History Of Alcoholic Pancreatitis Research Articles

Robotic Puestow for Chronic Pancreatitis

Introduction: Patients with chronic pancreatitis often present with debilitating pain that limits their day to day function. Numerous drainage and resection procedures have been described. For patients with dilation of the pancreatic duct, a lateral pancreaticojejunostomy (Puestow) can offer significant relief. These patients often have difficult pain control postoperatively due to chronic pain and a minimally invasive approach may offer a benefit. Methods: The accompanying figure demonstrates representative views from a video of a robotic Puestow. The patient had a history of alcoholic pancreatitis, with daily narcotic use. Imaging demonstrated dilated pancreatic duct to 11 mm with presence of intraductal stones, without significant disease in the head. She was motivated to pursue surgery and abstained from alcohol and tobacco products. The da Vinci Xi robotic system was used. The gastrocolic ligament was opened and gastropancreatic folds were divided. The superior and inferior borders of the pancreas were mobilized and a pancreatic ultrasound was performed to delineate the extent of duct dilation. The gastroepiploic vein and gastroduodenal artery were divided to access the neck and head of the pancreas. A longitudinal pancreatic ductotomy was created with cautery and stones were retrieved (top panel). A pancreaticojejejunal anastomosis was created in two layers using V-Loc sutures (bottom panel). Results: The patient recovered uneventfully and was discharged on POD 5. The patient was able to decrease her narcotic use with significant symptomatic improvement. Conclusion: Minimally invasive approaches to management of chronic pancreatitis should be considered to expedite recovery and weaning from narcotics.

PANCREATICO-PLEURAL FISTULA AND SUBSEQUENT FUNGAL EMPYEMA

SESSION TITLE: Medical Student/Resident Chest Infections Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: A rare pancreatitis complication is pancreatico-pleural fistula with empyema development being even more scarce. CASE PRESENTATION: A 48-year-old male with a history of alcoholic pancreatitis, subsequent mediastinitis with recurrent pleural effusions and pneumonia presented to the outpatient pulmonology office for persistent dyspnea. We ordered basic labs, showing significant leukocytosis and anemia, and a thoracentesis, removing 600 milliliters. Upon transferring to the hospital, further workup revealed elevated lipase and C-reactive protein. Pleural fluid studies indicated an amylase-rich exudative process. Chest-x ray showed bilateral pleural effusions and multilobar pneumonia. Computed Tomography (CT) Angiography of chest showed loculated moderate right and small left pleural effusion, multilobar pneumonia especially in lower lobes. CT of abdomen/pelvis showed acute pancreatitis and pancreatic cystic lesions in the head and uncinate process. We initiated broad coverage with Vancomycin, Cefepime, and Metronidazole. On day 3 of admission, a chest tube was placed and 6 doses of lytic therapy were administered. Endoscopic Retrograde Cholangio-Pancreatography (ERCP) was performed and confirmed pancreatico-pleural fistula (PPF). Thus, sphincterotomy was performed and a stent was placed; however, the pancreatic duct could not be cannulated. Video-Assisted Thoracoscopic Surgery was not indicated at this time. Pleural fluid cultures grew Candida Albicans and Micafungin was added. Upon receiving sensitivities, we discontinued the current regimen and started Fluconazole. Chest tube was removed on day 10 of admission. The patient was discharged home with instructions to continue Fluconazole for 6 weeks, weekly lab monitoring, repeat ERCP with pancreatic duct cannulation in 3 weeks, and repeat Chest x-ray in 2 months. DISCUSSION: PPF with pleural effusion is reported with an incidence of 0.4%. A pancreatic duct disruption causes persistent leakage of pancreatic secretions. Initially, a fluid collection forms, known as a pseudocyst. Eventually, the secretions can cause a spontaneous erosion into a neighboring organ or cavity, the pleural cavity in our case. Patients with PPF present similarly to pleural effusions, as they are recurrent and refractory to repeated thoracentesis. 1 In rare cases, an empyema can develop that can cause life-threatening sepsis. 2 Classical PPF patients are middle-aged men, chronic pancreatitis from alcoholism, dyspneic, no acute abdominal symptoms, left pleural effusions, pseudocyst on CT, and elevated pleural fluid amylase, lipase, and albumin. These were observed in our case, except bilateral pleural effusions, which has a 19% incidence compared to 74% for left sided. 1 CONCLUSIONS: As clinicians, we should consider the rare complications of PPF in the differential for patients with a history of pancreatitis presenting for dyspnea and sepsis. Reference #1: Machado, NO. Pancreaticopleural Fistula: Revisited. Diagnostic and Therapeutic Endoscopy. 2011;2012:1-5. Reference #2: Kim E, Ahn HY, Kim YD, Hoseok, Cho JS. Successful Diagnosis and Treatment of a Pancreaticopleural Fistula in a Patient Presenting with Unusual Empyema and Hemoptysis. Korean J Thorac Cardiovasc Surg. 2019;52(3):174-177. doi: 10.5090/kjtcs.2019.52.3.174. DISCLOSURES: No relevant relationships by Jacob Burch, source=Web Response No relevant relationships by James Choi, source=Web Response No relevant relationships by Rakesh Gami, source=Web Response No relevant relationships by Tyler Kemnic, source=Web Response No relevant relationships by Jason Liu Liu, source=Web Response No relevant relationships by Rohan Prasad, source=Web Response No relevant relationships by Fazal Raziq, source=Web Response No relevant relationships by Eric Smith, source=Web Response

