Articles: respiratory-distress-syndrome.
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A review of the recent literature concerning the Adult Respiratory Distress Syndrome (ARDS) and Multiple Organ Failure (MOF) is presented. We hypothesize that the two syndromes probably have a common pathophysiology, with ARDS as the first occurring organ failure. The clinical situations that may cause ARDS and MOF are characterized by massive and prolonged activation of the complement system. ⋯ Oxygen diffusion in the peripheral tissues is impeded by the same mechanism, ultimately resulting in organ failure. Hypoxia may cause additional microvascular lesions, as toxic oxygen radicals are produced during reoxygenation. The implications of this hypothesis for the prevention and therapy of ARDS and MOF are discussed.
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Arterial blood oxygenation improved repeatedly after sedation and paralysis in a 27-year-old woman requiring mechanical ventilation for the adult respiratory distress syndrome. Oxygen consumption and cardiac output decreased proportionately after paralysis so that the partial pressure of oxygen in mixed venous blood remained unchanged. Paralysis eliminated inspiratory distortion of the airway pressure waveform and prevented forceful use of expiratory musculature. A flow-related reduction of venous admixture or recruitment of lung volume may best explain the beneficial effect of muscle relaxation on arterial saturation.
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Surg. Clin. North Am. · Aug 1985
Review Comparative StudyControversies in the pathophysiology and fluid management of postoperative adult respiratory distress syndrome.
Physiologic changes that lead to the development of ARDS begin with the precipitating shock syndrome. Hypovolemia, pulmonary vasoconstriction, reduced myocardial performance, and diminished O2 transport typically precede the development of clinical ARDS after hemorrhage, trauma, postoperative conditions, and sepsis. Since shock lung is a complication of shock, it is not surprising that the antecedent clinical and physiologic events that characterize the shock state may be determinants of both the genesis and the outcome of ARDS. ⋯ They are uneven ventilation throughout the lung; redistribution of regional pulmonary blood flow between zones due to gravity; nonuniform pulmonary blood flow between individual metarteriolar-capillary networks because of local vasoconstriction; uneven systemic blood flow between organs; irregular systemic blood flow at the microcirculatory level, producing inadequate nutritional flow to the tissues; and redistribution of body water, leading particularly to fluid accumulation in the extracellular compartment, with expanded interstitial space and contracted plasma volume (hypovolemia). Pathogenic roles have been implicated for capillary leak, surfactant synthesis, erythrocyte and platelet aggregation, leukocyte margination in the pulmonary circulation, complement and kinin cascades, neurohumoral responses, histamine, serotonin, vasoactive peptides, and the metabolic products of arachidonic acid breakdown in pulmonary vessels. However, these potential pathogenic influences have yet to be described in terms of their temporal relationships to the natural physiologic history of ARDS; nor have their roles been evaluated in terms of mechanistic interrelationships.(ABSTRACT TRUNCATED AT 400 WORDS)
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Adult respiratory distress syndrome remains one of the most lethal conditions treated in surgical and medical intensive care units. Mortality rates of 50 per cent are still reported in recent reviews. Many risk factors are linked with an increased incidence of ARDS, but sepsis and direct pulmonary injury from aspiration, pulmonary contusion, and other forms of trauma are the most commonly associated risk factors. ⋯ Therapy should be started at this time and maintained while the etiologic factors are identified and treated. Minimal ventilatory support should be continued until the primary diseases have resolved and the multisystem impact of the critical illness has lessened. Weaning from inspiratory (IMV) support, manipulation of expiratory pressures (PEEP), and airway control should then be more easily accomplished and more successful in practice.
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In a 10-year period, 22 neonates with esophageal atresia (EA) and tracheoesophageal fistula (TEF) required high pressure ventilatory support soon after birth because of respiratory distress syndrome (RDS). Eleven of the 22 or 50% survived overall, but if the 5 patients who died before definitive surgical repair could be attempted are excluded, 11 of 17 or 65% survived. More importantly, 4 of 7 (57%) patients who had gastrostomy performed first survived while 7 of 10 (70%) who had fistula ligation performed first survived. ⋯ Resuscitation of such a patient is not possible until leakage from the esophagus is controlled by ligation of the fistula or transabdominal occlusion of the distal esophagus. Placement of a Fogarty catheter into the fistula via a bronchoscope is effective but may not be feasible in every case. Early thoracotomy and ligation of the fistula in patients with progressive RDS provides immediate improvement in ventilatory efficiency and relief of gastric distention.