletal sepsis. One child died. Prothrombotic screens were performed on the three surviving children, showing normal hematologic parameters. The severity of DVT complicating musculoskeletal sepsis is emphasized, particularly the potential for septic embolic complications. Deep vein thrombosis should be considered in any child with musculoskeletal sepsis, particularly when a limb is severely swollen or when there are pulmonary septic emboli.
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PMID:Deep vein thrombosis associated with pediatric musculoskeletal sepsis. 1196 48

Clinical hematologists are frequently consulted for the care of hospitalized patients with complicated coagulopathies. This chapter provides an update on the scientific and clinical advances noted in disseminated intravascular coagulation (DIC) and discusses the challenges in hemostasis consultation. In Section I, Dr. Marcel Levi reviews advances in our understanding of the pathogenic mechanisms of DIC. Novel therapeutic strategies that have been developed and evaluated in patients with DIC are discussed, as are the clinical trials performed in patients with sepsis. In Section II, Dr. Lawrence Leung provides an overview of the challenging problems in thrombosis encountered in the inpatient setting. Patients with deep vein thrombosis that is refractory to conventional anticoagulation and those with extensive mesenteric thrombosis as well as the evaluation of a positive PF4/heparin ELISA in a post-operative setting are discussed. Novel treatments for recurrent catheter thrombosis in dialysis patients is addressed as well. In Section III, Dr. Julie Hambleton reviews the hemostatic complications of solid organ transplantation. Coagulopathy associated with liver transplantation, contribution of underlying thrombophilia to graft thrombosis, drug-induced microangiopathy, and the indication for postoperative prophylaxis are emphasized. Dr. Hambleton reviews the clinical trials evaluating hemostatic agents in patients undergoing liver transplantation.
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PMID:Coagulation: consultative hemostasis. 1244 31

Sepsis and septic shock are the leading causes of death in non-cardiological intensive care units in developed countries despite recent advances in critical care medicine. Sepsis is the systemic inflammatory response to infection, often associated with hypoperfusion followed by tissue injury and organ failure. Activation of monocytes/macrophages and neutrophils with consecutive release of proinflammatory mediators and activation of the coagulation cascade, seem to play a key role in the pathogenesis of sepsis. Elimination of the septic focus,antimicrobial therapy and supportive treatment are the cornerstones of sepsis therapy. Adequate and rapid volume replacement and if necessary application of catecholamines are of highest priority to optimize tissue perfusion. Norepinephrine is the vasopressor of choice and dobutamine the preferred inotropic agent. Most experts recommend hemoglobin levels of 8-10 g/dl in severe sepsis. In addition,lung protective ventilatory strategies as well as enteral and parenteral nutrition are part of the clinical management of septic patients. In mechanically ventilated patients intensive insulin therapy to maintain blood glucose at a level between 80 and 110 mg/dl has significantly reduced mortality.Furthermore,prophylaxis of deep vein thrombosis and of stress ulcer bleeding are individually applied to septic patients. Treatment of septic patients with anti-mediator strategies or high dose AT III were not successful so far. In contrast,now two new promising treatment options may be emerging: application of small doses hydrocortisone and activated protein C [drotrecogin alfa (activated)]. Large and in part multicentric studies especially in the last 2 years now allow the practicing clinician to perform a partially evidence-based management of patients with sepsis. In addition, for the first time two options for specific therapy of sepsis,application of small doses hydrocortisone and activated protein C [drotrecogin alfa (activated)],are available which may further improve prognosis for septic patients.
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PMID:[Clinical management of patients with sepsis]. 1257 61

The pharmacotherapy of burn care has evolved from the first topical antibiotics instituted > 30 years ago. These have helped greatly to reduce the incidence of burn wound sepsis, but a better understanding of the principles of burn care has resulted in earlier burn wound excision and complete coverage with autograft, cadaver skin, synthetic dressings, and amnion. This has markedly reduced septic complications and ameliorated the hypermetabolic response to burn injury. The hypermetabolic response, which is mediated by hugely increased levels of circulating catecholamines, prostaglandins, glucagon and cortisol, causes profound skeletal muscle catabolism, immune deficiency, peripheral lipolysis, reduced bone mineralisation, reduced linear growth, and increased energy expenditure. Supportive therapy and pharmacological manipulation, acutely and during rehabilitation, with growth hormone, insulin and related proteins, oxandrolone and propranolol can ameliorate the hypermetabolic response, improving survival and long-term outcome. Despite judicious use of topical and systemic antibiotics, opportunistic nosocomial bacterial resistance threatens to annul the improved survival of patients with severe burns. Patterns of emerging resistance encountered in burn units need to be considered, in light of a decreasing antibiotic armamentarium. A holistic approach to pharmacotherapy of severely burned patients including current practice in antimicrobial control, analgesia, sedation, and anxiety management is required. Current therapy of frequently encountered problems, such as post-burn pruritus, prophylaxis of deep venous thrombosis and peptic ulceration, and pharmacological manipulation of inhalation injury in the burned patient is described. Current pharmacotherapy to ameliorate psychosocial problems associated with burns such as acute stress disorder, depression and post traumatic stress disorder are discussed. Better analgesics, newer antibiotics and immune stimulating drugs are required to reduce mortality and morbidity in large burns.
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PMID:Current pharmacotherapy for the treatment of severe burns. 1261 89

