Ann Thorac Surg 2015;100:2343–6
CASE REPORT SERRALHEIRO ET AL SPLENIC RUPTURE AND PARAESOPHAGEAL HERNIA
2343
Fig 3. Immunohistochemical staining and follow-up esophagoscopy. (A) Bcl-2-positive (magnification 20); (B) CD34-positive (magnification 20); (C) 1 month and (D) 2 months postoperatively, follow-up esophagoscopy demonstrated a wellhealed mucosa.
endoscopic piecemeal mucosal resection: a case report. Korean J Gastroenterol 2013;61:286–9. 5. Saito I, Tsuji Y, Sakaguchi Y, et al. Complications related to gastric endoscopic submucosal dissection and their managements. Clin Endosc 2014;47:398–403. 6. Guo J, Liu Z, Sun S, et al. Endosonography-assisted diagnosis and therapy of gastrointestinal submucosal tumors. Endosc Ultrasound 2013;2:125–33. 7. Wen G, Li M, Xu L, et al. Solitary fibrous tumor of the central nervous system: report of 2 cases and review of literature. Int J Clin Exp Pathol 2014;7:3444–8.
Splenic Rupture Caused by Giant Paraesophageal Hernia Pedro Serralheiro, MD, Bhaskar Kumar, MD, and Edward Cheong, MD Department of General Surgery, Norfolk and Norwich University Hospital, Norwich, United Kingdom
References 1. Sun J, Yu XR, Shi BB, Zheng J, Wu JT. CT features of retroperitoneal solitary fibrous tumor: report of three cases and review of the literature. World J Surg Oncol 2014;12:324. 2. Shin S, Choi YS, Shim YM, Kim HK, Kim K, Kim J. Enucleation of esophageal submucosal tumors: a single institution’s experience. Ann Thorac Surg 2014;97:454–9. 3. Li JJ, Shan HB, He LJ, et al. Extraesophageal saline during endoscopic submucosal dissection in a patient with early esophageal squamous cell carcinoma. Ann Thorac Surg 2014;98:1843–5. 4. Sekiguchi M, Matsuda T, Sekine S, et al. Repeatedly recurrent colon cancer involving the appendiceal orifice after Ó 2015 by The Society of Thoracic Surgeons Published by Elsevier
Splenic hemorrhage secondary to retching and vomiting from incarceration of paraesophageal hernia is a rare but life-threatening complication. Clinicians need to be aware of this complication in the event of sudden unexplained hemodynamic instability. Surgical intervention for the hernia is best performed as soon as possible once the patient is stabilized, before complications such as perforation or further bleeding occur. We report two cases of splenic rupture and intraperitoneal bleeding resulting from traction of the gastrosplenic pedicle 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2015.02.110
FEATURE ARTICLES
Recently, there have been some literature reviews on cases in which ESD was used to treat upper gastrointestinal submucosal tumors [2]. In this study, SFT was smoothly resected in patients with tumors’ sizes of 22 cm 3.5 cm without severe complications. Thus far, there have been no reports regarding the use of ESD for the treatment of esophageal SFTs. This is the first case in which ESD was performed to treat esophageal SFT. In conclusion, esophagus SFT is an extremely rare neoplasm in adult patients. Precise diagnosis is solely based on the correct interpretation of unique pathologic and immunohistochemical features. Because the use of ESD has recently increased, we propose that this case report is significant and will help validate the use of ESD as a feasible option for the treatment of esophageal SFT.
2344
CASE REPORT SERRALHEIRO ET AL SPLENIC RUPTURE AND PARAESOPHAGEAL HERNIA
Ann Thorac Surg 2015;100:2343–6
associated with retching and vomiting from a giant paraesophageal hernia. (Ann Thorac Surg 2015;100:2343–6) Ó 2015 by The Society of Thoracic Surgeons
P
araesophageal hernias (PEH) account for 5% to 10% of all hiatal hernias and are seen mainly in a growing population of elderly and middle-aged patients. The term giant paraesophageal hernia is used when more than 50% of the stomach is displaced above the diaphragm into an intrathoracic position [1]. Gastric volvulus, acute gastric outlet obstruction, strangulation with gastric wall necrosis, and perforation are well-documented presentations. Rarer presentations that have been described include hematemesis, hemorrhagic pancreatitis, respiratory distress by compression of the left main bronchus, or gastrobronchial and gastrocardiac fistula [1–4]. Atraumatic splenic rupture is a rare but potentially lifethreatening association of PEHs. This is believed to occur as a result of uncontrolled traction and stretching of the gastrosplenic pedicle from the elevated intraabdominal pressure of vomiting and retching. We report two cases of splenic rupture and intraperitoneal bleeding resulting from traction of the gastrosplenic pedicle associated with a giant PEH.
