There is ample clinical evidence suggesting that the presence of large axial or paraesophageal hernias may lead to iron deficiency anemia.So-called Cameron lesions,as well as other small mucosa erosions,in the sliding...There is ample clinical evidence suggesting that the presence of large axial or paraesophageal hernias may lead to iron deficiency anemia.So-called Cameron lesions,as well as other small mucosa erosions,in the sliding area of these diaphragmatic hernias lead to invisible chronic blood loss and consequently to iron depletion.While the spectrum of symptoms in these patients is large,anemia is often not the only indication and typically not the primary indication for surgical correction of diaphragmatic hernias.Drug treatment with proton pump inhibitors and iron substitution can alleviate anemia,but this is not always successful.To exclude other possible bleeding sources in the gastrointestinal tract,a comprehensive diagnostic program is necessary and reviewed in this manuscript.Additionally,we discuss controversies in the surgical management of paraesophageal hernias.展开更多
Background: Historically, the pathophysiology of Hiatal Hernias (HH) has not been fully understood. As a result, the surgical therapy of HH has focused primarily on gastrointestinal symptoms and Gastroesophageal Reflu...Background: Historically, the pathophysiology of Hiatal Hernias (HH) has not been fully understood. As a result, the surgical therapy of HH has focused primarily on gastrointestinal symptoms and Gastroesophageal Reflux (GERD). This treatment strategy has been associated with poor relief of symptoms and poor long-term outcomes. In fact, until recently, most patients with HH have been watched and referred for surgery as a last resort. Recent experience has shown that a large (giant) Hiatal Hernia (GHH) is a common problem known to impact adjacent organs such as the hearts and lungs. Those referred for surgical repair often complain of dyspnea, which is erroneously attributed to pulmonary compression or aspiration, but has been shown to be from tamponade caused from compression of the heart by herniated abdominal contents. This article reviews the present understanding of GHH, the cardiac complications which result from GHH, and the most advanced robotic minimally invasive surgical approach to the anatomic and physiologic repair of GHH. Methods: In a prospective cohort study, we evaluated patients undergoing RRHH with at least a 2-year follow-up. All patients undergoing elective (RRHH) were identified preoperatively and enrolled prospectively in this study. Preoperative characteristics, medical comorbidities, and clinical information were all recorded prospectively and recorded into a secure surgical outcomes database. All patients received the previously validated Gastroesophageal Reflux Disease-Health-Related Quality of Life (GERD-HRQL) questionnaire preoperatively and at postoperative time points of 1 month, 1 year, and 2 years. Patients routinely had a barium swallow postoperatively before discharge but did not undergo a barium swallow, an endoscopy, or a CT scan study at the 1-month time point unless indicated by symptoms. At 6 months, 1 year, and yearly intervals thereafter, all patients received an endoscopy study to ascertain the presence of a recurrence, regardless of symptoms. Recurrence was defined as over 2 cm or 10% of the stomach above the diaphragm detected by CT, esophagogram or endoscopy. In addition, an extensive search was conducted using Pub Med in order to extract references to the cardiovascular complications of HH. Results: 423 patients underwent RRHH. With a long-term follow-up, there was a significant decrease in the Median Symptom Severity Score from 42.0 preoperatively, to 3.0 postoperatively. Recurrence was seen in 5 patients (5/423) for a recurrence rate of 1.1%. Conclusion: This experience has been the basis of two important realizations: 1) all patients with GHH have at least some degrees of clinically relevant compression of the inferior vena cava and the left atrium which causes tamponade and cardiogenic dyspnea which completely resolves after successful surgical repair;and 2) primary care providers and gastroenterologists who usually treat patients for GHH repair rarely recognize cardiac compression and tamponade as the cause of the shortness of breath and gradual increase in dyspnea on exertion and progressive fatigability in these patients. This article reviews the present understanding of GHH, the cardiac complications which result from GHH and the most advanced robotic minimally invasive surgical approach to the anatomic and physiologic repair of GHH.展开更多
文摘There is ample clinical evidence suggesting that the presence of large axial or paraesophageal hernias may lead to iron deficiency anemia.So-called Cameron lesions,as well as other small mucosa erosions,in the sliding area of these diaphragmatic hernias lead to invisible chronic blood loss and consequently to iron depletion.While the spectrum of symptoms in these patients is large,anemia is often not the only indication and typically not the primary indication for surgical correction of diaphragmatic hernias.Drug treatment with proton pump inhibitors and iron substitution can alleviate anemia,but this is not always successful.To exclude other possible bleeding sources in the gastrointestinal tract,a comprehensive diagnostic program is necessary and reviewed in this manuscript.Additionally,we discuss controversies in the surgical management of paraesophageal hernias.
文摘Background: Historically, the pathophysiology of Hiatal Hernias (HH) has not been fully understood. As a result, the surgical therapy of HH has focused primarily on gastrointestinal symptoms and Gastroesophageal Reflux (GERD). This treatment strategy has been associated with poor relief of symptoms and poor long-term outcomes. In fact, until recently, most patients with HH have been watched and referred for surgery as a last resort. Recent experience has shown that a large (giant) Hiatal Hernia (GHH) is a common problem known to impact adjacent organs such as the hearts and lungs. Those referred for surgical repair often complain of dyspnea, which is erroneously attributed to pulmonary compression or aspiration, but has been shown to be from tamponade caused from compression of the heart by herniated abdominal contents. This article reviews the present understanding of GHH, the cardiac complications which result from GHH, and the most advanced robotic minimally invasive surgical approach to the anatomic and physiologic repair of GHH. Methods: In a prospective cohort study, we evaluated patients undergoing RRHH with at least a 2-year follow-up. All patients undergoing elective (RRHH) were identified preoperatively and enrolled prospectively in this study. Preoperative characteristics, medical comorbidities, and clinical information were all recorded prospectively and recorded into a secure surgical outcomes database. All patients received the previously validated Gastroesophageal Reflux Disease-Health-Related Quality of Life (GERD-HRQL) questionnaire preoperatively and at postoperative time points of 1 month, 1 year, and 2 years. Patients routinely had a barium swallow postoperatively before discharge but did not undergo a barium swallow, an endoscopy, or a CT scan study at the 1-month time point unless indicated by symptoms. At 6 months, 1 year, and yearly intervals thereafter, all patients received an endoscopy study to ascertain the presence of a recurrence, regardless of symptoms. Recurrence was defined as over 2 cm or 10% of the stomach above the diaphragm detected by CT, esophagogram or endoscopy. In addition, an extensive search was conducted using Pub Med in order to extract references to the cardiovascular complications of HH. Results: 423 patients underwent RRHH. With a long-term follow-up, there was a significant decrease in the Median Symptom Severity Score from 42.0 preoperatively, to 3.0 postoperatively. Recurrence was seen in 5 patients (5/423) for a recurrence rate of 1.1%. Conclusion: This experience has been the basis of two important realizations: 1) all patients with GHH have at least some degrees of clinically relevant compression of the inferior vena cava and the left atrium which causes tamponade and cardiogenic dyspnea which completely resolves after successful surgical repair;and 2) primary care providers and gastroenterologists who usually treat patients for GHH repair rarely recognize cardiac compression and tamponade as the cause of the shortness of breath and gradual increase in dyspnea on exertion and progressive fatigability in these patients. This article reviews the present understanding of GHH, the cardiac complications which result from GHH and the most advanced robotic minimally invasive surgical approach to the anatomic and physiologic repair of GHH.