Thiamine: An Underutilized Agent in Refractory Lactic Acidosis

SESSION TITLE: Fellow Case Report Poster - Critical Care II SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Lactic acid (LA) is a biomarker of unparalleled use in critical care practice,mainly by serving as index of perfusion and outcome predictor in circulatory and septic shock.Thiamine deficiency(TD) is an underappreciated cause of lactic acidosis in critically ill patients. Relative or absolute TD may occur de novo or develop rapidly in settings of low intake, sepsis, critical illness, alcoholism, malabsorptive states or psychiatric problems. We present a case of severe non-shock related lactic acidosis that resolved after high-dose thiamine administration. CASE PRESENTATION: A 44-year-old woman with a history of alcoholic pancreatitis,presented to the Emergency Department with epigastric pain and vomiting of 3 days duration after binge drinking with vodka. Vital signs were remarkable for temperature of 92.90F and respiratory rate of 35. She took no medications. Clinical examination was remarkable for Kussmaul’s breathing, mid-epigastric tenderness, hepatomegaly and warm extremities. Laboratory studies revealed WBC 19.2/mm3, Hb 5.8g/dL, PLT 107/mm3,pH 6.88, LA>15mmol/L, slightly elevated lipase and moderate transaminitis. She received 4 liters of normal saline, 2 units of packed red blood cells and antibiotics. LA decreased to 9.9mmol/L. TD was suspected and 500mg intravenous thiamine was given. LA levels subsequently decreased dramatically. DISCUSSION: Thiamine is an essential co-factor of aerobic glucose metabolism. TD is neither uncommon nor of negligible importance in critically ill patients. Studies report a prevalence of 10-30% among hospitalized patients not at epidemiological risk for it. Absence of “classic” symptoms and lack of point-of-care confirmatory tests make the identification of TD challenging. Interrelationship of TD and sepsis should not be ignored; therefore resuscitative efforts should be complemented by all measures targeting sepsis. Aggressive fluid resuscitation and transfusion led to a 33% decrease in LA, yet it remained markedly elevated.Additional fluids would have only led to fluid overload and associated complications. CONCLUSIONS: TD should be considered when abnormal tissue perfusion,oxygenation or medications seem unlikely causes of LA, especially when hyperlactatemia persists after fluid resuscitation. Early thiamine repletion in the appropriate context may reduce the morbidity that comes with aggressive fluid resuscitation in lactate-guided management algorithms. Reference #1: Crook M et al.Thiamine Deficiency:the importance of recognition and prompt management.Nutrition30(2014)953-954 DISCLOSURE: The following authors have nothing to disclose: Ismini Kourouni, Stefania Pirrotta, Joseph Mathew, Janet Shapiro No Product/Research Disclosure Information

