Articles: trauma.
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Pneumothoraces are classified as spontaneous, traumatic, and iatrogenic. Spontaneous pneumothoraces (SP) occur without recognized lung disease (primary, PSP) or due to an underlying lung disease (secondary, SSP). Treatment of PSP and SSP has been quite heterogeneous in the United States; adoption of the recently published American College of Chest Physicians guidelines will hopefully improve care. ⋯ Iatrogenic pneumothoraces appear most commonly due to transthoracic needle aspiration and may be treated in carefully selected patients with observation. The presence of underlying emphysema in the setting of an iatrogenic pneumothorax usually mandates placement of a drainage catheter. Newer mechanical ventilation modes and strategies may limit the development of positive pressure ventilation- related iatrogenic pneumothoraces.
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Patients with traumatic brain injury (TBI) have a high mortality and morbidity. This pilot study was undertaken to identify contributors to outcome in the early management of patients with TBI and to investigate the feasibility of a larger study. ⋯ Both initial GCS and severity of brain injury should be used to match TBI patients for injury severity in future studies. Lower initial GCS in deceased patients was likely due to greater severity of brain injury, although it is also possible that the lower GCS was due to decreased brain perfusion (perhaps reflecting inadequate resuscitation) in these patients. Volume of early fluid resuscitation, time to definitive therapy, and time of presentation to hospital may also be important determinants of patient outcome. A large case control outcome study is required to extend these observations.
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Pediatr Crit Care Me · Jul 2001
The Th1 versus Th2 cytokine profile in cerebrospinal fluid after severe traumatic brain injury in infants and children.
To further characterize the Th1 (proinflammatory) vs. the Th2 (antiinflammatory) cytokine profile after severe traumatic brain injury (TBI) by quantifying the ventricular cerebrospinal fluid concentrations of Th1 cytokines (interleukin [IL]-2 and IL-12) and Th2 cytokines (IL-6 and IL-12) in infants and children. DESIGN: Retrospective study. SETTING: University children's hospital. PATIENTS: Twenty-four children hospitalized with severe TBI (admission Glasgow Coma Scale score, <13) and 12 controls with negative diagnostic lumbar punctures. INTERVENTIONS: All TBI patients received standard neurointensive care, including the placement of an intraventricular catheter for continuous drainage of cerebrospinal fluid. MEASUREMENTS AND MAIN ⋯ This study confirms that IL-6 levels are increased in cerebrospinal fluid after TBI in infants and children. It is the first report of increased IL-12 levels in cerebrospinal fluid after TBI in infants and children. Further, it is the first to report on IL-2 and IL-4 levels in pediatric or adult TBI. These data suggest that selected members of both the Th1 and Th2 cytokine families are increased as part of the endogenous inflammatory response to TBI. Finally, in that both IL-6 and IL-12 (but neither IL-2 nor IL-4) can be produced by astrocytes and/or neurons, a parenchymal source for cytokines in the brain after TBI may be critical to their production in the acute phase after TBI.
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Early reports of late outcomes among survivors of ARDS indicated that most patients improved dramatically after their intensive care unit stay, and few lived with residua of their once-severe pulmonary injury. Over the last decade, a collection of new studies with improved methodology and novel questions has improved our understanding of life after ARDS. After reviewing these newer investigations in the context of previously published literature, we have drawn several preliminary conclusions: (1) Long-term survival after hospital discharge is unaffected by ARDS, but is strongly affected by ARDS risk factor and comorbidities. (2) Respiratory symptoms after ARDS are more prevalent than previously indicated, but improve over the first 12 months of recovery. (3) Pulmonary function testing reveals marked impairment soon after ARDS. ⋯ A small group of patients have severe impairment without improvement. (4) Quality of life, functional independence, and cognitive function are severely affected by ARDS, with dramatic improvement over the first year. Quality of life is lower than in matched critically ill controls. (5) Significant numbers of ARDS survivors suffer from posttraumatic stress syndrome. This is an exciting time for research in long-term outcomes of ARDS, with potential for future studies that validate these single-center hypotheses, explore their ramifications, and investigate the impacts of changing practices in the intensive care unit in the acute phase of ARDS.
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The acute respiratory distress syndrome (ARDS) is a life-threatening syndrome that may occur in any patient without any predisposition and that is mostly triggered by underlying processes such as sepsis, pneumonia, trauma, multiple transfusions, and pancreatitis. ARDS is defined by (1) acute onset, (2) bilateral infiltrates in chest x-rays, (3) absence of left ventricular failure, and (4) severe arterial hypoxemia with a PaO2/FiO2 ratio less than 200 mmHg. Still, ARDS is feared (mortality 30-40%) and relatively frequent (incidence between 13.5 per 100,000 to 75 per 100,000). ⋯ Despite ongoing and intensive scientific research in this area, the mechanisms underlying ALI/ARDS are still not completely understood, and until recently, there were no studies demonstrating any beneficial effect of a single treatment modality in ARDS. The recent report that a specific approach to ventilatory support can significantly reduce mortality in ARDS underscores the need for better understanding of the pathophysiological events occurring in this syndrome. This review therefore summarizes the current pathophysiological concepts underlying the evolution of acute hypoxemic respiratory failure and focuses on: (1) possible reasons for the development of ALI/ARDS; (2) cellular and humoral mediator responses leading to a sustained and self-perpetuating inflammation of the lung; (3) consequences with regard to fluid balance, pulmonary perfusion, ventilation, and efficiency of gas exchange; and (4) mechanisms underlying the aggravating complications commonly seen in ARDS, especially ventilator-associated lung injury, ventilator-associated pneumonia, and lung fibrosis.