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Volume Resuscitation (volume + resuscitation)
Selected AbstractsAnaphylaxis: Clinical concepts and research prioritiesEMERGENCY MEDICINE AUSTRALASIA, Issue 2 2006Simon GA Brown Abstract Anaphylaxis is a severe immediate-type hypersensitivity reaction characterized by life-threatening upper airway obstruction bronchospasm and hypotension. Although many episodes are easy to diagnose by the combination of characteristic skin features with other organ effects, this is not always the case and a workable clinical definition of anaphylaxis and useful biomarkers of the condition have been elusive. A recently proposed consensus definition is ready for prospective validation. The cornerstones of management are the supine position, adrenaline and volume resuscitation. An intramuscular dose of adrenaline is generally recommended to initiate treatment. If additional adrenaline is required, then a controlled intravenous infusion might be more efficacious and safer than intravenous bolus administration. Additional bronchodilator treatment with continuous salbutamol and corticosteroids are used for severe and/or refractory bronchospasm. Aggressive volume resuscitation, selective vasopressors, atropine (for bradycardia), inotropes that bypass the ,-adrenoreceptor and bedside echocardiographic assessment should be considered for hypotension that is refractory to treatment. Management guidelines continue to be opinion- and consensus-based, with retrospective studies accounting for the vast majority of clinical research papers on the topic. The clinical spectrum of anaphylaxis including major disease subgroups requires clarification, and validated scoring systems and outcome measures are needed to enable good-quality prospective observational studies and randomized controlled trials. A systematic approach with multicentre collaboration is required to improve our understanding and management of this disease. [source] Case Report of Cardiac Arrest, Abdominal Compartment Syndrome, and Thoracic Aortic Injury with Endovascular Repair of Thoracic Aortic TearJOURNAL OF CARDIAC SURGERY, Issue 4 2007Randy M. Stevens M.D. Currently, endografts are not FDA-approved for treating thoracic aortic injury (TAI). We report a case of TAI who presented in hemorrhagic shock and preoperative cardiac arrest who was successfully treated with large volume resuscitation, closed chest cardiac massage, exploratory laparotomy, and thoracic endografting. [source] Cardiovascular and Pulmonary Effects of Hetastarch Plus Hypertonic Saline Solutions during Experimental Endotoxemia in Anesthetized HorsesJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2006DACVIM, Lucas G. Pantaleon MV Background:Small volume resuscitation has been advocated as a beneficial therapy for endotoxemia in horses but this therapy has not been investigated in a prospective manner. The objective of this study was to determine the cardiopulmonary effects of small-volume resuscitation using hypertonic saline solution (HSS) plus Hetastarch (HES) during experimental endotoxemia in anesthetized horses. Hypothesis:Treatment of horses with induced endotoxemia using HES-HSS does not alter the response of various cardiopulmonary indices when compared to treatment with either small-or large-volume isotonic crystalloid solutions. Animals:Eighteen healthy horses were randomly assigned to 1 of 3 groups. Anesthesia was maintained with halothane. Endotoxemia was induced by administering 50 ,g/kg of Escherichia coli endotoxin IV. The horses were treated over 30 minutes with 15 mL/kg of balanced polyionic crystalloid solution (control), 60 mL/kg of balanced polyionic crystalloid solution (ISO), or 5 mL/kg of HSS followed by 10 mL/kg of HES (HSS-HES). Methods:Prospective randomized trial. Results:Cardiac output (CO) after endotoxin infusion increased significantly (P < .05) from baseline in all groups, whereas mean central venous pressure increased significantly (P < .05) in the ISO group only. Mean pulmonary artery pressure increased from baseline (P < .05) in horses treated with isotonic fluids and HSS-HES. There was no effect of treatment with HSS-HES on CO, systemic vascular resistance (SVR), mean arterial pressure, blood lactate concentrations, or arterial oxygenation. Conclusions and Clinical Importance: The use of HSS-HES failed to ameliorate the deleterious hemodynamic responses associated with endotoxemia in horses. The clinical value of this treatment in horses with endotoxemia remains unconfirmed. [source] Review article: diagnosis and management of mesenteric ischaemia with an emphasis on pharmacotherapyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2005P. L. Kozuch Summary Mesenteric ischaemia results from decreased blood flow to the bowel, causing cellular injury from lack of oxygen and nutrients. Acute mesenteric ischaemia (AMI) is an uncommon disorder with high morbidity and mortality, but outcomes are improved with prompt recognition and aggressive treatment. Five subgroups of AMI