A Case of Lower GI Bleeding Caused by Localized Amyloid Light-Chain Amyloidosis in the Small Intestine

Introduction: Amyloidosis is a disorder characterized by the abnormal deposition of extracellular amyloid fibrils that leads to disruption of tissue structure. Systemic amyloidosis can involve the gastrointestinal tract. The small intestine is the most commonly involved gastrointestinal site. However, cases of localized amyloid light-chain amyloidosis in the small intestine are rarely reported. Here we report a case of primary amyloidosis only in the small intestine without any other organ involvement. Case: A 73-year-old male with history of alcoholic pancreatitis, hypertension was transferred to our hospital with complaints of hematochezia before 2 days ago. Laboratory tests revealed that serum hemoglobin level decreased from 11.6 to 7.7 g/dL. There was no bleeding focus on gastroduodenoscopic and colonoscopic examination. Contrast enhanced CT enterography for evaluation of small bowel bleeding showed that two sites of aneurysmal dilatation of small bowel loops with concentric wall thickening (Figure 1a, 1b). Balloon enteroscopy to examine the lesions in the small bowel detected cystic mucosal lesion with hemorrhagic surface change with easily touch bleeding below the 2nd portion of duodenum (Figure 2a). For control of bleeding, he underwent surgery of small bowel resection. There were 2 segmental lesions (5cm in the jejunum, 8cm in the ileum) of small bowel wall dilatation. Also small bowel between the lesions showed distended and edematous in the operation finding (Figure 2b). Histologic examination of the specimen revealed amyloid deposition (Figure 3a) and positive Congo red staining in the small intestine (Figure 3b). According to the results of immunohistochemistry, deposits of amyloid were positive for amyloid kappa (Figure 3c), lambda (Figure 3d), but negative for amyloid A. Therefore the results were indicative of amyloid light-chain (AL) amyloidosis. Bone marrow biopsy for evaluation of systemic amyloidosis founded that no definite evidence of plasma cell disorder. Serum and urine electrophoresis revealed no monoclonal gammopathy. There was no evidence of other organ involvement. In conclusion, he was diagnosed with localized AL amyloidosis in the small intestine. He was followed-up as an outpatient without history of re-bleeding and complaining of other symptom.Figure 1Figure 2Figure 3Conclusion: Localized amyloidosis in the small intestine can manifest the symptom of lower GI bleeding. Because our patient underwent resection of involved small intestine without any other treatment, it needs to follow-up about progression to systemic disease, re-bleeding and any other complications.

Complicated pancreatic disease management--radiologist/interventionist batting cleanup?

