and Edgar D. Guzman-Arrieta3
(1)
Department of Surgery Advocate Illinois Masonic Medical Center, University of Illinois Metropolitan Group Hospitals Residency in General Surgery, Chicago, IL, USA
(2)
University of Illinois at Chicago, Chicago, IL, USA
(3)
Vascular Specialists – Hattiesburg Clinic, Hattiesburg, MS, USA
Keywords
DiaphragmSeptum transversumPhrenic nerveDiaphragmatic herniaMedian arcuate ligament syndrome1.
All of the following contribute to the formation of the diaphragm except
(a)
Septum transversum
(b)
Glisson’s capsule
(c)
Visceral peritoneum
(d)
Pleuroperitoneal membranes
(e)
Dermatomes from T6 to T12
Comments
The septum transversum forms the central part of the diaphragm in the adult. This mesodermal structure originates in the neck at C3 level. From there, it descends bringing its innervation from C3 to C5, forming the phrenic nerve. In fish, the diaphragm is immediately below the gills and heart, at a level that would correspond to the human neck. As the lungs developed in evolution, the septum transversum was displaced caudally. This migration explains referred pain to the neck from diaphragmatic irritation, inferior wall myocardial infarctions, and basal pneumonia (Fig. 6.1).
Fig. 6.1
Gills (branchium) of the fish act as the lungs. The septum transversum of the fish lies in the neck distal to the heart. During evolution, the septum transversum remained below the developing lungs and maintained innervation by the cervical nerves. This explains why pain from a myocardial infarction, or from diseases effecting the diaphragm are referred to the neck and shoulder
The septum transversum does not completely separate the abdomen from the thorax. Posterolateral to it are the pleuroperitoneal canals, which are obliterated by the pleuroperitoneal membranes. During the 8th week of gestation, the diaphragmatic descent is complete. The central portion of the diaphragm joins, the body wall circumferentially (T6 anteriorly to T12 posteriorly). The mesodermal body wall contributes muscular tissue to the peripheral diaphragm. This component of the diaphragmatic musculature receives segmental innervation. Irritation to the peripheral diaphragm may produce referred pain along the T6–T12 dermatomes. Lastly, the dorsal mesentery provides connective tissue to the posterior midline of the diaphragm.
Answer
b
2.
Mark the incorrect statement:
(a)
Morgagni hernias occur anteriorly, through the attachments of the diaphragm to the xiphoid process.
(b)
Bochdalek hernias occur posterolaterally, representing a defect of the pleuroperitoneal membranes.
(c)
Diaphragmatic eventration consists of pathologic elevation of the diaphragm, without a loss in continuity.
(d)
Pulmonary hypoplasia is commonly associated with congenital diaphragmatic hernias.
(e)
Congenital short esophagus is a common anomaly present in children.
Comments
Diaphragmatic hernias may occur through any of the normal orifices of the diaphragm as well as through abnormal orifices. The most significant congenital diaphragmatic hernias are Bochdalek hernias, which occur through a defect in the contribution of the pleuroperitoneal membranes to the posterolateral diaphragm. In this pathology, invasion of the thorax by abdominal contents prevents normal lung development which may lead to neonatal hypoxemia. These hernias are more frequent and symptomatic on the left, due to the presence of the liver on the right [2, 4].
Morgagni–Larrey hernias occur in the central part of the anterior diaphragm, where the internal mammaries exit the chest. They are not very large and are not associated with lung hypoplasia. They are diagnosed later in life due to their tendency to incarcerate [5]. Of note, Bochdalek and Morgagni–Larrey hernias are unique in that the sac has two serosal layers, derived from the peritoneum and pleura [6] (Fig. 6.2).
Fig. 6.2
Congenital diaphragmatic hernias (CDH) result from the improper or delayed fusion of the central tendon (septum transversum), posterolateral pleuroperitoneal canals, and peripheral T6–T12 somites. Other associated congenital anomalies, especially cardiac, may lead to severe morbidity and mortality. Non-closure of the pleuroperitoneal canals results in the Bochdalek hernia which is often associated with pulmonary hypoplasia. These hernias are common on the left side as the large neonatal liver often covers right-sided defects. In neonates, this hernia presents as a surgical emergency. Morgagni hernias are anterior and between the fusion of sternocostal somites. Diagnosis of CDH is today largely made during prenatal ultrasound. Modern surgical treatment has shifted from emergency to semi-elective after stabilization
Diaphragmatic eventration occurs due to the lack of muscularization of the diaphragm (congenital) or phrenic nerve injury (acquired) [7]. True congenitally short esophagus is a rare entity in the newborn. The esophagus is normal; there is a supradiaphragmatic stomach with no hernial sac, no displacement of the left gastric artery, and normal phrenoesophageal ligament. There is considerable debate surrounding its true congenital origin [8].
Answer
e
3.
In relation to hiatal hernias, all of the following are correct except:
(a)
An enlarged esophageal hiatus and a weak phrenoesophageal ligament favor the occurrence of a sliding esophageal hernia.
(b)
Sliding hernias are so named because the stomach forms part of the hernial sac.
(c)
Symptomatic paraesophageal hernias may be treated nonoperatively.
(d)
Paraesophageal hiatal hernias do not disturb the position of the GE junction.
(e)
Combined hiatal hernias behave as sliding hiatal hernias.
Comments
Hiatal hernias are classified into [9]:
Sliding, where the esophagogastric junction is above the diaphragm
Paraesophageal or rolling, occurring through the esophageal hiatus but with the GE junction in its normal location
Combined, which has a sliding and rolling component (the most frequent)
Complex, when organs other than the esophagus or stomach herniate (Fig. 6.3)
Fig. 6.3
The normal gastroesophageal junction (GEJ) is below the diaphragm. A functional lower esophageal sphincter (LES), external sphincter function provided by the crura, and an intra-abdominal esophagus are the key factors in preventing esophageal reflux. In a sliding hernia, the GEJ and LES are both above the diaphragm, and a part of the stomach is covered by the hernia sac. In paraesophageal hernia, the GEJ and LES are in the anatomical position, but a part of the stomach herniates into the chest covered with the hernia sac. Depending on the size of the hernia and the size of the defect, paraesophageal hernias may strangulate in the chest producing a serious surgical emergency.
The normal esophagogastric junction lies to the left of the midline, with a 2–3 cm segment of intra-abdominal esophagus. The existence of the abdominal esophagus is fundamental in avoiding gastroesophageal reflux. Even though there is no anatomic lower esophageal sphincter, there is surely a functional sphincter. Positive intra-abdominal pressure exerted on the intra-abdominal diaphragm causes its collapse and prevents reflux [10]. The treatment of sliding hiatal hernias for all intents and purposes is that of reflux esophagitis, rather than the correction of the anatomic defect per se. The same concept applies to combined hiatal hernias.
In the past, there was agreement on the need to repair all paraesophageal hernias promptly. More recently, this belief has been challenged, and watchful waiting of asymptomatic or minimally symptomatic hernias is a viable alternative. Controversy also exists regarding the best method of repair: open vs. laparoscopic, transthoracic vs. transabdominal and with or without antireflux procedure. There is also discussion regarding the benefits or using mesh for the repair and performing esophageal lengthening procedures. While paraesophageal hernias classically present after the fifth decade of life, this hernias may occur due to traumatic diaphragmatic injury at any age. Very often the history of trauma may be absent or remote [11, 12].
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