LAUSR

We are grateful for the thoughtful consideration inspired by our article, particularly as clinical interest in primary antibiotic therapy for acute appendicitis continues to grow. To ensure clarity, the essential points in the article should be stated accurately. Our goal was “To determine the frequency of luminal obstruction on appendiceal graded compression sonography (US) in patients with uncomplicated appendicitis and test the hypothesis that this frequency is similar to the failure rates of primary antibiotic therapy for uncomplicated appendicitis when treatment selection is based on CT findings.” The data confirmed this hypothesis, supporting “the possibility that undiagnosed luminal obstruction may account for treatment failures when patients are selected by CT for primary antibiotic therapy.” We discussed a potential “role for US in selecting patients without luminal obstruction for antibiotic therapy” with luminal obstruction on US possibly being “a leading indicator” of subsequent antibiotic failure. A fluid-filled appendix does not equate to luminal obstruction because intraluminal fluid can be present in normal patients as well as patients who have enteritis. Additionally, we are not aware of a specific defensible criterion for appendiceal “distension” on sonography. Thus, we sought a more rigorous, workable definition of luminal obstruction and for this we utilized “proximal appendicolithiasis or lymphoid hyperplasia which completely obliterated the appendiceal lumen and was accompanied by fluid or other material filling the lumen upstream from the obstructing lesion.” We focused on appendicolithiasis and lymphoid hyperplasia because these findings are sonographically identifiable and are much more frequent, in our experience, than other obstructive processes such as parasites and neoplasia. This early work was not designed to address all possible obstructing processes. Regarding lymphoid hyperplasia, its sonographic appearance and criteria for its diagnosis have been described and well discussed in the literature. The present study and the study by Xu et al differ fundamentally from one another, addressing different questions in different patient populations using different study designs. For example, the present study included only patients with appendicitis; the earlier study included patients with appendicitis and patients without appendicitis. One would not expect their results to be the same. The mechanism(s) leading to the failure of primary antibiotic treatment are not known to be the same as those leading to the initial onset of appendicitis, to our knowledge, and we believe that they could well be different given the different biological states involved. We caution against presuming that processes associated (or not associated) with initial appendicitis are also associated (or not associated) with antibiotic failure—whether obstructive or nonobstructive, and whether related to lymphoid hyperplasia, appendicolithiasis, or still other processes. Further to this, we stated, “the mechanisms underlying the progression of established appendicitis may differ from those contributing to the initial onset of appendicitis.” We look forward to further elucidation of the processes involved in these different events. Because an association between luminal obstruction and antibiotic treatment failure “would clearly have great clinical importance,” we reiterate our hope that our findings will indeed lead to further investigation.