VG Med IF 001SM stomach herniation of stomach, compressive atelectasis Paraesophageal hernia, gastric volvulus CT stomach herniation of stomach, compressive atelectasis Paraesophageal hernia, gastric volvulus CT 79F N/V and abdominal pain
<
<
Sidney Messier MS4
Paraesophageal Hernia with Gastric Volvulus and Compressive Atelectasis CT abdomen and chest, axial and coronal planes, demonstrate herniation of the stomach through the esophageal hiatus into the thoracic cavity, consistent with a paraesophageal hiatal hernia. The gastric fundus and body are displaced superiorly with an abnormal organoaxial rotation, and there is associated compressive atelectasis of the adjacent left lower lobe. Findings are characteristic of a paraesophageal hernia complicated by gastric volvulus, a condition that may present with nausea, vomiting, and epigastric pain due to mechanical obstruction or vascular compromise. Differential considerations for a large retrocardiac mass on imaging include hiatal hernia, mediastinal cyst, or diaphragmatic hernia; however, the presence of rugal folds and intrathoracic stomach contour confirms the diagnosis. (PMID: 35549254) Prompt recognition is essential as volvulus can progress to ischemia or perforation, requiring urgent surgical evaluation. Chronic cases may cause postprandial fullness, dyspnea, or anemia from Cameron ulcers. (PMID: 29261800) Paraesophageal hernias differ from sliding hernias in that the gastroesophageal junction remains fixed below the diaphragm while the gastric fundus herniates above, increasing risk for strangulation. Sidney Messier MS4 – TheCommonVein.com (001SM)
2. Findings
Sidney Messier MS4
herniation compressive atelectasis
Paraesophageal Hernia
Gastric Volvulus
Finding
Definition
Comment
Paraesophageal Hernia
A type of hiatal hernia where the gastric fundus and/or other abdominal contents herniate into the thorax through the esophageal hiatus, adjacent to a normally positioned or displaced gastroesophageal junction.
Type II involves herniation of the fundus with a normal GE junction position, Type III is a combination of a sliding hernia and a paraesophageal hernia, and Type IV includes other abdominal organs.
This condition is present in up to 60% of individuals over 50 years old, though many remain asymptomatic.
Symptomatic patients may experience dysphagia, post-prandial pain, and reflux. Complications can be severe, including gastric volvulus, obstruction, and respiratory issues from lung compression.
Sánchez-Pernaute, A et al. World J Emerg Surg. 2025
Gastric Volvulus
An abnormal rotation of the stomach of at least 180 degrees around one of its axes, which can lead to a closed-loop obstruction, strangulation, and ischemia.
It is classified as organoaxial (rotation along the long axis, more common in adults) or mesenteroaxial (rotation along the short axis).
Gastric volvulus is a rare but potentially life-threatening surgical emergency.
It is most commonly a complication of a paraesophageal hernia. The classic presentation is Borchardt’s triad: severe epigastric pain, intractable retching without vomiting, and the inability to pass a nasogastric tube.
Patel, S et al. StatPearls. 2024
Compressive Atelectasis
A form of lung collapse caused by external pressure on the lung tissue.
In the context of a large paraesophageal hernia, herniated abdominal contents increase intrathoracic pressure, compressing the adjacent lung parenchyma and leading to volume loss.
While respiratory symptoms like dyspnea can occur with large hernias, significant atelectasis is a rare complication.
The mechanical compression reduces transmural pressure across the alveoli, causing them to collapse. This finding highlights the significant mass effect that a large intrathoracic hernia can exert.
Gastric volvulus is an abnormal rotation of the stomach of more than 180 degrees around one of its axes, which can lead to a closed-loop obstruction.
When it occurs in the context of a paraesophageal hernia (PEH), it signifies the herniation of the stomach through the esophageal hiatus with subsequent twisting.
Paraesophageal hernias are characterized by the herniation of the gastric fundus, and potentially other portions of the stomach, into the thoracic cavity adjacent to the esophagus, while the gastroesophageal junction may remain in its normal intra-abdominal position (Type II) or be displaced into the thorax as well (Type III, mixed).
Cause
Gastric volvulus can be primary, due to the laxity of the gastric ligaments (gastrohepatic, gastrocolic, gastrosplenic, and gastrophrenic), or secondary to an underlying anatomical abnormality.
The most common predisposing factor for secondary gastric volvulus is a paraesophageal hiatal hernia.
