2003 OPEN FORUM Abstracts
HIGH FREQUENCY OSCILLATORY VENTILATION IN SICKLE CELL CRISIS-ACUTE CHEST SYNDROME.
Stephen Hepditch RRT, John Davies RRT, Neil MacIntyre MD. Duke University Medical Center, Durham NC.
Introduction: Acute chest syndrome (ACS) in the setting of sickle cell crisis presents a unique challenge in maintaining adequate oxygenation in the critically ill patient. The respiratory failure in ACS involves microvascular injury/thrombi along with edema, atelectasis and superimposed infection. We reasoned that the "lung protective" ventilatory support provided by high frequency oscillatory ventilation (HFOV) might be particularly well suited for patients with ACS.
Case Summary: A 29 year-old male with a known history of Sickle Cell disease presented to the ED with a chief complaint of chest and joint pain that developed after an upper respiratory tract infection. He was admitted to the hospital and treated with hydration, antibiotics, oxygen and opiods for pain control. He subsequently developed worsening dyspnea and chest pain along with the development of diffuse bilateral infiltrates on chest radiograph. A diagnosis of ACS was made and he was transferred to the ICU. Arterial blood gases at the time showed: pH 7.30, PCO2 67, PO2 67 on FiO2 1.0 via facemask. He was emergently intubated and for the next 48 hours required substantial PEEP (10-14 cm H2O) and FiO2 (0.7-1.0) to maintain PO2 levels above 60 mm Hg. PCO2 levels ranged from 70-80 mmHg despite plateau pressure requirements of 30-35 cm H2O. In an effort to reduce the FiO2 and airway pressure requirements, he was placed on HFOV with a mean pressure of 25 cm H2O. The rate was 5 Hz and the initial FiO2 was 1.0. The first ABG on HFOV showed marked improvement: pH 7.29, PCO2 63 and PO2 106. After 7 days of HFOV, his FiO2 requirement had decreased to 0.5 and his mean airway pressure was down to 21 cm H2O. He was transitioned back to conventional ventilation and extubated 3 days later. He was ultimately discharged from the hospital, 20 days after admission to the ICU.
Discussion: The putative advantage to HFOV is that it will provide good alveolar recruitment and CO2 transport with lower maximal distending pressures and FiO2 requirements than conventional ventilation. Because of this, HFOV is felt to result in a lower risk of ventilator induced lung injury (VILI). These features may be particularly important in ACS for several reasons: First, the microvascular injury of ACS may make the lung particularly prone to VILI from high distending pressures. Second, the red blood cell sickling phenomenon is very oxygen sensitive and ventilator strategies maximizing PO2 (without causing VILI) are particularly important. Third, we can speculate that the lower tidal pressure swings in HFOV may be beneficial to the injured microvasculature in ACS. Fourth, although not observed in this patient, others have suggested that HFOV might be beneficial in facilitating secretion removal in ACS.