Case Reports
FEATURE ARTICLES
Patient 1 A 78-year-old woman with known pleural mesothelioma was hospitalized with epigastric pain and vomiting. Clinical examination revealed no evidence of hemodynamic compromise and no peritonitis. Routine blood tests were within normal values (hemoglobin [Hb], 127 g/L). Computed tomography (CT) of the thorax and abdomen and gastroscopy revealed an intrathoracic stomach with volvulus. Two tubes were placed endoscopically: a nasojejunal tube for enteral feeding and a nasogastric tube for draining the stomach. A decision was made to perform an urgent laparoscopic surgical repair after a period of feeding and stabilization. During the next two days, the Hb dropped precipitously to 78 g/L (hematocrit, 0.238). A 2-unit blood transfusion was given, and an urgent CT of the abdomen demonstrated, besides the unchanged giant PEH, a large perisplenic hematoma with free fluid in the pelvis (Fig 1). The patient did not have a history of trauma before the admission. Owing to her frailty and underlying diagnosis of mesothelioma, surgical repair was performed in a semiurgent manner rather than immediately. Ten days later a laparoscopic repair was attempted. There was evidence of previous hemorrhage in the left upper quadrant with dense adhesions and hematoma, but no active hemorrhage.
Fig 1. Computed tomographic image of giant paraesophageal hernia and a large perisplenic fluid collection (patient 1).
Given the history of mesothelioma, the hernia sac was densely adherent to the pleura and a decision was made to convert to open surgery. Her postoperative recovery was uncomplicated. A follow-up CT angiogram did not show any evidence of splenic artery pseudoaneurysm or progression of the perisplenic hematoma.
Patient 2 Accepted for publication Feb 2, 2015. Address correspondence to Dr Serralheiro, NNUH, General Surgery, Colney Ln, Norwich NR47UY, UK; e-mail: [email protected].
A 73-year-old man was hospitalized as a result of collapse after an episode of generalized abdominal pain and persistent vomiting. There was no history of trauma.
Ann Thorac Surg 2015;100:2343–6
CASE REPORT SERRALHEIRO ET AL SPLENIC RUPTURE AND PARAESOPHAGEAL HERNIA
2345
The patient’s Hb remained stable, and he was discharged 10 days after admission. A follow up CT of the thorax, abdomen, and pelvis showed a static, organizing, perisplenic hematoma with homogeneously enhanced spleen. An elective laparoscopic PEH repair was performed 2 months after the original admission. The patient made an uneventful recovery from surgery. Follow-up CT angiogram did not show any evidence of splenic artery pseudoaneurysm or progression of the perisplenic hematoma.
Comment
Clinical examination revealed no hemodynamic compromise and no peritonitis. The electrocardiogram was normal, and routine blood tests were within normal values (Hb, 133 g/L; hematocrit, 0.408). The following day his Hb dropped to 86 g/L and hematocrit to 0.265. A 4-unit blood transfusion was commenced. Urgent CT angiogram revealed a giant unobstructed PEH and a large perisplenic fluid collection with free fluid throughout the abdomen (Fig 2). Conservative management was pursued with a low threshold for surgical exploration in the event of hemodynamic compromise, as there was no active extravasation of contrast or splenic hilar vessel damage.
FEATURE ARTICLES
Fig 2. Computed tomographic image of giant paraesophageal hernia and a large perisplenic fluid collection (patient 2).
