Authors’ reply

We would like to thank Dr. Ł. Krupa and colleagues for their interest and important comments on our paper published recently in Polish Archives of Internal Medicine. In their letter, they raise the same questions that we have asked ourselves in the setting of such a complex medical situation. Due to the word limit, it is only possible to enclose partial information about the patient’s clinical status, so we appreciate the opportunity to elaborate on the subject. We decided to share this case despite its fatal course to underline the importance of detailed evaluation of the anatomy of pseudocysts as well as general condition of the patient to establish the optimal choice of treatment. We agree that uncomplicated and asymptomatic pseudocysts can be safely managed with a conservative approach, and the presence of symptoms (eg, persistent pain, weight loss, or vomiting) as well as development of local and systemic complications are indications for invasive treatment. At that time, we discussed with surgical and gastroenterology teams the necessity, urgency, as well as the optimal method of intervention and its timeliness. In this specific situation, the location of the pseudocyst was rather unfavorable for endoscopic drainage; the distance between the stomach wall and the thin wall of the pseudocyst was approximately 1.9 cm, and did not change significantly after large-volume paracentesis. These specific factors, combined with abnormal coagulation test results (international normalized ratio of 1.5 and decreased prothrombin percentage), the initial need for anticoagulation, and a possibility of malignancy were considered to confer a high risk of bleeding, which is a serious complication that may occur especially in immature pseudocysts with a gastric lumen–pseudocyst wall distance greater than 1.5 cm. The occurrence of a hemorrhage and rupture of the pseudocyst were a tragic confirmation of this hazard. The clinical presentation and patient’s history suggested acute-on-chronic pancreatitis, with an estimated time of onset of less than 4 weeks prior to the presentation. Implementation of supportive treatment consisting of the abovementioned paracentesis resulted in improvement of the patient’s physical condition, including the reduction of abdominal pain, inflammatory markers, amylase and lipase activity, and normalization of coagulation test results. We would like to highlight that after careful evaluation, we decided to postpone the intervention, preferably endoscopic ultrasound–guided treatment, for up to 14 days to allow the wall of the pseudocyst to mature and become thicker, which would make the procedure less likely to cause complications.1-3

Another question regarding the diagnosis of spontaneous bacterial peritonitis (SBP) may remain a topic of academic discussion. SBP most commonly occurs in patients with liver cirrhosis and ascites. However, it may develop as a consequence of any disease that results in the accumulation of ascitic fluid, for example, Budd–Chiari syndrome, portal vein thrombosis, pancreatitis, or neoplasms. This serious complication occurs in approximately 10% to 25% of patients with ascites, with a relatively high incidence of in-hospital mortality.4,5 We agree that the cause of ascites in the presented case was multifactorial, and it was not possible to clearly interpret the laboratory tests results in such a complex medical situation encompassing pancreatic ascites as well as pancreatitis and its complications. Since the chances for effective treatment were time-dependent before the possible onset of septic shock with multiorgan failure, we decided to start antibiotic therapy. Blood and ascitic fluid cultures came back negative, which is relatively common in SBP. Additionally, our patient did not meet the Runyon’s criteria for secondary bacterial peritonitis and responded to treatment with broad-spectrum antibiotics.

We hope that this response clarified, at least to some extent, our point of view.