Gastric volvulus implies torsion of the stomach to 180° or more along 1 of its 2 axes: the vertical axis connecting the esophagus to the greater curvature (omento-axial), or the horizontal axis between the greater and lesser curvatures (mesentero-enteric).4 Gastric volvulus can be primary or secondary. Primary gastric volvulus (one third of cases) occurs below the diaphragm in the absence of any diaphragmatic or intra-abdominal abnormality and results from slack gastric stabilizing ligaments. Secondary gastric volvulus (the other two thirds of cases) develops above the diaphragm, usually in the setting of a pre-existing diaphragmatic defect. Six percent of cases of gastric volvulus occur in pediatric patients.4 Most, however, occur in the 5th decade of life due to predisposing conditions, such as a paraesophageal hiatal hernia, trauma to the diaphragm, or diaphragmatic paralysis.4 The prevalence of diaphragmatic herniation, recently recognized as a complication after LVAD explantation, has been reported to be as high as 15.9% for unrepaired defects versus 4.3% for defects that are repaired at the time of explantation.1–3 To the best of our knowledge, gastric volvulus in such a patient has not previously been reported.
The clinical symptoms of gastric volvulus vary from acute to chronic, depending on the degree of obstruction of the lumen and on the presence or absence of strangulation of the blood supply to the gastric wall.5 Patients who have acute symptoms tend to present with sudden, severe pain localized to the upper abdomen or lower chest. On physical examination, the upper abdomen is often distended and is occasionally tympanic. Untreated, these patients can die of such complications as ulceration, perforation, hemorrhage, pancreatic necrosis, and omental avulsion.5,6 Of note, rare cases of cardiac tamponade due to a severely distended intra-thoracic stomach have also been reported.7,8 The chronic symptoms usually include vague upper abdominal or respiratory complaints, which are difficult to directly ascribe to underlying gastric volvulus.
Gastric volvulus is generally diagnosed by means of radiology. Initial suspicion arises from the identification of abnormal gas shadows in the upper abdomen or lower chest on plain radiography. Computed tomographic scanning with oral contrast medium or esophagogram can then be used to establish the diagnosis and define the gastric anatomy.9 Laboratory test results, including elevated amylase or alkaline phosphatase, are not sufficiently specific to be useful in the diagnosis.
Early recognition and prompt surgical correction are the mainstays of therapy for gastric volvulus.10 Mortality rates as high as 30% to 50% have been reported when complications of unoperated gastric volvulus develop. Surgical options include open or laparoscopic reduction of the hernia.11 If the stomach is found to be necrotic intraoperatively, partial or full resection also becomes necessary. Otherwise, reduction of the volvulus should be followed either by fixation of the stomach within the abdomen or by correction of the predisposing factors mentioned above. A midline abdominal laparotomy is generally the preferred approach.1 In patients who have acute obstruction, decompression of the stomach via nasogastric suction can help relieve symptoms before surgery.
This case highlights the need for increased awareness of the diaphragmatic complications that can occur after LVAD explantation so that appropriate tests can be ordered to make an early diagnosis. It also emphasizes the need for primary repair of all diaphragmatic defects remaining after LVAD explantation in order to prevent this life-threatening complication.