Articles: respiratory-distress-syndrome.
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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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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.
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Southern medical journal · Jul 1985
Case ReportsAdult respiratory distress syndrome due to malignant histiocytosis.
While a 23-year-old man was being evaluated for a two-month history of night sweats, fever, and weight loss, he had the typical clinical, radiologic, and laboratory findings of adult respiratory distress syndrome (ARDS). After a diagnosis of malignant histiocytosis (MH) was established by lymph node biopsy, review of an earlier lung biopsy initially interpreted as nonspecific revealed malignant histiocytes. He failed to respond to combination chemotherapy and died as a result of progressive respiratory failure.
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In 16 anesthetized dogs, low-pressure pulmonary edema was induced by the intravenous infusion of oleic acid (0.02 mL/kg). One group of four animals served as controls. In the remaining 12 animals, the pulmonary capillary wedge pressure (Pcwp) was lowered in an effort to decrease the accumulation of extravascular lung water (EVLW). ⋯ In four dogs, reduction of the Pcwp did not decrease the accumulation of EVLW but did reduce the rate of accumulation. In animals in which the EVLW reached a minimum, restoration of Pcwp to baseline values did not increase edema, while the control animals continued to deteriorate. Presumably, changes in tissue and lymphatic dynamics compensated for the increased capillary permeability.