Other risk factors include advanced age, other diaphragmatic defects such as traumatic rupture or phrenic nerve paralysis, and previous gastroesophageal surgery.
Large paraesophageal hernias, which allow for increased gastric mobility within the chest, significantly elevate the risk of volvulus.
Pathophysiology
The development of gastric volvulus in a PEH involves the rotation of the herniated stomach around an axis.
The most common type is organoaxial volvulus (approximately 59-74% of cases), where the stomach rotates along its long axis, connecting the cardia and the pylorus. This often results in the greater curvature moving superiorly while the lesser curvature moves inferiorly.
The less common mesenteroaxial volvulus involves rotation around the short axis, perpendicular to the long axis, which can displace the antrum superior to the gastroesophageal junction.
Rotation exceeding 180 degrees can cause a closed-loop obstruction of both the gastric inlet and outlet.
This obstruction leads to progressive gastric distention from trapped fluid and gas, which increases intragastric pressure.
The twisting of the gastric mesentery can compromise the blood supply, leading to venous congestion, ischemia, necrosis, and eventual perforation.
Strangulation is a significant risk, particularly with acute organoaxial volvulus.
Structural Result
The anatomical derangement involves the displacement of the stomach into the thoracic cavity, with the fundus and/or body situated above the diaphragm.
In organoaxial volvulus, this leads to an inversion of the stomach’s normal orientation.
The rotation can create a physical obstruction at the gastroesophageal junction and the pylorus.
Persistent obstruction and ischemia can result in gastric wall edema, hemorrhage, mucosal ulceration, full-thickness necrosis, and perforation, leading to peritonitis or mediastinitis.
Functional Impact
The primary functional consequence is foregut obstruction.
Acute, complete obstruction presents with the Borchardt triad (seen in up to 70% of acute organoaxial cases): severe epigastric pain, intractable retching with non-productive emesis, and the inability to pass a nasogastric tube.
The obstruction prevents the passage of food and gastric secretions, leading to gastric distention and the symptoms of early satiety and postprandial fullness in chronic or intermittent cases.
Vascular compromise leads to gastric ischemia, which if not corrected, results in gastric gangrene and perforation, a state associated with sepsis and hemodynamic instability.
Imaging
Plain Radiography: Chest X-rays may reveal a retrocardiac air-fluid level or a gas-filled viscus in the lower chest, consistent with an intrathoracic stomach. Abdominal films might show a large, distended stomach with a paucity of distal bowel gas. A double air-fluid level may be seen on upright films.
Upper GI Barium Study: This is a highly sensitive and specific examination that can confirm the diagnosis by demonstrating the abnormal position and orientation of the stomach. Findings include an inverted or ‘upside-down’ stomach, positioning of the cardia and pylorus at the same level, and obstruction to the flow of contrast.
Computed Tomography (CT): CT is often the preferred modality in the emergency setting as it can rapidly confirm the diagnosis, define the type of volvulus, identify the points of torsion, and assess for complications like ischemia (seen as lack of wall enhancement or pneumatosis), perforation, and the presence of a PEH. It can show the stomach herniated into the thorax with the greater curvature lying superior to the lesser curvature in an organoaxial volvulus.
Labs
Laboratory tests are generally non-diagnostic for gastric volvulus.
Findings are often nonspecific and may reflect complications such as dehydration, electrolyte disturbances from vomiting, or sepsis from gastric necrosis.
An elevated lactate level may be present in the setting of ischemia or necrosis.
Hyperamylasemia and elevated alkaline phosphatase have been reported but are not consistent findings.
Treatment
The management of acute gastric volvulus is a surgical emergency.
Initial management includes fluid resuscitation, correction of electrolyte abnormalities, and gastric decompression via a nasogastric tube, though passage may be difficult or impossible in organoaxial volvulus.
In stable patients without signs of ischemia, endoscopic detorsion can be attempted.
Definitive treatment is surgical and involves reduction of the herniated stomach, detorsion of the volvulus, resection of any necrotic tissue, repair of the diaphragmatic hiatus (crural repair), and often an anti-reflux procedure (fundoplication) or gastropexy to prevent recurrence.
The procedure can be performed via an open or laparoscopic approach, with laparoscopy being associated with shorter hospital stays.
Prognosis
The prognosis of gastric volvulus is highly dependent on the speed of diagnosis and intervention.
In acute gastric volvulus, delays in treatment can lead to gastric strangulation and necrosis, which significantly increases mortality.
