The impact of spontaneous ventilation on distribution of lung aeration in patients with acute respiratory distress syndrome: airway pressure release ventilation versus pressure support ventilation.

BACKGROUND: In this study, we sought to determine which mode, airway pressure release ventilation (APRV) or pressure support ventilation (PSV), decreases atelectasis more in patients with acute lung injury/acute respiratory distress syndrome (ARDS). METHODS: This was a retrospective study in the intensive care unit. Between 2006 and 2007, we identified 18 patients with acute lung injury/ARDS who received either APRV or PSV and had a helical computed tomography scan twice in 3 days. RESULTS: Computed tomography data from the APRV and PSV groups (n = 9 each) were analyzed for 3-dimensional reconstruction and volumetry. Aerated lung regions (normally aerated, poorly aerated, nonaerated, and hyperinflated) were identified by their densities in Hounsfield units. The Pao(2)/Fio(2) ratio and alveolar-arteriolar oxygen gradient after ventilation were improved in both groups (P = 0.008); however, the improvements in the APRV group exceeded those in the PSV group when delivered with equal mean airway pressure (P = 0.018 and 0.015, respectively). Atelectasis decreased significantly from 41% (range, 17%-68%) to 19% (range, 6%-40%) (P = 0.008) and normally aerated volume increased significantly from 29% (range, 13%-41%) to 43% (range, 25%-56%) (P = 0.008) in the APRV group, whereas lung volume did not change in the PSV group. CONCLUSIONS: Spontaneous ventilation during APRV improves lung aeration by decreasing atelectasis. PSV for gas exchange is effective but not sufficient to improve lung aeration. These results indicate that APRV is more efficient than PSV as a mode of primary ventilatory support to decrease atelectasis in patients with ARDS.

Hemorrhagic shock and encephalopathy syndrome--the markers for an early HSES diagnosis.

BACKGROUND: The hemorrhagic shock and encephalopathy syndrome (HSES) is a devastating disease that affects young children. The outcomes of HSES patients are often fatal or manifesting severe neurological sequelae. We reviewed the markers for an early diagnosis of HSES. METHODS: We examined the clinical, biological and radiological findings of 8 patients (4 months to 9 years old) who met the HSES criteria. RESULTS: Although cerebral edema, disseminated intravascular coagulopathy (DIC), and multiple organ failure were seen in all 8 cases during their clinical courses, brain computed tomography (CT) scans showed normal or only slight edema in 5 patients upon admission. All 8 patients had normal platelet counts, and none were in shock. However, they all had severe metabolic acidosis, which persisted even after 3 hours (median base excess (BE), -7.6 mmol/L). And at 6 hours after admission (BE, -5.7 mmol/L) they required mechanical ventilation. Within 12 hours after admission, fluid resuscitation and vasopressor infusion for hypotension was required. Seven of the patients had elevated liver enzymes and creatine kinase (CK) upon admission. Twenty-four hours after admission, all 8 patients needed vasopressor infusion to maintain blood pressure. CONCLUSION: CT scan, platelet count, hemoglobin level and renal function upon admission are not useful for an early diagnosis of HSES. However, the elevated liver enzymes and CK upon admission, hypotension in the early stage after admission with refractory acid-base disturbance to fluid resuscitation and vasopressor infusion are useful markers for an early HSES diagnosis and helpful to indicate starting intensive neurological treatment.