Article

Pulmonary accumulation of polymorphonuclear leukocytes in the adult respiratory distress syndrome.

Critical Care Medicine (Impact Factor: 6.12). 12/1982; 10(11):712-8. DOI: 10.1097/00003246-198211000-00003
Source: PubMed

ABSTRACT The polymorphonuclear leukocyte (PMN) plays an integral role in the development of permeability pulmonary edema associated with the adult respiratory distress syndrome (ARDS). This report describes 3 patients with ARDS secondary to systemic sepsis who demonstrated an abnormal diffuse accumulation of Indium (111In)-labeled PMNs in their lungs, without concomitant clinical or laboratory evidence of a primary chest infection. In one patient, the accumulation of the pulmonary activity during an initial pass suggested that this observation was related to diffuse leukoaggregation within the pulmonary microvasculature. A 4th patient with ARDS was on high-dose corticosteroids at the time of a similar study, and showed no pulmonary accumulation of PMNs, suggesting a possible reason for the reported beneficial effect of corticosteroids in human ARDS.

0 Bookmarks
 · 
42 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Acute lung injury (ALI) and acute respiratory distress syndrome are characterized by protein rich alveolar edema, reduced lung compliance, and acute severe hypoxemia. A degree of pulmonary hypertension (PH) is also characteristic, higher levels of which are associated with increased morbidity and mortality. The increase in right ventricular (RV) afterload causes RV dysfunction and failure in some patients, with associated adverse effects on oxygen delivery. Although the introduction of lung protective ventilation strategies has probably reduced the severity of PH in ALI, a recent invasive hemodynamic analysis suggests that even in the modern era, its presence remains clinically important. We therefore sought to summarize current knowledge of the pathophysiology of PH in ALI.
    AJP Lung Cellular and Molecular Physiology 01/2012; 302(9):L803-15. · 3.52 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: C-reactive protein (CRP) has been studied as a marker of systemic inflammation and outcome in a number of diseases, but little is known about its characteristics in ARDS. We sought to examine plasma levels of CRP in patients with ARDS and their relationship to outcome and measures of illness severity. We measured CRP levels in 177 patients within 48 h of disease onset and tested the association of protein level with 60-day mortality, 28-day daily organ dysfunction scores, and number of ventilator-free days. We found that CRP levels were significantly lower in nonsurvivors when compared with survivors (p = 0.02). Mortality rate decreased with increasing CRP decile (p = 0.02). An increasing CRP level was associated with a significantly higher probability of survival at 60 days (p = 0.005). This difference persisted after adjustment for age and severity of illness in a multivariable model (p = 0.009). Multivariable models were also used to show that patients in the group with higher CRP levels had significantly lower organ dysfunction scores (p = 0.001) and more ventilator-free days (p = 0.02). Increasing plasma levels of CRP within 48 h of ARDS onset are associated with improved survival, lower organ failure scores, and fewer days of mechanical ventilation. These data appear to be contrary to the established view that CRP is solely a marker of systemic inflammation.
    Chest 06/2009; 136(2):471-80. · 5.85 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Seizures and epilepsy may occur secondarily to a wide range of infectious (parasites, bacteria, viruses, or fungi) and inflammatory diseases of the central nervous system, either as the primary manifestation or as part of a diffuse encephalopathy. The pathogenesis and clinical expression of the seizure disorder vary widely from one disease to another, and even across different types of infection with the same agent. While a myriad of infective agents invading the central nervous system may cause seizures, most frequent causes include cerebral malaria, neurocysticercosis, bacterial meningitis or encephalitis, bacterial abscesses, tuberculosis, viral encephalitis, and cryptococcosis. Seizures may also be associated with inflammatory, noninfectious disorders including Rasmussen encephalitis and neurosarcoidosis. Treatment of seizures associated with infection or inflammation usually involves symptomatic management, including antiepileptic drug therapy, and treatment for the underlying disorder. Recognition of infectious- or inflammatory-related acute or remote symptomatic seizures has important therapeutic and prognostic implications.
    Handbook of Clinical Neurology 01/2012; 108:601-20.