The mortality rate for an acute volvulus can range from 30% to 50% when complicated by vascular compromise.
Patients who undergo emergency surgery for gastric necrosis or perforation have a mortality rate of around 30%.
For patients treated surgically before the onset of irreversible ischemia, outcomes are generally good with minimal morbidity.
However, recurrence can occur, particularly after laparoscopic repair without adequate fixation.
Hernia: The term “hernia” originates from the Greek word “hernios,” meaning a “bud” or “shoot,” aptly describing the protrusion of an organ through an abnormal opening.
Paraesophageal: Derived from Greek “para-” (beside) and “oisophagos” (esophagus), indicating the location of the hernia adjacent to the esophagus.
Gastric: From the Greek “gaster,” meaning “stomach” or “belly.”
Volvulus: From the Latin “volvere,” which means “to roll” or “to turn,” describing the twisting of the stomach upon itself.
AKA / Terminology
Paraesophageal Hernia (PEH): Often referred to as a Type II, III, or IV hiatal hernia, depending on the extent of herniation and the position of the gastroesophageal junction. It is sometimes colloquially termed an “upside-down stomach” when the entire organ herniates into the thorax.
Gastric Volvulus: Classified by the axis of rotation: Organoaxial (rotation along the long axis from the GE junction to the pylorus, most common and often associated with PEH) or Mesenteroaxial (rotation along the short axis from the lesser to the greater curvature). A combined type also exists.
Historical Notes
The earliest written accounts of hernias appear in the Egyptian Ebers Papyrus around 1550 BC. Mummified pharaohs, including Ramses V, show evidence of inguinal hernias.
The first description of a hiatal hernia was by Bowditch in 1853. However, it was not widely recognized as a clinical entity until the first half of the 20th century.
In 1926, Åkerlund proposed the term “hiatus hernia” and classified it into the three types still used today.
The first description of gastric volvulus was by Berti in 1866 during an autopsy. The first successful operation for the condition was performed by Berg in 1896.
Early surgical attempts to treat hernias were often crude and included methods like castration. The “Age of Dissection” in the mid-1700s led to a better understanding of anatomy, paving the way for more refined techniques.
The first elective surgical repair for a hiatal hernia was reported by Angelo Soresi in 1919.
Cultural or Practice Insights
The evolution of hernia surgery reflects major shifts in medical practice. Early procedures were fraught with peril until the advent of anesthesia and Joseph Lister’s principles of antiseptic surgery in the 19th century.
Ambroise Paré’s revolutionary move away from cauterizing wounds with boiling oil to using a soothing balm marked a pivotal shift toward the “gentle art of surgery,” emphasizing minimizing patient suffering.
The understanding of hiatal hernia surgery evolved from simple anatomical repair to a more complex physiological restoration, appreciating its link to gastroesophageal reflux, a connection solidified in the 1950s by surgeons like Allison and Barrett.
Notable Figures or Contributions
Giovanni Battista Morgagni (1682-1771): Considered the father of modern pathological anatomy, he correlated clinical symptoms with post-mortem findings in his seminal work De Sedibus et Causis Morborum. He provided the first description of the anterior diaphragmatic hernia that now bears his name, the Morgagni hernia.
Ambroise Paré (1510-1590): A French barber-surgeon considered one of the fathers of surgery. He revolutionized battlefield medicine, reintroduced the use of ligatures for amputations instead of cauterization, and championed a more humane approach to patient care.
Edoardo Bassini (1844-1924): An Italian surgeon who is the progenitor of modern hernia repair. He developed a durable anatomical repair for inguinal hernias based on a deep understanding of the anatomy and was a pioneer in prospectively studying patient outcomes.
Borchardt (1904): Described the classic triad of symptoms for acute gastric volvulus: 1) severe epigastric pain, 2) retching without vomiting, and 3) the inability to pass a nasogastric tube. This triad is present in up to 70% of acute cases.
Rudolph Nissen (1896-1981): A surgeon who developed the Nissen fundoplication, a landmark procedure to correct gastroesophageal reflux, often performed in conjunction with hiatal hernia repair.
Quotes and/or Teaching Lines
“Je le pansai, Dieu le guérit” (“I bandaged him, God healed him.”) – A famous quote by Ambroise Paré, reflecting his philosophy on the role of the surgeon.
