Articles: respiratory-distress-syndrome.
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Critical care medicine · May 1989
Sepsis syndrome: a valid clinical entity. Methylprednisolone Severe Sepsis Study Group.
The sepsis syndrome represents a systemic response to infection and is defined as hypothermia (temperature less than 96 degrees F) or hyperthermia (greater than 101 degrees F), tachycardia (greater than 90 beat/min), tachypnea (greater than 20 breath/min), clinical evidence of an infection site and with at least one end-organ demonstrating inadequate perfusion or dysfunction expressed as poor or altered cerebral function, hypoxemia (PaO2 less than 75 torr), elevated plasma lactate, or oliguria (urine output less than 30 ml/h or 0.5 ml/kg body weight.h without corrective therapy). One hundred ninety-one patients with the sepsis syndrome were evaluated prospectively and comprised the placebo group of a multicenter trial of methylprednisolone in sepsis syndrome and septic shock. Forty-five percent of the patients were found to be bacteremic. ⋯ Mortality for the patients with sepsis syndrome who did not develop shock was 13%. Mortality for the groups of patients with shock on admission and shock postadmission was 27.5% and 43.2%, respectively. Forty-seven percent of the bacteremic patients developed shock after study admission compared to 29.6% of the nonbacteremic patients (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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Southern medical journal · May 1989
Case ReportsSeptic shock and acute respiratory distress syndrome after salpingitis caused by Streptococcus pyogenes group A.
A 32-year-old woman with acute salpingitis had signs and symptoms of sepsis, with hypotension, renal failure, acute respiratory distress syndrome, and disseminated intravascular coagulation. Streptococcus pyogenes group A was grown from blood cultures taken at the onset of illness, and salpingitis was confirmed at laparotomy. The patient recovered after appropriate antimicrobial and intensive supportive therapy.
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ARDS is a pulmonary injury syndrome associated with a variety of clinical disorders. The pathophysiology of ARDS has been clarified substantially in the past several years. ⋯ The mortality rate in ARDS remains high despite advances in elucidating of pathogenesis. Newer approaches to management stress earlier identification of patients and specific therapy aimed at interfering with the damage produced by toxic mediators of pulmonary injury.
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Nineteen patients with ARDS or pneumonia who were ventilated with PcIRV on the Siemens-Elema Servo 900 C were retrospectively reviewed. The PcIRV reduced peak airway pressure, PEEP, increased Paw, and improved ventilation and oxygenation in these patients. When these patients were compared with themselves on prior conventional IPPV, all had a decrease in PIP, an increase in Paw and most had a decrease in VE, with no change in PaCO2 and an increase in PaO2. ⋯ High levels of PIP and PEEP during IPPV have been identified as risk factors in the development of barotrauma and residual parenchymal pulmonary damage. We propose that PcIRV allows for adequate ventilation and oxygenation with decreases in PIP, extrinsically added PEEP and inspired O2 concentration. This mode of ventilation may decrease the morbidity associated with IPPV utilizing high PIP and PEEP.
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Am. Rev. Respir. Dis. · May 1989
Comparative StudyThe role of airflow resistance in patients with the adult respiratory distress syndrome.
Although reduced lung compliance is a hallmark of the adult respiratory distress syndrome (ARDS), the role of increased airflow resistance in this disorder has not been well studied. Because animal models of ARDS show marked increases in airflow resistance and because mediators known to participate in lung parenchymal injury have also been implicated in models of increased airway reactivity, we hypothesized that increased airflow resistance is a major contributor to altered lung mechanics in human ARDS. We studied 10 mechanically ventilated patients with ARDS (criteria: PaO2 less than or equal to 70 mm Hg breathing FIO2 greater than or equal to 0.4; bilateral pulmonary roentgenographic infiltrates; Ppaw less than or equal to 18 mm Hg) measuring dynamic (Cdyn) and static (Cstat) compliance, airflow resistance across the lungs (RL), shunt fraction (QS/QT breathing FIO2 = 1.0), minute ventilation (VE), (a/A)PO2, dead space to tidal volume ratio (VD/VT), airflow (pneumotachograph), transpulmonary pressure (intratracheal pressure minus esophageal pressure) and volume (integrated from flow) at 50 L/min peak flow rate. ⋯ RL correlated with peak pressure, but did not correlate with VE, shunt, (a/A)PO2, or VD/VT. We conclude that increased pulmonary airflow resistance contributes significantly to the altered lung mechanics in ARDS. These data are consistent with studies of animal models of ARDS and long-term survivors of ARDS and may be secondary to tissue factors, airway hyperreactivity, or airway inflammation.