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Strangulated parahiatal hernia: Not just another paraesophageal hernia
CASE REPORTS
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Strangulated Parahiatal Hernia: Not Just Another Paraesophageal Hernia Todd L. Demmy, MD, Theresa M. Boley, RN-C, MSN, and Jack J. Curtis, MD Division of Cardiothoracic Surgery, University of Missouri, Columbia, Missouri
Exploratory thoracotomy was necessary to establish the diagnosis of a rare incarcerated parahiatal hernia. Symptomatology, signs, and radiographic findings are compared with those of paraesophageal hernias. (Ann Thorae Surg 1994;58:226-7)
P
arahiatal hernia is an extremely rare abnormality that occurs from muscular diaphragmatic defects separate from the esophageal hiatus [1]. Its rarity has led to doubts regarding its existence [2]. A 48-year-old woman presented 7 days after the acute onset of upper abdominal pain that was sharp and radiated from beneath her left breast into her back. She complained of progressive shortness of breath, and 2 days before admission a nonproductive cough developed. She had episodic nausea and emesis but at the time of admission was tolerating a regular diet with a diminished appetite. There was no history of previous trauma. Physical examination showed an obese woman in no acute distress. Her vital signs included a temperature of 37.8°C, a pulse of 110 beats/min, and a respiratory rate of 18 breaths/min. There were decreased breath sounds and dullness to percussion in the left lower hemithorax. Stool guaiac test was negative. Her white blood cell count was 13,100 IJL The admission chest roentgenogram showed a large left pleural effusion but no air-fluid level. Diagnostic thoracentesis yielded sterile blood-tinged exudative fluid. Repeat chest roentgenogram demonstrated a retrocardiac air-fluid level for which a computed tomographic scan and emergency esophagogram were obtained (Fig 1). Exploratory left thoracotomy revealed a perforated necrotic stomach, densely adherent to the left lower lobe. The stomach had herniated and strangulated through a small (1 to 2 em) diaphragmatic defect that was separate from and 4 ern lateral to the esophageal hiatus. The diaphragmatic defect was extended radially and the stomach was repaired in two layers. The diaphragm was closed with a monofilament nonabsorbable suture and the pleura was decorticated and drained. Her postoperative course was complicated by sepsis from a subpulmonic empyema that was drained via a posterior seventh rib resection on the 14th postoperative day. Eventually, the patient made slow progress and was discharged on the 42nd postoperative day. Accepted for publication Oct 5, 1993. Address reprint requests to Dr Demmy, Division of Cardiothoracic Surgery, University of Missouri, 245 Major Hall, Dc119.0, Columbia, MO 65212.
© 1994 by The Society of Thoracic Surgeons
Comment Typical paraesophageal hernias occur "naturally" through gradually enlarging defects in the phrenoesophagealligament. They may occur postoperatively through a surgically enlarged esophageal hiatus or a defect like the relaxing diaphragm incision used in early Belsey antireflux operations [3]. In this latter group, the defect is separated from esophageal hiatus and mimics the rare naturally occurring parahiatal hernia. Failure of the embryonic pleuroperitoneal canal to obliterate is the theory for the etiology of naturally occurring parahiatal hernias [4]. The distance between the hernia and the hiatus will determine the distortion of the esophagogastric junction and the resultant symptoms (Fig 2). Paraesophageal hernia symptoms may be grouped conveniently into those of obstruction (nausea, vomiting, dysphagia) and those that indicate problems caused by the distended herniated stomach (pain, bleeding from
A
B
Fig 1. (A) Computed tomogram of incarcerated parahiatal hernia showingan air-fluid leveland surrounding effusion. Inset shows corresponding lateral chest roentgenogram with retrocardiac air-fluid level. (B) Gastrografin (Squibb Diagnostic, Princeton, NJ) swallow shows no abnormality at the esophagogastric junction. Although no gastric abnormalities were identified originally on this limited examination, thereappears to be a gastric deformity corresponding to the hernia site (arrow). 0003-4975/94/$7.00
CASE REPORT MULDER ET AL POST-ARTERIAL SWITCH COARCTATION
Ann Thorac Surg
1994;58:227-9
227
7. Vallieres E, Waters PF. Incarcerated parahiatal hernia with
gastric necrosis. Ann Thorac Surg 1987;44:82-3. 8. Pearson FG, Cooper JD, lives R, Todd TRJ, Jamieson WRE. Massive hiatal hernia with incarceration: a report of 53 cases. Ann Thorac Surg 1983;35:45-51.
