Y. El-Gohary1, A. Fleming2, T. Beazely2, A. Abdelhafeez1, J. Estepp3, J. Hankins3, A. Davidoff1, A. Murphy1 1St. Jude Children’s Research Hospital,Pediatric Surgery,Memphis, TN, USA 2University of Tennessee Health Sciences Center,Memphis, TN, USA 3St. Jude Children’s Research Hospital,Hematology,Memphis, TN, USA
Introduction:
Acute chest syndrome (ACS), defined by a new pulmonary infiltrate on chest radiograph and one or more of the following symptoms: chest pain, fever greater than 38.5 Celsius, respiratory symptoms, and/or relative hypoxemia, is a life-threatening complication in patients with sickle cell disease (SCD). Patients with SCD are at high-risk of developing ACS following anesthesia. Here we sought to determine the risk factors for developing ACS after splenectomy in children with SCD.
Methods:
We retrospectively reviewed medical records of all children with SCD who underwent splenectomy at our institution between 1997-2017. Variables evaluated included age, SCD subtype, surgical method, operative time, splenic volume, total morphine equivalents administered, pain scale score (Face, Legs, Activity, Cry, Consolability (FLACC) scale), and peri-operative transfusions. Determination of the area under the curve (AUC) for FLACC score was calculated as a function of time. Categorical variables were compared using the Student’s t-test with a significance threshold of p<0.05
Results:
Sixty-six patients (n=50, HbSS; n=11, HbSC; and n=5 HbSβ -thalassemia) underwent splenectomy at a mean (SD) of 5.4 (±4.5) years of age. There were 36 males and 30 females. A laparoscopic approach was used in almost all cases (n=65, 98.5%). Of the laparoscopic procedures, 14 (21.5%) were single site, and two (3.1%) were converted to open partial splenectomy. One patient had an open partial splenectomy. Ten (15.2%) children developed ACS. No child died from postoperative ACS during this 20-year period. Children who developed postoperative ACS had similar operative times, perioperative RBC transfusions, preoperative hemoglobin levels and splenic volumes compared to those who did not develop ACS. Children who developed ACS had higher postoperative mean FLACC scores (6.2 ±3.0 versus 2.8 ±1.8, respectively; p <0.01), higher FLACC AUCs (117.9 ±56.1 versus 52.0 ± 33, respectively; p=0.01), and received more total morphine equivalents (1.6mg/kg ±1.5 versus 0.8 ±0.8, respectively; p = 0.01), compared to children who did not develop ACS
Conclusion:
The dogma of postoperative fever being due to atelectasis does not apply to SCD patients, and surgeons must be made aware of ACS as potentially fatal complication. Despite most of our patients undergoing minimally invasive surgery and receiving preoperative transfusions, our postoperative ACS rate is similar to the reported literature. In our cohort, ACS was associated with moderate to severe postoperative pain and narcotic use, supporting the investigation of non-narcotic pain control options in this patient population.