Abstract The long term results of various interventional procedures used in the treatment of patients with chronic pancreatic fistulas or severe pancreatic pain syndrome, after failure of both surgery and endoscopic catheterization, are described. Five patients were divided into two groups. Group 1 contained three patients with recurrent severe abdominal pain with superimposed episodes of acute pancreatitis. Two patients had undergone prior Whipple procedures but remained symptomatic. The third had a 6-yr history of alcoholic pancreatitis. All three had failed selective pancreatic endoscopy because of a proximal pancreatic duct stricture. The pancreatic duct was dilated to between 7 and 10 mm by CT or ultrasound imaging. Group 2 patients had pancreaticocutaneous fistulas that developed after surgical and percutaneous pseudocyst drainage. Both patients’ fistulas had been unresponsive to therapy with somatostatin analogues, and had been controlled by means of percutaneous drains. Patients were treated under either general anesthesia (two patients, patient preference) or conscious sedation. Each received preprocedure antibiotics and had normal coagulation profiles. Oral contrast was given to opacify the colon the night before the procedure. Ultrasound or fluoroscopic guidance was used to puncture the pancreatic duct, either directly or through the stomach (after placement of T fasteners). The procedures were then individualized to fit the particular pathology and anatomical situation. At least one procedure required endoscopic assistance (rendezvous procedure) for guidewire stabilization to deliver an angioplasty catheter across a pancreatic duct stricture. The criteria for successful treatment included partial or complete relief of abdominal pain, with normalization of pancreatic duct caliber in group 1 and cure of the pancreatic fistulas in group 2 without recurrent episodes of pancreatitis. All three patients in group 1 had prompt relief of abdominal pain after placement of percutaneous pancreatic duct drains. All had return to normal caliber of the pancreatic duct by imaging. One patient had a recurrent episode of abdominal pain after drain removal, but this was found to be due to a ureteral stricture. The details of the procedures for treating the fistulas have been previously reported (1) . Cope and colleagues’ report assesses long term efficacy of these interventions. Both patients with fistulas were cured out to 5-yr follow-up after removal of their drains. None of these percutaneous procedures showed early complications such as leakage of pancreatic juice, sepsis, hemorrhage, or acute pancreatitis, as determined symptomatically by hematological screening and abdominal imaging. The authors conclude that percutaneous pancreatic duct drainage and stent placement is safe in selected cases. It is particularly useful when endoscopic stent placement is unsuccessful and surgery too risky. They also suggest several other situations in which this technique may be beneficial.

Complicated pancreatic disease management—radiologist/interventionist batting cleanup?

The long term results of various interventional procedures used in the treatment of patients with chronic pancreatic fistulas or severe pancreatic pain syndrome, after failure of both surgery and endoscopic catheterization, are described. Five patients were divided into two groups. Group 1 contained three patients with recurrent severe abdominal pain with superimposed episodes of acute pancreatitis. Two patients had undergone prior Whipple procedures but remained symptomatic. The third had a 6-yr history of alcoholic pancreatitis. All three had failed selective pancreatic endoscopy because of a proximal pancreatic duct stricture. The pancreatic duct was dilated to between 7 and 10 mm by CT or ultrasound imaging. Group 2 patients had pancreaticocutaneous fistulas that developed after surgical and percutaneous pseudocyst drainage. Both patients’ fistulas had been unresponsive to therapy with somatostatin analogues, and had been controlled by means of percutaneous drains. Patients were treated under either general anesthesia (two patients, patient preference) or conscious sedation. Each received preprocedure antibiotics and had normal coagulation profiles. Oral contrast was given to opacify the colon the night before the procedure. Ultrasound or fluoroscopic guidance was used to puncture the pancreatic duct, either directly or through the stomach (after placement of T fasteners). The procedures were then individualized to fit the particular pathology and anatomical situation. At least one procedure required endoscopic assistance (rendezvous procedure) for guidewire stabilization to deliver an angioplasty catheter across a pancreatic duct stricture. The criteria for successful treatment included partial or complete relief of abdominal pain, with normalization of pancreatic duct caliber in group 1 and cure of the pancreatic fistulas in group 2 without recurrent episodes of pancreatitis. All three patients in group 1 had prompt relief of abdominal pain after placement of percutaneous pancreatic duct drains. All had return to normal caliber of the pancreatic duct by imaging. One patient had a recurrent episode of abdominal pain after drain removal, but this was found to be due to a ureteral stricture. The details of the procedures for treating the fistulas have been previously reported (1). Cope and colleagues’ report assesses long term efficacy of these interventions. Both patients with fistulas were cured out to 5-yr follow-up after removal of their drains. None of these percutaneous procedures showed early complications such as leakage of pancreatic juice, sepsis, hemorrhage, or acute pancreatitis, as determined symptomatically by hematological screening and abdominal imaging. The authors conclude that percutaneous pancreatic duct drainage and stent placement is safe in selected cases. It is particularly useful when endoscopic stent placement is unsuccessful and surgery too risky. They also suggest several other situations in which this technique may be beneficial.