Only one case of splenic rupture secondary to PEH has been reported in the literature [3]. This rare but important life-threatening complication should always be considered as a reason for sudden hemodynamic compromise or unexplained anemia in a patient with PEH. Lack of awareness of this rare complication may lead to a missed diagnosis, which may be fatal. Splenic rupture secondary to PEH is an important differential diagnosis that must always be kept in mind in the event of sudden unexplained instability or sharp fall in Hb well below baseline, and a low threshold should be applied to obtain cross-sectional imaging to visualize the spleen. In this situation, surgical intervention needs to be performed in an urgent manner because of the potential risks of disastrous complications (such as gastric perforation or further splenic bleeding), once the patient is stabilized as much as possible, to minimize perioperative risk, albeit avoiding unacceptable delays in intervention. A number of interesting technical points that are worthy of discussion have arisen from our experience. Caution needs to be applied in operating on these patients as the spleen remains at risk of further disruption. Our experience would suggest that the chance of this is reduced through such an approach. In terms of surgical approach it may be argued that open repair may be the safer approach from the outset, although our results in patient 2 would suggest that a laparoscopic repair is safe and feasible. In patient 1 the decision to convert to open surgery was owing to the difficulty in dissecting the hernia sac off the diseased pleura in an elderly, frail patient rather than splenic bleeding. A trial laparoscopic dissection can be safely performed with a low threshold for conversion to open surgery, if required. During laparoscopy, pneumoperitoneum should be established gradually, with low intraabdominal pressures, to minimize gastrosplenic pedicle traction and rebleeding. Close cooperation throughout the procedure with the anesthetic team, who should remain vigilant for any hemodynamic instability, is important. These patients must have blood available to cover the possibility of hemorrhage requiring urgent transfusion. Patient 1 had atypical antibodies necessitating a request of blood from a different regional center. The most difficult area of the hernia sac dissection may be in the vicinity of the left crus of the
2346
CASE REPORT TURIY ET AL ANOMALOUS CORONARY ORIGIN IN HLHS
diaphragm, where adhesions can be particularly dense. Throughout the operation, attention and care should be applied to prevent further traction to the gastrosplenic ligament and disturbing any perisplenic hematoma. It would be advisable to avoid dissection of the short gastric vessels in the construction of a fundoplication. Based on our experience and limited reports in the literature we postulate that traction exerted on the gastrosplenic pedicle against the hernia rim of the diaphragmatic defect, generated during the period of vomiting and retching, may have resulted in an avulsion injury to the spleen. Measures to minimize retching and vomiting should be instituted early in the management, such as nasogastric tube decompression and regular antiemetics. In conclusion, clinicians managing patients with a PEH must not only be aware of this rare complication but also be prepared to intervene in an urgent manner, avoiding life-threatening sequelae.
References
FEATURE ARTICLES
1. Mori T, Nagao G, Sugiyama M. Paraesophageal hernia repair. Ann Thorac Cardiovasc Surg 2012;18:297–305. 2. K€ ohler G, Koch OO, Antoniou SA, Emmanuel K, Pointner R. “Acute intrathoracic stomach!” How should we deal with complicated type IV paraesophageal hernias? Hernia 2014 Jul 25; [Epub ahead of print]. 3. Szwerc MF, Landreneau RJ. Splenic rupture as a consequence of giant paraesophageal hernia. Ann Thorac Surg 2000;70: 1727–8. 4. Polomsky M, Hu R, Sepesi B, et al. A population-based analysis of emergent vs. elective hospital admissions for an intrathoracic stomach. Surg Endosc 2010;24:1250–5.
Anomalous Origin of Coronary Artery From Main Pulmonary Artery in Hypoplastic Left Heart Syndrome Yuliya Turiy, MD, MPH, William Douglas, MD, and Duraisamy Balaguru, MD Divisions of Pediatric Cardiology and Pediatric Cardiovascular Surgery, University of Texas Health Science Center, Houston, Texas
