Pulmonary Manifestations of Systemic Disease: Pulmonary Manifestation of Systemic Disease |

Sickle Cell Crisis and Its Effects on Pulmonary Arterial Pressure FREE TO VIEW

Enrique Calvo-Ayala, MD; Amanda Liggett, MD; Matthew McLaughlin, MD
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Eastern Virginia Medical School, Norfolk, VA

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):1066A. doi:10.1016/j.chest.2016.08.1173
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SESSION TITLE: Pulmonary Manifestation of Systemic Disease

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 26, 2016 at 01:30 PM - 02:30 PM

PURPOSE: To determine the magnitude of the change in pulmonary artery pressures as estimated by transthoracic echocardiogram (TTE) in subjects with an acute sickle cell crisis.

METHODS: Design: Retrospective chart review. Subjects: Adult subjects with the diagnosis of Sickle Cell Disease (SCD) and at least two TTE’s performed within three years, with one performed during an acute sickle cell crisis.

RESULTS: Twelve patients were included. 70% of subjects were female. The mean age was 35.4. The mean estimated systolic pulmonary artery pressure (eSPAP) measured was 42.7 mmHg (SD=17.2) and 71.7 mmHg (SD = 28), in TTE's performed as outpatient while not in an acute sickle cell crisis and inpatient during an acute sickle cell crisis, respectively (p<0.001). The eSPAP mean difference between measurement while in and not in crisis was 29 mmHg (SD = 20.8). A Pearson Correlation Coefficient for outpatient versus inpatient eSPAP revealed a moderate positive correlation (R=0.67; p < 0.05). The prevalence of pulmonary hypertension, as defined by eSPAP >40 mmHg, was 100% while in crisis compared to 50% while not in crisis (p=0.005).

CONCLUSIONS: This study confirms the presence of a significant difference between eSPAP measured while subjects have an acute vaso-occlusive crisis as compared to the pressure measured while outpatient without a crisis. Also, the study demonstrates the high prevalence of pulmonary hypertension when eSPAP is measured during crisis. 50% of patients had normal outpatient eSPAP (<40 mmHg), and 83% of those had an eSPAP < 67 mmHg while in crisis. We hypothesize that if the eSPAP is <67 mmHg while in crisis, the eSPAP is likely to become normal after the episode. Prospective studies to confirm our findings are needed.

CLINICAL IMPLICATIONS: We determined that the eSPAP increases by 29 mmHg on average when subjects with SCD have an acute vaso-occlusive crisis, and that the prevalence of pulmonary hypertension is high while in crisis. An eSPAP measured during vaso-occlusive crisis below 67mmHg may predict a normalization of eSPAP after the crisis resolves.

DISCLOSURE: The following authors have nothing to disclose: Enrique Calvo-Ayala, Amanda Liggett, Matthew McLaughlin

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