As a result of advanced technology, dramatic developments in the area of new anticoagulant and antithrombotic drugs appear to have made a profound impact on the use of LMWHs. Furthermore, because porcine mucosal heparin is used for the preparation of these agents, it is likely that alternative drugs with comparable pharmacologic and clinical efficacy are sought. Antithrombin drugs such as argatroban and hirudin are already approved for alternative management of heparin-compromised patients. Their efficacy in other indications is less superior. The development of specific anti-Xa drugs is slow. Although these agents may inhibit factor Xa and thrombin generation, none of them are capable of mimicking the polytherapeutic effects of LMWHs and thus can only be given in drug combinations. Synthetic and recombinant protein-derived anti-tissue factor agents have also been developed. These drugs only inhibit the tissue factor-mediated process and are limited in their therapeutic spectrum. Plasma-derived and recombinant serine protease inhibitors (serpins) are also available for the management of thrombotic and inflammatory disorders, but these agents cannot be given subcutaneously. Furthermore, because they are proteins, antibodies to these agents are generated. Nucleic acid derivatives (natural and synthetic aptomers) are developed for intravenous administration, but they are relatively weak antithrombotic agents. Dermatans, heparans, and chondroitin sulfates represent nonheparin GAGs, and, in mono-compositional and polycompositional form, these drugs are mainly used for the intravenous management of DVT prophylaxis. They can be given to patients who are heparin compromised. Synthetic heparinomimetics include heparin consensus-binding oligosaccharides and synthetic oligosaccharides with non-serpin affinity. In addition, binding oligosaccharides are conjugated with antithrombin agents to mimic the anti-Xa/anti-IIa activities of heparin. Biotechnology using bacterial and yeast cultures, aqua cultures for marine products, and plant carbohydrates have been the focus of developing heparin analogues. Development of these agents is in the early phase; however, it is likely that this approach may provide a reasonable alternative to LMWHs. Despite these developments, it is unlikely that any of these drugs will have a profound impact on the use of LMWHs in the near future. Unfractionated heparin and LMWHs collectively represent an important group of polypharmacologic drugs without which the management of thrombosis and vascular disorders would not be possible. The continual development of LMWHs in expanded indications did not comprise the use of unfractionated heparin in surgical and interventional cardiovascular indications. Ever since their introduction in the 1980s, the use of LMWHs has continually increased. This is primarily because of expanded indications and growing awareness among the clinicians. It is likely that once an antidote is developed and additional information is available on the mechanism of action of LMWHs, these drugs may gradualty be used for surgery patients. Despite these developments, it is likely that unfractionated heparin will continue to be used for specific indications. Drug combinations with heparins may necessitate dose adjustments, but it is unclear whether unilateral reduction of heparins will be optimal. The coming years will provide useful clinical and applied data on the improved use of unfractionated heparin. LMWHs, and pentasaccharide in the management of thrombotic and cardiovascular disorders. In addition, use of these drugs will be extended to many conditions, including cancer, inflammation, sepsis, and autoimmune diseases. Polytherapeutic approaches emphasizing LMWHs as primary and secondary drugs will also have an impact on the management of thrombotic and nonthrombotic disorders. Ultra-LMWHs and synthetic heparinomimetics, such as fondaparinux, that exhibit a narrow pharmacologic spectrum will only be useful in specific indications and in combination with other drugs.
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PMID:Heparin, low-molecular-weight heparins, and heparin pentasaccharide: basic and clinical differentiation. 1262 73

Thrombosis of the internal jugular vein is a rare event but one that can have serious consequences. Most cases reported in the literature have occurred in patients with indwelling central venous catheters, in association with head and neck sepsis, or in hypercoagulable states. However, a small number of cases have been associated with in vitro fertilization and more often with the ovarian hyperstimulation syndrome (OHSS). We report the case of a 30-year-old woman heterozygous for both the prothrombin 3' UTR mutation and for the factor V Leiden mutation who presented with a proximal deep vein thrombosis following in vitro fertilization. She subsequently developed an internal jugular vein thrombosis extending into the subclavian and axillary vein despite therapeutic anticoagulation with a low molecular weight heparin. Thromboembolic events can occur in the absence of other clinical features of OHSS, especially in patients with underlying prothrombotic abnormalities. Neck pain and swelling in a pregnant woman, especially one that has undergone in vitro fertilization, should be taken seriously and investigated with duplex scanning and/or MRI. Women with a personal or family history of thrombosis undergoing in vitro fertilization should be made fully aware of the potential thrombotic risks and should be considered for a thrombophilia screen.
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PMID:Deep vein thrombosis followed by internal jugular vein thrombosis as a complication of in vitro fertilization in a woman heterozygous for the prothrombin 3' UTR and factor V Leiden mutations. 1287 33


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