We report a case of anomalous origin of the left anterior descending coronary artery (LAD) from the main pulmonary artery in a child with hypoplastic left heart syndrome (mitral atresia/aortic atresia). Mechanical circulatory support was necessary because of the inability to wean from cardiopulmonary bypass after the Norwood procedure. The patient died at 4 months of age having continued depressed right ventricular function. The diagnosis was made during a catheterization performed 6 weeks after surgery because of concern for stenosis of Blalock-Taussig shunt. We believe his prolonged postoperative recovery and eventual demise can partially be Ó 2015 by The Society of Thoracic Surgeons Published by Elsevier
Ann Thorac Surg 2015;100:2346–8
attributed to lack of cardioplegia to the anomalous LAD territory during surgery. (Ann Thorac Surg 2015;100:2346–8) Ó 2015 by The Society of Thoracic Surgeons
C
oronary artery (CA) anomalies have been reported in small proportion of patients with hypoplastic left heart syndrome (HLHS). An autopsy study of 216 specimens found 49 (22%) that had coronary anomalies: 39 cases of coronary fistulas (all in mitral stenosis and aortic atresia), 9 cases of other CA anomalies such as high takeoff and hypoplasia of CAs and single CA, and only one case of anomalous origin of the left coronary artery (LCA) from the right pulmonary artery (RPA). These latter 10 cases were associated with mitral atresia/aortic atresia anatomy [1]. In addition, several case reports describe anomalous origin of the CA from the RPA in HLHS [2–6]. Anomalies reported include LCA from RPA, circumflex coronary artery from RPA, and right CA from RPA. A large retrospective review of 552 patients with HLHS found 6 patients with anomalous LCA arising from RPA [7]. The association of anomalous origin of the CA from a branch pulmonary artery with HLHS is rare and appears to be more common with the mitral atresia/aortic atresia (MA/AA) type of HLHS. We report a case of HLHS (MA/ AA) associated with anomalous origin of left anterior descending coronary artery (LAD) from the main pulmonary artery. Failure to recognize this associated defect may have contributed to postoperative myocardial dysfunction, the need for mechanical circulatory support, and eventual poor outcome. The patient was born at an outside hospital at term with a birth weight of 2.1 kg. Low oxygen saturations and a heart murmur prompted a hyperoxia test and echocardiography. Diagnosis of HLHS (MA/AA) was made. CAs were well visualized and appeared apparently normal. Prostaglandin infusion was started, and he was transferred to our institution for further management. Because of low birth weight, the patient underwent a modified hybrid procedure with bilateral pulmonary artery banding without complications at 10 days of age. Prostaglandin infusion was continued. A Norwood procedure with 4-mm modified Blalock-Taussig (BT) shunt and debanding of pulmonary arteries was performed at 45 days of age. A polytetrafluoroethylene graft on the innominate artery (eventually used for the BT shunt) was used for arterial cannulation. Cardioplegia was given during a brief period of circulatory arrest with snares on the distal innominate artery (distal to the shunt insertion), left common carotid and subclavian arteries, the ductus arteriosus, and a clamp on the descending aorta. In the operating room, poor right ventricular (RV) systolic Accepted for publication Jan 27, 2015. Address correspondence to Dr Balaguru, University of Texas Health Science Center at Houston, 6410 Fannin St, Houston, TX 77030; e-mail: [email protected].
0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2015.01.077
CASE REPORT SERRALHEIRO ET AL SPLENIC RUPTURE AND PARAESOPHAGEAL HERNIA
2343
Fig 3. Immunohistochemical staining and follow-up esophagoscopy. (A) Bcl-2-positive (magnification 20); (B) CD34-positive (magnification 20); (C) 1 month and (D) 2 months postoperatively, follow-up esophagoscopy demonstrated a wellhealed mucosa.
endoscopic piecemeal mucosal resection: a case report. Korean J Gastroenterol 2013;61:286–9. 5. Saito I, Tsuji Y, Sakaguchi Y, et al. Complications related to gastric endoscopic submucosal dissection and their managements. Clin Endosc 2014;47:398–403. 6. Guo J, Liu Z, Sun S, et al. Endosonography-assisted diagnosis and therapy of gastrointestinal submucosal tumors. Endosc Ultrasound 2013;2:125–33. 7. Wen G, Li M, Xu L, et al. Solitary fibrous tumor of the central nervous system: report of 2 cases and review of literature. Int J Clin Exp Pathol 2014;7:3444–8.