Fig 2. The morecommon paraesophageal herniation (left) and the rare parahiatal hernia (right) are differentiated by the interveningdiaphragmatic muscle in the latter.
gastric venous obstruction, anemia, respiratory distress from lung compression) [1-3, 5-8]. Most of our patient's symptoms were in this second group. Her vomiting was a transient early symptom, and her barium swallow did not show esophageal obstruction. The patient's radiographic findings were similar to reports of incarcerated paraesophageal hernias with an elevated left hemidiaphragm and an air-fluid level in the left lower chest. However, the hernia orifice was sufficiently tight to prevent filling of the incarcerated segment with contrast from the upper gastrointestinal or the computed tomographic examination. Therefore, although contrast studies are usually helpful in the diagnosis of paraesophageal hernias, the radiographic absence of obstruction or supradiaphragmatic contrast may not exclude the diagnosis of parahiatal hernia. Incarcerated parahiatal hernias may be less virulent than their paraesophageal counterpart when they are smaller and allow less stomach to herniate and necrose. The bridge of diaphragm muscle may prevent gastric inversion and volvulus that is associated with a rapidly lethal clinical course in paraesophageal hernias [2]. Earlier diagnosis in this patient may have been made by dismissing lung abscess as a diagnosis because of the paucity of pulmonary symptoms. Focusing on the abdominal complaints and performing gastroscopy could have been diagnostic. This case report further substantiates the existence of parahiatal hernias. The relative lack of obstructive symptoms or radiographic findings is due to separation of the hernia from the esophageal hiatus and warrants distinction of this entity from true paraesophageal hernias.
Coarctation Developing After Arterial Switch Repair for Transposition of the Great Arteries Han J. G. H. Mulder, MD, Gilles L. Kaan, MD, Aagje Nijveld, MD, Anton van Oort, MD, Jelle Barentsz, MD, and Leon K. Lacquet, MD Departments of Thoracic and Cardiac Surgery, Pediatric Cardiology, and Radiology, University Hospital St. Radboud, Nijmegen, the Netherlands
We describe 2 patients with simple transposition of the great arteries in whom coarctation of the aorta developed after uncomplicated arterial switch operation. Both patients showed no symptoms or signs of this coarctation at the time of arterial switch operation. (Ann Thorae Surg 1994;58:227-9)
D
uring the past 10 years the neonatal arterial switch operation (ASO) has found increasing favor as the therapy of choice for transposition of the great arteries (TGA) [I, 2]. Midterm follow-up results support the theoretic advantages of the ASO. The main late complications seem to be pulmonary stenosis and aortic regurgitation [3]. Complete TGA associated with coarctation of the aorta (CoA) is a known and not so rare anatomic entity [4]. Very rare is the development of CoA after the ASO. Muster and associates [5] reported 3 patients with TGA in whom kinking of the aortic arch developed after ASO, resulting in a "nee-coarctation." Di Donato and colleagues [6] presented, as an incidental finding, a TGA patient in whom a genuine CoA developed after ASO. We present 2 patients in whom a typical, isthmus CoA developed after uncomplicated ASO for simple TGA.
Case Reports
Patient 1 References 1. Ellis FH. Diaphragmatic hiatal hernias: recognizingand treating the major types. Postgrad Med 1990;88:113-24.
2. Hill LD. Incarcerated paraesophageal hernia: a surgical emergency. Am J Surg 1973;126:286-91. 3. Streitz JM, Ellis FH. Iatrogenic paraesophageal hiatus hernia. Ann Thorac Surg 1990;50:446-9. 4. Wells LJ. Development of the human diaphragm and pleural sacs. In: Contributions to embryology. Washington, DC: Carnegie Institute, 1954;35:109-34. 5. Borchardt M. Zur Pathologie und Therapie des MagenvolvuIus. Arch Klin Chir 1904;74:244--60. 6. Ozdemir LA, Burke WA, Ikins PM. Paraesophageal hernia: a life-threatening disease. Ann Thorac Surg 1973;16:547-54. © 1994 by The Society of Thoracic Surgeons
Patient 1 is a boy operated on for TGA at the age of 2 days and weight of 3,400 g. The preoperative morphologic diagnosis was based on echocardiography. Specific attention was paid to a possible CoA, but it was excluded before and after prostaglandin treatment. External pressure measurements of arms and legs showed no difference. The ASO was performed with an uncomplicated postoperative course. Accepted for publication Oct 13, 1993. Address reprint requests to Dr Kaan, Department of Thoracic and Cardiac Surgery, University Hospital St. Radboud, Box 9101, 6500 HB Nijmegen, the Netherlands.
