|Year : 2019 | Volume
| Issue : 2 | Page : 84-88
Acute necrotizing pancreatitis after esophagectomy: A nail in the coffin?
Abhay K Kattepur, Nizamudheen M Pareekutty, John J Alapatt, Satheesan Balasubramanian
Department of Surgical Oncology, Malabar Cancer Centre, Thalassery, Kerala, India
|Date of Web Publication||30-Dec-2019|
Dr. Abhay K Kattepur
Department of Surgical Oncology, Malabar Cancer Centre, Thalassery 670103, Kerala.
Source of Support: None, Conflict of Interest: None
Postoperative pancreatitis is an extremely rare complication associated with a high mortality rate. This report describes the case of a 62-year-old man who developed acute necrotizing pancreatitis post transhiatal esophagectomy for esophageal adenocarcinoma. The diagnosis can be challenging, first, owing to the confounding similarities of anastomotic leak in the postoperative period, and second, the rarity of this entity, which precludes a clinical suspicion at the outset. Hence, the appearance of pancreatitis becomes the final “nail in the coffin” in such patients who run the risk of death or severe long-term morbidity.
Keywords: Amylase, anastomotic leak, carcinoma esophagus, esophagectomy, pancreatitis
|How to cite this article:|
Kattepur AK, Pareekutty NM, Alapatt JJ, Balasubramanian S. Acute necrotizing pancreatitis after esophagectomy: A nail in the coffin?. J Curr Oncol 2019;2:84-8
| Introduction|| |
Surgery for esophageal cancer is not without its attendant risks. Being a supra-major surgery, surgical and nonsurgical complications can directly and indirectly influence outcomes in the perioperative period. Depending on the tumor location and the general condition of the patient, a transthoracic esophagectomy (TTE) or a transhiatal esophagectomy (THE) can be performed with comparable oncological outcomes,, although, the former is associated with higher pulmonary complications. Large volume centers around the world have also shown acceptable morbidity and mortality rates.,
Postoperative pancreatitis is a dreaded complication that commonly occurs after pancreatic or gastric surgeries. Acute pancreatitis occurring after esophagectomy is rare. The severity can vary, ranging from a milder form, with transient elevation in serum amylase levels, often resolving with conservative management, to a severe, necrotizing pancreatitis that is associated with multi-organ dysfunction syndrome (MODS) and high mortality rates. The exact cause of such postoperative pancreatitis remains speculative. This report describes a case of acute severe pancreatitis in a patient after THE for carcinoma esophagus.
| Case Report|| |
A 62-year-old man, who was diabetic and a reformed smoker, presented with dysphagia for solids of 3 months. No history of vomiting, abdominal pain, cough with expectoration, or regurgitation of feeds was observed. Clinical examination was unremarkable. Endoscopy revealed a growth in the lower esophagus extending into the gastroesophageal junction (GEJ), cardia, and proximal part of gastric fundus. Biopsy showed moderately differentiated adenocarcinoma. Computed tomography (CT) showed a thickening involving the distal esophagus, GEJ, and cardia with perigastric adenopathy. The patient was staged as cT3N2 disease and was planned for neoadjuvant chemotherapy. He received four cycles of FLOT (5-fluorouracil, leucovorin, oxaliplatin, and docetaxel)-based chemotherapy. Response assessment showed near complete endoscopic and radiological response.
The patient underwent THE, proximal gastrectomy, and D2 lymphadenectomy. Intraoperatively, a minor parenchymal transection injury to the pancreatic parenchyma during dissection of stations 10 and 11 was observed. On postoperative day (POD) 1, the patient developed atrial fibrillation (AF) and increased output from the left Intercostal drain. Elevated serum (413 IU/L) and drain (1912 IU/L) amylase levels raised the suspicion of acute pancreatitis. The patient was started on broad-spectrum antibiotics. The neck wound was opened and inspected. The anastomosis was found to be healthy. Over the subsequent 3 days, the general condition of the patient remained stable. On POD 5, the intercostal tube drainage turned bilious. At this point with an elevated drain fluid amylase and “bile in the drain,” there was a high index of clinical suspicion for it to be an anastomotic leak than anything else. Hence, without radiological imaging, the patient was taken up for emergency reexploration. Intraoperatively, anastomotic leak was confirmed. He underwent gastric conduit disconnection with cervical esophagostomy and feeding jejunostomy. Florid pancreatitis with saponification of the complete lesser and part of the greater omentum with pancreatic ascites was found. In addition, necrosis of the distal edge of the gastric conduit was noted.