Splenic Rupture Caused by Giant Paraesophageal Hernia Pedro Serralheiro, MD, Bhaskar Kumar, MD, and Edward Cheong, MD Department of General Surgery, Norfolk and Norwich University Hospital, Norwich, United Kingdom
References 1. Sun J, Yu XR, Shi BB, Zheng J, Wu JT. CT features of retroperitoneal solitary fibrous tumor: report of three cases and review of the literature. World J Surg Oncol 2014;12:324. 2. Shin S, Choi YS, Shim YM, Kim HK, Kim K, Kim J. Enucleation of esophageal submucosal tumors: a single institution’s experience. Ann Thorac Surg 2014;97:454–9. 3. Li JJ, Shan HB, He LJ, et al. Extraesophageal saline during endoscopic submucosal dissection in a patient with early esophageal squamous cell carcinoma. Ann Thorac Surg 2014;98:1843–5. 4. Sekiguchi M, Matsuda T, Sekine S, et al. Repeatedly recurrent colon cancer involving the appendiceal orifice after Ó 2015 by The Society of Thoracic Surgeons Published by Elsevier
Splenic hemorrhage secondary to retching and vomiting from incarceration of paraesophageal hernia is a rare but life-threatening complication. Clinicians need to be aware of this complication in the event of sudden unexplained hemodynamic instability. Surgical intervention for the hernia is best performed as soon as possible once the patient is stabilized, before complications such as perforation or further bleeding occur. We report two cases of splenic rupture and intraperitoneal bleeding resulting from traction of the gastrosplenic pedicle 0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2015.02.110
FEATURE ARTICLES
Recently, there have been some literature reviews on cases in which ESD was used to treat upper gastrointestinal submucosal tumors [2]. In this study, SFT was smoothly resected in patients with tumors’ sizes of 22 cm 3.5 cm without severe complications. Thus far, there have been no reports regarding the use of ESD for the treatment of esophageal SFTs. This is the first case in which ESD was performed to treat esophageal SFT. In conclusion, esophagus SFT is an extremely rare neoplasm in adult patients. Precise diagnosis is solely based on the correct interpretation of unique pathologic and immunohistochemical features. Because the use of ESD has recently increased, we propose that this case report is significant and will help validate the use of ESD as a feasible option for the treatment of esophageal SFT.
2344
CASE REPORT SERRALHEIRO ET AL SPLENIC RUPTURE AND PARAESOPHAGEAL HERNIA
Ann Thorac Surg 2015;100:2343–6
associated with retching and vomiting from a giant paraesophageal hernia. (Ann Thorac Surg 2015;100:2343–6) Ó 2015 by The Society of Thoracic Surgeons
P
araesophageal hernias (PEH) account for 5% to 10% of all hiatal hernias and are seen mainly in a growing population of elderly and middle-aged patients. The term giant paraesophageal hernia is used when more than 50% of the stomach is displaced above the diaphragm into an intrathoracic position [1]. Gastric volvulus, acute gastric outlet obstruction, strangulation with gastric wall necrosis, and perforation are well-documented presentations. Rarer presentations that have been described include hematemesis, hemorrhagic pancreatitis, respiratory distress by compression of the left main bronchus, or gastrobronchial and gastrocardiac fistula [1–4]. Atraumatic splenic rupture is a rare but potentially lifethreatening association of PEHs. This is believed to occur as a result of uncontrolled traction and stretching of the gastrosplenic pedicle from the elevated intraabdominal pressure of vomiting and retching. We report two cases of splenic rupture and intraperitoneal bleeding resulting from traction of the gastrosplenic pedicle associated with a giant PEH.
Case Reports
FEATURE ARTICLES
Patient 1 A 78-year-old woman with known pleural mesothelioma was hospitalized with epigastric pain and vomiting. Clinical examination revealed no evidence of hemodynamic compromise and no peritonitis. Routine blood tests were within normal values (hemoglobin [Hb], 127 g/L). Computed tomography (CT) of the thorax and abdomen and gastroscopy revealed an intrathoracic stomach with volvulus. Two tubes were placed endoscopically: a nasojejunal tube for enteral feeding and a nasogastric tube for draining the stomach. A decision was made to perform an urgent laparoscopic surgical repair after a period of feeding and stabilization. During the next two days, the Hb dropped precipitously to 78 g/L (hematocrit, 0.238). A 2-unit blood transfusion was given, and an urgent CT of the abdomen demonstrated, besides the unchanged giant PEH, a large perisplenic hematoma with free fluid in the pelvis (Fig 1). The patient did not have a history of trauma before the admission. Owing to her frailty and underlying diagnosis of mesothelioma, surgical repair was performed in a semiurgent manner rather than immediately. Ten days later a laparoscopic repair was attempted. There was evidence of previous hemorrhage in the left upper quadrant with dense adhesions and hematoma, but no active hemorrhage.
Fig 1. Computed tomographic image of giant paraesophageal hernia and a large perisplenic fluid collection (patient 1).
Given the history of mesothelioma, the hernia sac was densely adherent to the pleura and a decision was made to convert to open surgery. Her postoperative recovery was uncomplicated. A follow-up CT angiogram did not show any evidence of splenic artery pseudoaneurysm or progression of the perisplenic hematoma.
Patient 2 Accepted for publication Feb 2, 2015. Address correspondence to Dr Serralheiro, NNUH, General Surgery, Colney Ln, Norwich NR47UY, UK; e-mail: [email protected].
A 73-year-old man was hospitalized as a result of collapse after an episode of generalized abdominal pain and persistent vomiting. There was no history of trauma.