0003-4975/94/$7.00
_
Strangulated Parahiatal Hernia: Not Just Another Paraesophageal Hernia Todd L. Demmy, MD, Theresa M. Boley, RN-C, MSN, and Jack J. Curtis, MD Division of Cardiothoracic Surgery, University of Missouri, Columbia, Missouri
Exploratory thoracotomy was necessary to establish the diagnosis of a rare incarcerated parahiatal hernia. Symptomatology, signs, and radiographic findings are compared with those of paraesophageal hernias. (Ann Thorae Surg 1994;58:226-7)
P
arahiatal hernia is an extremely rare abnormality that occurs from muscular diaphragmatic defects separate from the esophageal hiatus [1]. Its rarity has led to doubts regarding its existence [2]. A 48-year-old woman presented 7 days after the acute onset of upper abdominal pain that was sharp and radiated from beneath her left breast into her back. She complained of progressive shortness of breath, and 2 days before admission a nonproductive cough developed. She had episodic nausea and emesis but at the time of admission was tolerating a regular diet with a diminished appetite. There was no history of previous trauma. Physical examination showed an obese woman in no acute distress. Her vital signs included a temperature of 37.8°C, a pulse of 110 beats/min, and a respiratory rate of 18 breaths/min. There were decreased breath sounds and dullness to percussion in the left lower hemithorax. Stool guaiac test was negative. Her white blood cell count was 13,100 IJL The admission chest roentgenogram showed a large left pleural effusion but no air-fluid level. Diagnostic thoracentesis yielded sterile blood-tinged exudative fluid. Repeat chest roentgenogram demonstrated a retrocardiac air-fluid level for which a computed tomographic scan and emergency esophagogram were obtained (Fig 1). Exploratory left thoracotomy revealed a perforated necrotic stomach, densely adherent to the left lower lobe. The stomach had herniated and strangulated through a small (1 to 2 em) diaphragmatic defect that was separate from and 4 ern lateral to the esophageal hiatus. The diaphragmatic defect was extended radially and the stomach was repaired in two layers. The diaphragm was closed with a monofilament nonabsorbable suture and the pleura was decorticated and drained. Her postoperative course was complicated by sepsis from a subpulmonic empyema that was drained via a posterior seventh rib resection on the 14th postoperative day. Eventually, the patient made slow progress and was discharged on the 42nd postoperative day. Accepted for publication Oct 5, 1993. Address reprint requests to Dr Demmy, Division of Cardiothoracic Surgery, University of Missouri, 245 Major Hall, Dc119.0, Columbia, MO 65212.
© 1994 by The Society of Thoracic Surgeons
Comment Typical paraesophageal hernias occur "naturally" through gradually enlarging defects in the phrenoesophagealligament. They may occur postoperatively through a surgically enlarged esophageal hiatus or a defect like the relaxing diaphragm incision used in early Belsey antireflux operations [3]. In this latter group, the defect is separated from esophageal hiatus and mimics the rare naturally occurring parahiatal hernia. Failure of the embryonic pleuroperitoneal canal to obliterate is the theory for the etiology of naturally occurring parahiatal hernias [4]. The distance between the hernia and the hiatus will determine the distortion of the esophagogastric junction and the resultant symptoms (Fig 2). Paraesophageal hernia symptoms may be grouped conveniently into those of obstruction (nausea, vomiting, dysphagia) and those that indicate problems caused by the distended herniated stomach (pain, bleeding from
A
B
Fig 1. (A) Computed tomogram of incarcerated parahiatal hernia showingan air-fluid leveland surrounding effusion. Inset shows corresponding lateral chest roentgenogram with retrocardiac air-fluid level. (B) Gastrografin (Squibb Diagnostic, Princeton, NJ) swallow shows no abnormality at the esophagogastric junction. Although no gastric abnormalities were identified originally on this limited examination, thereappears to be a gastric deformity corresponding to the hernia site (arrow). 0003-4975/94/$7.00
CASE REPORT MULDER ET AL POST-ARTERIAL SWITCH COARCTATION
Ann Thorac Surg
1994;58:227-9
227
7. Vallieres E, Waters PF. Incarcerated parahiatal hernia with
gastric necrosis. Ann Thorac Surg 1987;44:82-3. 8. Pearson FG, Cooper JD, lives R, Todd TRJ, Jamieson WRE. Massive hiatal hernia with incarceration: a report of 53 cases. Ann Thorac Surg 1983;35:45-51.