On POD 15 (from the first surgery and POD 10 from the reexploration), a bilious abdominal drain output was observed. As the general condition of the patient was acceptable with no hemodynamic instability or features of peritonitis, he was closely monitored. Total parenteral nutrition was started, and tube feeds were withheld. On POD 17, a sudden drop in hemoglobin with associated bleeding from the drain was observed. Splenic artery pseudoaneurysm with intra-abdominal bleed was suspected. CT showed moderate ascites with bleed within the perisplenic region [Figure 1]A and B. The patient was taken for exploration with peritoneal lavage. Intraoperatively, infected clot and necrotic material were found in peripancreatic region with small area of pancreatic necrosis and bleed from the areas around the splenic artery. Pancreatic necrosectomy with thorough peritoneal lavage was undertaken. Hemostatic pack was placed in the oozy area, and the abdomen was closed. [Figure 2] depicts the laboratory trends during the postoperative period.
|Figure 1: (A) Axial CT showing moderate ascites with fluid enhancement around the spleen, suggestive of bleed. (B) Axial CT scan showing bulky pancreas|
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|Figure 2: Trend of various laboratory parameters during the postoperative period|
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The patient gradually recovered from surgery. He continued to have bilious drain output, which resolved over next 15 days. During this period, the patient’s clinical recovery was complicated with fungal sepsis, which was treated with antifungals. He was discharged on POD 30 after the second exploration (i.e., 55th day after first surgery). The final histopathology report showed residual adenocarcinoma with positive periesophageal nodes (ypT2N2) and negative margins. He is currently not planned for any form of adjuvant chemotherapy because of stormy postoperative course and delayed recovery. At the present time (POD 120), the patient is alive, tolerating enteral (feeding jejunostomy) feeds with fairly well-controlled analgesia.
| Discussion|| |
The aforementioned case highlights that there is indeed a definite, albeit small risk of postoperative pancreatitis after esophagectomy, and a high degree of suspicion is needed for diagnosis. The overall incidence is, however, rare (<0.5%) as per literature review., In our case, the patient had developed AF, which was the first red flag, showing that he was veering away from the normal postoperative course. The minor elevation of both serum and intercostal drain amylase levels raised our suspicion of an anastomotic leak. On neck wound exploration, as there were no features of anastomotic dehiscence, we assumed it as a case of acute mild pancreatitis (no organ failure, systemic complications, or hemodynamic instability were observed) and started him on a conservative line of management. The biochemical diagnostic criteria of acute pancreatitis are defined as the three times increase in upper limit of the normal serum value of amylase or lipase in association with upper abdominal pain or confirmatory radiological confirmation.
The most common manifestation is a deviation from the normal clinical course in an otherwise stable patient. The clinical features of an anastomotic leak can overlap with that of acute pancreatitis (as postoperative pancreatitis can itself manifest as an anastomotic leak compounding the worsening of a patient). In our case, the pertinent question that begs to be asked is “Did the postoperative pancreatitis cause the ensuing anastomotic leak and gastric conduit necrosis or is it vice versa?” It seems to be a case of the classic “chicken or the egg paradox.” As there were evidences of florid pancreatitis and distal gastric conduit necrosis in the emergency exploratory laparotomy, and review of literature showed that around one-third of the patients also develop conduit necrosis and its attendant complications, the plausible reason being a microcirculatory failure or thrombosis of arterioles supplying the conduit during the systemic inflammatory response syndrome (SIRS) state, we believed it could be a case of acute pancreatitis following the surgical procedure.
Two reports by Blom et al. and Kawamorita et al. describe similar clinical situations [Table 1]. The former has reported four patients with postoperative pancreatitis. These patients are generally elderly with or without preexisting comorbidities. The onset can be acute but variable with respect to time of presentation. The presence of high levels of amylase in drains or chest tubes may heighten clinical suspicion, although lower levels do not exclude one. The mortality rate is over 50%, with hopeful survivors having long-term morbidity. In another study by Berkelmans et al., the role of serum and drain amylase in detecting anastomotic leaks after esophagectomy was evaluated. In this study, however, one patient with postoperative pancreatitis was excluded from the analysis. The authors concluded that patients with anastomotic leaks have a higher value of both serum and drain amylase levels with a specificity of around 95%. In our patient, a high drain amylase level helped us make a diagnosis of pancreatitis, although it could possibly hint towards an early leak.