Ann Thorac Surg 2015;100:2343–6
CASE REPORT SERRALHEIRO ET AL SPLENIC RUPTURE AND PARAESOPHAGEAL HERNIA
2345
The patient’s Hb remained stable, and he was discharged 10 days after admission. A follow up CT of the thorax, abdomen, and pelvis showed a static, organizing, perisplenic hematoma with homogeneously enhanced spleen. An elective laparoscopic PEH repair was performed 2 months after the original admission. The patient made an uneventful recovery from surgery. Follow-up CT angiogram did not show any evidence of splenic artery pseudoaneurysm or progression of the perisplenic hematoma.
Comment
Clinical examination revealed no hemodynamic compromise and no peritonitis. The electrocardiogram was normal, and routine blood tests were within normal values (Hb, 133 g/L; hematocrit, 0.408). The following day his Hb dropped to 86 g/L and hematocrit to 0.265. A 4-unit blood transfusion was commenced. Urgent CT angiogram revealed a giant unobstructed PEH and a large perisplenic fluid collection with free fluid throughout the abdomen (Fig 2). Conservative management was pursued with a low threshold for surgical exploration in the event of hemodynamic compromise, as there was no active extravasation of contrast or splenic hilar vessel damage.
FEATURE ARTICLES
Fig 2. Computed tomographic image of giant paraesophageal hernia and a large perisplenic fluid collection (patient 2).
Only one case of splenic rupture secondary to PEH has been reported in the literature [3]. This rare but important life-threatening complication should always be considered as a reason for sudden hemodynamic compromise or unexplained anemia in a patient with PEH. Lack of awareness of this rare complication may lead to a missed diagnosis, which may be fatal. Splenic rupture secondary to PEH is an important differential diagnosis that must always be kept in mind in the event of sudden unexplained instability or sharp fall in Hb well below baseline, and a low threshold should be applied to obtain cross-sectional imaging to visualize the spleen. In this situation, surgical intervention needs to be performed in an urgent manner because of the potential risks of disastrous complications (such as gastric perforation or further splenic bleeding), once the patient is stabilized as much as possible, to minimize perioperative risk, albeit avoiding unacceptable delays in intervention. A number of interesting technical points that are worthy of discussion have arisen from our experience. Caution needs to be applied in operating on these patients as the spleen remains at risk of further disruption. Our experience would suggest that the chance of this is reduced through such an approach. In terms of surgical approach it may be argued that open repair may be the safer approach from the outset, although our results in patient 2 would suggest that a laparoscopic repair is safe and feasible. In patient 1 the decision to convert to open surgery was owing to the difficulty in dissecting the hernia sac off the diseased pleura in an elderly, frail patient rather than splenic bleeding. A trial laparoscopic dissection can be safely performed with a low threshold for conversion to open surgery, if required. During laparoscopy, pneumoperitoneum should be established gradually, with low intraabdominal pressures, to minimize gastrosplenic pedicle traction and rebleeding. Close cooperation throughout the procedure with the anesthetic team, who should remain vigilant for any hemodynamic instability, is important. These patients must have blood available to cover the possibility of hemorrhage requiring urgent transfusion. Patient 1 had atypical antibodies necessitating a request of blood from a different regional center. The most difficult area of the hernia sac dissection may be in the vicinity of the left crus of the
2346
CASE REPORT TURIY ET AL ANOMALOUS CORONARY ORIGIN IN HLHS
diaphragm, where adhesions can be particularly dense. Throughout the operation, attention and care should be applied to prevent further traction to the gastrosplenic ligament and disturbing any perisplenic hematoma. It would be advisable to avoid dissection of the short gastric vessels in the construction of a fundoplication. Based on our experience and limited reports in the literature we postulate that traction exerted on the gastrosplenic pedicle against the hernia rim of the diaphragmatic defect, generated during the period of vomiting and retching, may have resulted in an avulsion injury to the spleen. Measures to minimize retching and vomiting should be instituted early in the management, such as nasogastric tube decompression and regular antiemetics. In conclusion, clinicians managing patients with a PEH must not only be aware of this rare complication but also be prepared to intervene in an urgent manner, avoiding life-threatening sequelae.