Borchardt’s Triad: The constellation of severe epigastric pain, nonproductive retching, and inability to pass a nasogastric tube is a classic teaching point for the diagnosis of acute gastric volvulus.
“There are five duties of surgery: to remove what is superfluous, to restore what has been dislocated, to separate what has grown together, to reunite what has been divided, and to redress the defects of nature.” – Ambroise Paré, outlining the scope of surgical practice in the 16th century.
1. Weakness or attenuation of which structure is the primary anatomical defect leading to the development of a paraesophageal hernia?
2. In an organoaxial gastric volvulus, which arterial supplies are most immediately at risk of compromise due to torsion and stretching, potentially leading to fundal and greater curvature ischemia?
3. A patient presenting with severe epigastric pain, nonproductive retching, and the inability to pass a nasogastric tube is exhibiting which classic clinical sign of acute gastric volvulus?
4. Hiatal hernias are classified into four types. Which type is the most common, accounting for over 90% of cases, and is characterized by the displacement of the gastroesophageal junction above the diaphragm?
5. On a contrast-enhanced CT scan, what is the key imaging feature that distinguishes a mesenteroaxial volvulus from an organoaxial volvulus?
6. In the context of a large paraesophageal hernia, what is the pathophysiological mechanism for developing compressive atelectasis?
7. A Type IV paraesophageal hernia is diagnosed on imaging when, in addition to the stomach, which other structures are seen herniating into the thoracic cavity?
Part B
1. Weakness or attenuation of which structure is the primary anatomical defect leading to the development of a paraesophageal hernia?
A) Gastrosplenic ligament
❌
Incorrect.
The gastrosplenic ligament tethers the stomach to the spleen; its laxity is associated with gastric volvulus but is not the primary cause of hiatal herniation.
B) Gastrohepatic ligament
❌
Incorrect.
The gastrohepatic ligament connects the stomach to the liver; its integrity is not the principal barrier to hiatal herniation.
C) Phrenoesophageal ligament
✅
Correct.
The phrenoesophageal ligament, an extension of the endothoracic and transversalis fascia, anchors the esophagus to the diaphragm.
Laxity or attenuation of this ligament allows for the stomach or other viscera to herniate through the esophageal hiatus.
Kahrilas PJ, World J Gastroenterol, 2008.
D) Crus of the diaphragm
❌
Incorrect.
While a widened diaphragmatic hiatus, formed by the crura, is necessary for herniation, the primary failure is the deterioration of the phrenoesophageal ligament that normally seals this junction.
2. In an organoaxial gastric volvulus, which arterial supplies are most immediately at risk of compromise due to torsion and stretching, potentially leading to fundal and greater curvature ischemia?
A) Right gastric and right gastroepiploic arteries
❌
Incorrect.
These vessels supply the pyloric end and right side of the greater curvature.
While they can be compromised, the splenic artery branches are more acutely affected in organoaxial rotation.
B) Short gastric and left gastroepiploic arteries
✅
Correct.
In organoaxial volvulus, the stomach rotates along its long axis.
This rotation stretches and can occlude the short gastric arteries and the left gastroepiploic artery, which arise from the splenic artery and supply the fundus and the superior portion of the greater curvature.
Teague WJ, J Paediatr Child Health, 2000.
C) Gastroduodenal and superior pancreaticoduodenal arteries
❌
Incorrect.
These arteries supply the duodenum and pancreas and are not directly involved in the vascular compromise of an isolated gastric volvulus.
D) Left gastric and right gastric arteries
❌
Incorrect.
The left gastric artery, supplying the lesser curvature, can be compromised.
However, the short gastric arteries supplying the fundus are typically the most vulnerable due to stretching at the gastrosplenic ligament.
3. A patient presenting with severe epigastric pain, nonproductive retching, and the inability to pass a nasogastric tube is exhibiting which classic clinical sign of acute gastric volvulus?
A) Charcot’s triad
❌
Incorrect.
Charcot’s triad (fever, jaundice, right upper quadrant pain) is associated with ascending cholangitis.
B) Borchardt’s triad
✅
Correct.
Borchardt’s triad consists of severe epigastric pain, retching without vomiting, and the inability to pass a nasogastric tube.
It is considered diagnostic for acute gastric volvulus and is present in approximately 70% of cases.
Carter R, Br J Surg, 1980.
C) Beck’s triad
❌
Incorrect.
Beck’s triad (hypotension, jugular venous distension, muffled heart sounds) is indicative of cardiac tamponade.