have been identified, with superior mesenteric artery embolism (SMAE) the most common. Older age and cardiovascular disease are common risk factors for AMI, excepting acute mesenteric venous thrombosis (AMVT), which affects younger patients with hypercoaguable states. AMI is characterized by sudden onset of abdominal pain; a benign abdominal exam may be observed prior to bowel infarction. Conventional angiography and more recently, computed tomography angiography, are the cornerstones of diagnosis. Correction of predisposing conditions, volume resuscitation and antibiotic treatment are standard treatments for AMI, and surgery is mandated in the setting of peritoneal signs. Intra-arterial vasodilators are used routinely in the treatment of non-occlusive mesenteric ischaemia (NOMI) and also are advocated in the treatment of occlusive AMI to decrease associated vasospasm. Thrombolytics have been used on a limited basis to treat occlusive AMI. A variety of agents have been studied in animal models to treat reperfusion injury, which sometimes can be more harmful than ischaemic injury. Chronic mesenteric ischaemia (CMI) usually is caused by severe obstructive atherosclerotic disease of two or more splanchnic vessels, presents with post-prandial pain and weight loss, and is treated by either surgical revascularization or percutaneous angioplasty and stenting. [source] Colonic ischaemia and intra-abdominal hypertension following open repair of ruptured abdominal aortic aneurysmBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2009K. Djavani Background: The aim was to investigate the association between colonic ischaemia and intra-abdominal pressure (IAP) after surgery for ruptured abdominal aortic aneurysm (rAAA). Methods: Sigmoid colon perfusion was monitored with an intramucosal pH (pHi) tonometer. Patients with a pHi of 7·1 or less were treated for suspected hypovolaemia with intravenous colloids and colonoscopy. IAP was measured every 4 h. Patients with an IAP of 20 mmHg or more had neuromuscular blockade, relaparotomy or both. Results: A total of 52 consecutive patients had open rAAA repair; 30-day mortality was 27 per cent. Eight patients died shortly after surgery. Fifteen were not monitored for practical reasons; mortality in this group was 33 per cent. IAP and pHi were measured throughout the stay in intensive care in the remaining 29 patients. Monitoring led to volume resuscitation in 25 patients, neuromuscular blockade in 16, colonoscopy in 19 and relaparotomy in two. One patient died in this group. Twenty-three of 29 patients had a pHi of 7·1 or less, of whom 15 had a pHi of 6·9 or less. Sixteen had an IAP of 20 mmHg or more, of whom ten also had a pHi below 6·90. Peak IAP values correlated with the simultaneously measured pHi (r = ,0·39, P = 0·003). Conclusion: Raised IAP is an important mechanism behind colonic hypoperfusion after rAAA repair. Monitoring IAP and timely intervention may improve outcome. Copyright © 2009 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Preclinical Studies with Adrenomedullin and Its Binding Protein as Cardiovascular Protective Agents for Hemorrhagic ShockCARDIOVASCULAR THERAPEUTICS, Issue 3-4 2006Rongqian Wu ABSTRACT Traumatic injury is a major, largely unrecognized public health problem in the US that cuts across race, gender, age, and economic boundaries. The resulting loss of productive life years exceeds that of any other disease, with societal costs of $469 billion annually. Most trauma deaths result either from insufficient tissue perfusion due to excessive blood loss, or the development of inflammation, infection, and vital organ damage following resuscitation. Clinical management of hemorrhagic shock relies on massive and rapid infusion of fluids to maintain blood pressure. However, the majority of victims with severe blood loss do not respond well to fluid restoration. The development of effective strategies for resuscitation of traumatic blood loss is therefore critically needed. We have recently discovered that the vascular responsiveness to a recently-discovered potent vasodilatory peptide, adrenomedullin (AM) is depressed after severe blood loss, which may be due to downregulation of a novel specific binding protein, AM binding protein-1 (AMBP-1). Using three different animal models of hemorrhage (controlled hemorrhage with large volume resuscitation, controlled hemorrhage with low volume resuscitation, and uncontrolled hemorrhage with minimum resuscitation), we have shown that cell and organ injury occurs after hemorrhage despite fluid resuscitation. Administration of AM/AMBP-1 significantly improves cardiac output, heart performance and tissue perfusion, attenuates hepatic and renal injury, decreases pro-inflammatory cytokines, prevents metabolic acidosis, and reduces hemorrhage-induced mortality. Thus, administration of AM/AMBP-1 appears to be a novel and useful approach for restoring cardiovascular responses, preventing organ injury, and reducing mortality after hemorrhagic shock. [source] | ||||||||||