References
FEATURE ARTICLES
1. Mori T, Nagao G, Sugiyama M. Paraesophageal hernia repair. Ann Thorac Cardiovasc Surg 2012;18:297–305. 2. K€ ohler G, Koch OO, Antoniou SA, Emmanuel K, Pointner R. “Acute intrathoracic stomach!” How should we deal with complicated type IV paraesophageal hernias? Hernia 2014 Jul 25; [Epub ahead of print]. 3. Szwerc MF, Landreneau RJ. Splenic rupture as a consequence of giant paraesophageal hernia. Ann Thorac Surg 2000;70: 1727–8. 4. Polomsky M, Hu R, Sepesi B, et al. A population-based analysis of emergent vs. elective hospital admissions for an intrathoracic stomach. Surg Endosc 2010;24:1250–5.
Anomalous Origin of Coronary Artery From Main Pulmonary Artery in Hypoplastic Left Heart Syndrome Yuliya Turiy, MD, MPH, William Douglas, MD, and Duraisamy Balaguru, MD Divisions of Pediatric Cardiology and Pediatric Cardiovascular Surgery, University of Texas Health Science Center, Houston, Texas
We report a case of anomalous origin of the left anterior descending coronary artery (LAD) from the main pulmonary artery in a child with hypoplastic left heart syndrome (mitral atresia/aortic atresia). Mechanical circulatory support was necessary because of the inability to wean from cardiopulmonary bypass after the Norwood procedure. The patient died at 4 months of age having continued depressed right ventricular function. The diagnosis was made during a catheterization performed 6 weeks after surgery because of concern for stenosis of Blalock-Taussig shunt. We believe his prolonged postoperative recovery and eventual demise can partially be Ó 2015 by The Society of Thoracic Surgeons Published by Elsevier
Ann Thorac Surg 2015;100:2346–8
attributed to lack of cardioplegia to the anomalous LAD territory during surgery. (Ann Thorac Surg 2015;100:2346–8) Ó 2015 by The Society of Thoracic Surgeons
C
oronary artery (CA) anomalies have been reported in small proportion of patients with hypoplastic left heart syndrome (HLHS). An autopsy study of 216 specimens found 49 (22%) that had coronary anomalies: 39 cases of coronary fistulas (all in mitral stenosis and aortic atresia), 9 cases of other CA anomalies such as high takeoff and hypoplasia of CAs and single CA, and only one case of anomalous origin of the left coronary artery (LCA) from the right pulmonary artery (RPA). These latter 10 cases were associated with mitral atresia/aortic atresia anatomy [1]. In addition, several case reports describe anomalous origin of the CA from the RPA in HLHS [2–6]. Anomalies reported include LCA from RPA, circumflex coronary artery from RPA, and right CA from RPA. A large retrospective review of 552 patients with HLHS found 6 patients with anomalous LCA arising from RPA [7]. The association of anomalous origin of the CA from a branch pulmonary artery with HLHS is rare and appears to be more common with the mitral atresia/aortic atresia (MA/AA) type of HLHS. We report a case of HLHS (MA/ AA) associated with anomalous origin of left anterior descending coronary artery (LAD) from the main pulmonary artery. Failure to recognize this associated defect may have contributed to postoperative myocardial dysfunction, the need for mechanical circulatory support, and eventual poor outcome. The patient was born at an outside hospital at term with a birth weight of 2.1 kg. Low oxygen saturations and a heart murmur prompted a hyperoxia test and echocardiography. Diagnosis of HLHS (MA/AA) was made. CAs were well visualized and appeared apparently normal. Prostaglandin infusion was started, and he was transferred to our institution for further management. Because of low birth weight, the patient underwent a modified hybrid procedure with bilateral pulmonary artery banding without complications at 10 days of age. Prostaglandin infusion was continued. A Norwood procedure with 4-mm modified Blalock-Taussig (BT) shunt and debanding of pulmonary arteries was performed at 45 days of age. A polytetrafluoroethylene graft on the innominate artery (eventually used for the BT shunt) was used for arterial cannulation. Cardioplegia was given during a brief period of circulatory arrest with snares on the distal innominate artery (distal to the shunt insertion), left common carotid and subclavian arteries, the ductus arteriosus, and a clamp on the descending aorta. In the operating room, poor right ventricular (RV) systolic Accepted for publication Jan 27, 2015. Address correspondence to Dr Balaguru, University of Texas Health Science Center at Houston, 6410 Fannin St, Houston, TX 77030; e-mail: [email protected].
0003-4975/$36.00 http://dx.doi.org/10.1016/j.athoracsur.2015.01.077