D) Cushing’s triad
❌
Incorrect.
Cushing’s triad (hypertension, bradycardia, irregular respirations) is a sign of increased intracranial pressure.
4. Hiatal hernias are classified into four types. Which type is the most common, accounting for over 90% of cases, and is characterized by the displacement of the gastroesophageal junction above the diaphragm?
A) Type I (Sliding)
✅
Correct.
Type I, or sliding hiatal hernia, accounts for more than 90-95% of all cases.
It is defined by the symmetrical ascent of the gastroesophageal junction through the diaphragmatic hiatus into the thorax.
Sfara A, J Med Life, 2011.
B) Type II (Paraesophageal)
❌
Incorrect.
Type II is a true paraesophageal hernia where the gastric fundus herniates alongside a normally positioned gastroesophageal junction.
It is much less common than Type I.
C) Type III (Mixed)
❌
Incorrect.
Type III is a combination of Type I and Type II, with both the gastroesophageal junction and the gastric fundus herniating into the thorax.
D) Type IV (Complex)
❌
Incorrect.
Type IV involves the herniation of the stomach plus another abdominal organ (e.g., colon, spleen) into the chest.
This is the rarest type.
5. On a contrast-enhanced CT scan, what is the key imaging feature that distinguishes a mesenteroaxial volvulus from an organoaxial volvulus?
A) The greater curvature is located superior to the lesser curvature.
❌
Incorrect.
Inversion of the greater and lesser curvatures is the characteristic feature of an organoaxial volvulus, where the stomach rotates on its long axis.
B) The stomach appears horizontally oriented in the thorax.
❌
Incorrect.
This finding is more consistent with organoaxial volvulus, where the stomach rotates along its cardiopyloric line.
C) The antropyloric region is positioned superior to the gastroesophageal junction.
✅
Correct.
In a mesenteroaxial volvulus, the stomach rotates around its short axis (perpendicular to the cardiopyloric line).
This results in an “upside-down” stomach, where the antrum and pylorus are displaced superiorly, often lying above the level of the fundus and gastroesophageal junction.
Peterson CM, Radiographics, 2009.
D) A “bird’s beak” sign is seen at the point of torsion.
❌
Incorrect.
A “beaking” or tapering at the point of obstruction can be seen in both types of volvulus and is not a specific distinguishing feature between them.
It indicates the location of the twist.
6. In the context of a large paraesophageal hernia, what is the pathophysiological mechanism for developing compressive atelectasis?
A) Direct phrenic nerve palsy from the herniated sac.
❌
Incorrect.
While phrenic nerve injury is a known complication of surgery in this area, it is not the primary mechanism of atelectasis from the hernia itself.
B) Increased intrapleural pressure and mass effect from the intrathoracic stomach.
✅
Correct.
A large intrathoracic hernia exerts a significant mass effect, compressing the adjacent lung parenchyma.
This reduces transmural pressure, leading to alveolar collapse and the development of compression (or passive) atelectasis.
Naunheim KS, Ann Thorac Surg, 2004.
C) Aspiration pneumonitis leading to parenchymal consolidation.
❌
Incorrect.
While aspiration is a risk with large hernias due to GERD and obstruction, it leads to inflammatory consolidation, which is a different entity from compressive atelectasis.
D) Bronchial obstruction from direct compression by the herniated organ.
❌
Incorrect.
While theoretically possible, direct bronchial obstruction is extremely rare.
The more common mechanism is diffuse compression of the lung parenchyma rather than focal airway obstruction.
7. A Type IV paraesophageal hernia is diagnosed on imaging when, in addition to the stomach, which other structures are seen herniating into the thoracic cavity?
A) Only omentum
❌
Incorrect.
Herniation of omentum along with the stomach is common but does not by itself define a Type IV hernia.
B) Other abdominal organs such as the colon, spleen, or small intestine
✅
Correct.
A Type IV hernia is characterized by a large diaphragmatic defect that allows other abdominal organs (most commonly the colon, spleen, omentum, or small intestine) to herniate into the chest alongside the stomach.
Luketich JD, J Am Coll Surg, 2012.
C) The duodenum and head of the pancreas
❌
Incorrect.
The duodenum and pancreatic head are retroperitoneal structures and are exceptionally rarely involved in hiatal hernias.
D) The liver and gallbladder
❌
Incorrect.
Herniation of the liver is extremely rare and not the defining feature of a Type IV paraesophageal hernia.
