Resuscitation
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Randomized Controlled Trial Comparative Study Clinical Trial
The rapid infusion system: a superior method for the resuscitation of hypovolemic trauma patients.
The rapid infusion system (RIS), which can deliver fluids/blood products rapidly at precise rates and normothermic conditions, was compared with conventional fluid administration (CFA) in a randomized study of 36 hypovolemic trauma patients. Admission stratification criteria of the groups were similar relative to age, Glasgow Coma Score (GCS), Injury Severity Score (ISS) and plasma lactate. Despite the lack of difference in blood loss between the 24-h survivors of the two groups, the CFA group required greater total fluids (23.6/20.21), red blood cells (5.5/4.61), fresh frozen plasma (FFP) (2.8/1.91), platelets (523/204 ml), and crystalloids (12.9/10.61). ⋯ The PTT and PT were related to the degree of lactic acidosis (P = 0.0001) and hypothermia (P = 0.001) but not to the amount of FFP given (P = 0.14). The hospital costs, days in the ICU, and days on the ventilator were greater for the CFA group, as was the incidence of pneumonia (0/11 vs. 6/17; P = 0.03). Hypovolemic trauma patients resuscitated with the RIS needed fewer fluid/blood products and had less coagulopathy; more rapid resolution of hypoperfusion acidosis; better temperature preservation; and fewer hospital complications than those resuscitated with conventional methods of fluid/blood product administration.
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Awareness during anesthesia is as old as anesthesia itself. Using muscle relaxing drugs, operations can be done on a relaxed but fully aware patient. ⋯ This article reviews the subject from some aspects including its causes, signs, tests and medico-legal points. Awareness during anesthesia can be looked at as 'the invisible scars of surgery.'
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A previously established model in awake rats of hemorrhagic shock (HS) with 25% spontaneous survival rate (without resuscitation) was used to evaluate the effects of 4 novel life-supporting first aid (LSFA) measures on survival time and rate. After shed blood volume (SBV) of 3.25 ml/100 g, withdrawn over 20 min, hemodynamic and respiratory responses were recorded to 3 h and survival to 24 h. ⋯ Compared with group I, median survival times during HS 0-3 h were longer in groups II and III; and self-resuscitation attempts were longer in groups II, III and IV. We conclude that in untreated severe hemorrhagic shock, chances of survival to delayed arrival of advanced life support with i.v. fluid resuscitation might be increased with O2 inhalation and/or moderate external cooling.
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A simple rat model was developed for the study of spontaneous survival after volume-controlled hemorrhage. The objective was to determine in awake, unrestrained rats the shed blood volume (SBV) in ml/100 g body weight that without fluid resuscitation, would result in either a high or a low percentage of survivors within 24 h. About 24 h after cannulation under light anesthesia, the awake rats were insulted with arterial blood withdrawal at a constant rate over 20 min, while mean arterial pressure (MAP) was monitored (N = 78). ⋯ SBV of 2.50 ml/100 g should be suitable for testing additional insults. SBV of 3.00 ml/100 g should be suitable for testing resuscitative therapies. The model should be modified to allow monitoring of key variables after hemorrhage.
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The immediate organ damage seen after multiple trauma and in shock is a typical example of non-bacterial inflammation triggered by activation of various mediators of both the humoral and cellular systems. Anaphylatoxins and the low-flow syndrome during the shock phase account for increased PMN* margination, which in turn causes pulmonary leukostasis and may provoke massive mediator release by PMN (oxygen radicals, proteinases, eicosanoids, PAF etc). This probably leads to severe endothelial cell damage, especially in the lung. ⋯ TNF is secreted by monocytes/macrophages (MO/MA) in response to LPS. Via macrophage derived cytokines and by LPS there is activation of endothelial cells, with increased adhesiveness for PMN. Both due to this increased adhesiveness and the presence of LPS and cytokines, PMN undergo massive activation, which causes mediator release and tissue damage.(ABSTRACT TRUNCATED AT 400 WORDS)