Fig 2. The morecommon paraesophageal herniation (left) and the rare parahiatal hernia (right) are differentiated by the interveningdiaphragmatic muscle in the latter.
gastric venous obstruction, anemia, respiratory distress from lung compression) [1-3, 5-8]. Most of our patient's symptoms were in this second group. Her vomiting was a transient early symptom, and her barium swallow did not show esophageal obstruction. The patient's radiographic findings were similar to reports of incarcerated paraesophageal hernias with an elevated left hemidiaphragm and an air-fluid level in the left lower chest. However, the hernia orifice was sufficiently tight to prevent filling of the incarcerated segment with contrast from the upper gastrointestinal or the computed tomographic examination. Therefore, although contrast studies are usually helpful in the diagnosis of paraesophageal hernias, the radiographic absence of obstruction or supradiaphragmatic contrast may not exclude the diagnosis of parahiatal hernia. Incarcerated parahiatal hernias may be less virulent than their paraesophageal counterpart when they are smaller and allow less stomach to herniate and necrose. The bridge of diaphragm muscle may prevent gastric inversion and volvulus that is associated with a rapidly lethal clinical course in paraesophageal hernias [2]. Earlier diagnosis in this patient may have been made by dismissing lung abscess as a diagnosis because of the paucity of pulmonary symptoms. Focusing on the abdominal complaints and performing gastroscopy could have been diagnostic. This case report further substantiates the existence of parahiatal hernias. The relative lack of obstructive symptoms or radiographic findings is due to separation of the hernia from the esophageal hiatus and warrants distinction of this entity from true paraesophageal hernias.
Coarctation Developing After Arterial Switch Repair for Transposition of the Great Arteries Han J. G. H. Mulder, MD, Gilles L. Kaan, MD, Aagje Nijveld, MD, Anton van Oort, MD, Jelle Barentsz, MD, and Leon K. Lacquet, MD Departments of Thoracic and Cardiac Surgery, Pediatric Cardiology, and Radiology, University Hospital St. Radboud, Nijmegen, the Netherlands
We describe 2 patients with simple transposition of the great arteries in whom coarctation of the aorta developed after uncomplicated arterial switch operation. Both patients showed no symptoms or signs of this coarctation at the time of arterial switch operation. (Ann Thorae Surg 1994;58:227-9)
D
uring the past 10 years the neonatal arterial switch operation (ASO) has found increasing favor as the therapy of choice for transposition of the great arteries (TGA) [I, 2]. Midterm follow-up results support the theoretic advantages of the ASO. The main late complications seem to be pulmonary stenosis and aortic regurgitation [3]. Complete TGA associated with coarctation of the aorta (CoA) is a known and not so rare anatomic entity [4]. Very rare is the development of CoA after the ASO. Muster and associates [5] reported 3 patients with TGA in whom kinking of the aortic arch developed after ASO, resulting in a "nee-coarctation." Di Donato and colleagues [6] presented, as an incidental finding, a TGA patient in whom a genuine CoA developed after ASO. We present 2 patients in whom a typical, isthmus CoA developed after uncomplicated ASO for simple TGA.
Case Reports
Patient 1 References 1. Ellis FH. Diaphragmatic hiatal hernias: recognizingand treating the major types. Postgrad Med 1990;88:113-24.
2. Hill LD. Incarcerated paraesophageal hernia: a surgical emergency. Am J Surg 1973;126:286-91. 3. Streitz JM, Ellis FH. Iatrogenic paraesophageal hiatus hernia. Ann Thorac Surg 1990;50:446-9. 4. Wells LJ. Development of the human diaphragm and pleural sacs. In: Contributions to embryology. Washington, DC: Carnegie Institute, 1954;35:109-34. 5. Borchardt M. Zur Pathologie und Therapie des MagenvolvuIus. Arch Klin Chir 1904;74:244--60. 6. Ozdemir LA, Burke WA, Ikins PM. Paraesophageal hernia: a life-threatening disease. Ann Thorac Surg 1973;16:547-54. © 1994 by The Society of Thoracic Surgeons
Patient 1 is a boy operated on for TGA at the age of 2 days and weight of 3,400 g. The preoperative morphologic diagnosis was based on echocardiography. Specific attention was paid to a possible CoA, but it was excluded before and after prostaglandin treatment. External pressure measurements of arms and legs showed no difference. The ASO was performed with an uncomplicated postoperative course. Accepted for publication Oct 13, 1993. Address reprint requests to Dr Kaan, Department of Thoracic and Cardiac Surgery, University Hospital St. Radboud, Box 9101, 6500 HB Nijmegen, the Netherlands.
0003-4975/94/$7.00