The severity of pancreatitis can vary. In its severest form, pancreatic necrosis with its attendant complications of SIRS and MODS can lead to stormy postoperative recovery with a rapid downhill course. Approximately 50% of patients in earlier reports developed pancreatic necrosis. Around one-third of the patients also developed conduit necrosis and its attendant complications, the plausible reason being a microcirculatory failure or thrombosis of arterioles supplying the conduit during the SIRS state.
Pancreatitis, postoperatively, could be due to multiple factors: handling of the pancreas during lymphadenectomy or mobilization of the stomach producing microtrauma leading to edema, duct obstruction, and inflammation; devascularization of the pancreas during dissection; intraoperative hypotension and massive blood loss; and microthrombi within the pancreatic blood vessels leading to ischemia and diminished trypsin inhibition postoperatively, all could contribute to its development.,
The causes relevant to our case in question were the patient’s neoadjuvant chemotherapy regimen, oxaliplatin, and rarely docetaxel-induced acute pancreatitis. In all cases, patients had developed acute pancreatitis immediately after administration of the chemotherapeutic drug. In our case, whether these drugs, in addition to the minor pancreatic parenchymal injury precipitated the development of acute pancreatitis is difficult to substantiate. Morphine and fentanyl are the commonly used opioids intraoperatively and as postoperative analgesics. As these drugs can cause Sphincter of Oddi More Details spasm, they are better avoided in acute pancreatitis. At present, no clinical evidence linking morphine with increased risk, causing or aggravating pancreatitis, is present. This patient did receive both fentanyl at the time of induction of anesthesia and morphine as a part of his epidural analgesia. A randomized trial has shown that epidural analgesia can improve pancreatic perfusion and reduce severity in predicted severe acute pancreatitis. On reviewing the case file, no other possible offending drugs that could result in acute pancreatitis were available.
The splenic artery tends to be embedded or in close relation with the upper border of pancreas. More often than not, meticulous dissection of station 10 and 11 (nodes along the splenic artery and the hilum) results in minor injury to pancreatic parenchyma as it had happened in our case. Usually this degree of injury may result in a transient elevation of serum amylase levels and will not manifest as acute severe pancreatitis. One of the major causes postulated is pancreatic microcirculatory hypoperfusion, and the pancreas is exquisitely sensitive to arterial and venous ischemia, and infarction of a major vessel is not required to cause pancreatic necrosis. In our case, the patient did not have any major intraoperative hypotensive period, but in the immediate postoperative period, he had developed AF that could have resulted in hypotension and transient hypoperfusion of the pancreas, initiating the cascade of acute pancreatitis.
Pancreatic necrosis per se is associated with mortality rate of 10%–20%. Pancreatic necrosis is a complication, which occurs mostly 3 days after pancreatitis has begun. Contrast-enhanced CT imaging to diagnose necrosis needs only to be carried out after 3 days. Initially, the pancreatic necrosis is sterile, and subsequently, it may get infected. Treatment includes drainage (either percutaneous or endoscopic) of the pancreatic bed along with the management of fluid, electrolyte balance, adequate nutrition to tide over the catabolic phase, and appropriate antibiotics. Surgical drainage or necrosectomy is indicated when lesser invasive techniques fail to improve the patient’s condition or in cases of infected pancreatic necrosis. Even in case of infected pancreatic necrosis, surgical necrosectomy can be delayed in stable patients for as long as 4 weeks by continuing antibiotics. It is wise to do a feeding jejunostomy in the first reexploration rather than rely on the disconnected gastric conduit for feeding as it may further progressively undergo necrosis, and as in our case, a second adverse event should be anticipated in the form of a splenic artery pseudoaneurysm or bleed, which may occur later.
| Conclusion|| |
Postoperative pancreatitis with pancreatic necrosis after esophagectomy remains a devastating complication with high rates of morbidity and mortality. In all postoperative cases, there is a wide spectrum of causes and interplay of multiple factors that it might be difficult to ascertain a burden of proof to a particular event, the two major events being an anastomotic leak and acute pancreatitis. A few lessons learnt from the aforementioned case report are as follows: preoperatively, avoiding the probable offending drugs and immediately reviewing the drug chart of patient to stop drugs that may worsen the pancreatitis; intraoperatively, preventing hypotensive episodes and careful tissue handling of the pancreas; and postoperatively, high levels of drain amylase on POD 1, (if anastomotic leak is ruled out and intraoperatively if the pancreas has been handled) should be high index of suspicion for postoperative pancreatitis. Prognosis is grave, and its management may require multiple reexplorations, surgical necrosectomy, and prolonged intensive care but may ultimately save the patient as it happened in our case.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
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[Figure 1], [Figure 2]