Kursk State Medical University



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THE KURSK STATE MEDICAL UNIVERSITY

Department of surgical diseases № 1

Diaphragmatic hernias

Information for self-training of English-speaking students

The chair of surgical diseases N 1 (Chair-head - prof. S.V.Ivanov)

By ass. professor M.V. Yakovleva

KURSK-2010

I. Introduction

Diaphragmatic hernias is the most wide-spread pathology of the diaphragm. They may arise due to anomaly of the diaphragm development, its traumatic damages and other causes. The common phenomenon for all hernias is coming out of the abdominal organs in the thoracic cavity from defect in diaphragm, from natural apertures and from weak zone that is stretched.

II. General aim of the lesson.

General aim of the lesson includes:

1. acquiring knowledge about symptomatology of the different diaphragmatic hernias.

2. acquiring practical skills of the patients’ objective examination.

3. mastering of the instrumental examinations main principles.

4. determination of the indications for surgical treatment and choosing the mode of it or conservative therapy of patients with diaphragmatic hernias.

Tasks for self-training.

After individual studying of the material every student is supposed:

a) to know

1. ethiology of different types of diaphragmatic hernias.

2. classification of the diaphragmatic hernias.

3. clinical picture of these diseases

4. instrumental methods of diaphragmatic hernias examinations: US-scanning, CT-scanning, X-ray examinations, endoscopy

5. surgical modes for management of different varieties of diaphragmatic hernias

b) to be able

1. to find out main complains and accumulate anamnesis in cases of diaphragmatic hernias

2. to assess the obtained results of the endoscopy and X-ray examinations

3. to carry out objective examination of patients with diaphragmatic hernias

4. to determine indications for surgical correction of different kinds of diaphragmatic hernias.

III. Initial level of knowledge.

Anatomo-physiological data about the esophagus, stomach, diaphragm diseases.

A student should revise the material on the underlined items.

IV. Brief outline of the topic (obligatory material for acquisition)

Diaphragmatic hernias are the most widespread pathology of the diaphragm. The common symptom for all diaphragmatic hernias is the prolapse of the abdominal organs in the thoracic cavity through the congenital gaps (certebrocostal and sternocostal trigones) or through dilated natural apertures in the diaphragm and through traumatic opening.

Classification of the diaphragmatic hernias:

I. by the origin:

1. congenital

2. acquired

a) traumatic

b) non traumatic

II. by the localization:

1. hernias of the aponeurotic tendon

2. hernias of the muscular part of the diaphragm

3. hernias of the musculotendinous part of the diaphragm

4. hernias of the gaps and natural openings.

III. by the presence of the hernial sack

1. true

2. false

IV. by the clinical course

1. acute

2. chronic

V. by the clinical picture

1. incarcerated

2. non-incarcerated

a) reducible

b) irreducible

VI. by the hernia size

1. small

2. medium-sized

3. large

VII. by the quantity

1. solitary

2. multiple

Traumatic diaphragmatic hernias

The cause of its development is open or closed damages of the diaphragm. Eventration of the organs through the opening in diaphragm happens in the moment of trauma or some time after trauma (sometimes months or years later).

The left part of the diaphragm is damaged more often than the right one. The rupture of both diaphragm parts takes place very seldom. The rupture is formed on the border of the muscular and tendineos parts of the diaphragm.

The main clinical symptoms are: gastrointestinal and cardio-respiratory.

Gastrointestinal symptoms depend on the kinds of organs that dislocate in the thoracic cavity. They usually are: dysphagy, vomiting, pain in the upper part of the abdomen and other symptoms of the acute (chronic) torsion or acute (chronic) intestinal obstruction.

Cardiorespiratory symptoms usually depend on the rate of the heart dislocation and lungs compression.

These symptoms include full-blown evident dispnea, tachycardia, cyanosis, cough and sometimes collapse.

The main instrumental examinations are:

1. X-ray examination with barium swallow examination of the digestive tract

2. laparoscopy

3. diagnostical pneumoperitoneum

The main complications of the diaphragmatic hernias:

1. torsion of the stomach

2. intestinal obstruction

3. pericardial tamponade

4. ulceration of the stomach or bowel wall with the following perforation.

All traumatic hernias must be operated. The principle of surgery treatment is the suppression of the organs dislocation and suture of the diaphragm defect.

The opening in diaphragm is sutured with lavsan (catgut is not used). The duplication in the diaphragm opening is more reliable method. In case of suture tension the suture line can be strengthened by allograft

Hiatal hernia.

Anatomy

The diaphragm is a musculotendinous partition separating the thoracic and abdominal cavities. It's periphery consists of skeletal muscle fibres which merge centrally with an aponeurotic tendon. The diaphragm has a pronounced convexity toward the thorax and has two domes or cupolas, the right usually lying at a higher level than the left.

Musculature

Peripherally thr diaphragmatic muscle is attached to the sternum, the costal margin and the vertebral column. The sternal attachment is by two small slips to the posterior surface of the xiphisternum. The costal attachment is to the inner surface of the lower six ribs and costal cartilages by slips that interdigitate with those of transversus abdominis.

The diaphragm attaches to the vertebral column by two crura (pillars), one on each side of the abdominal aorta. Both crura are anchored to the sides of the upper two lumbar vertebral bodies while the longer right crus is also attached to the third lumbar vertebra. The crura are linked in front of the aorta by the median arcuate ligament, the fibres interdigitating as they ascend towards thecentral tendon. Lateral to each crus thr diaphragm attaches to the transverse process of the first lumbar vertebra by the medial arcuate ligament (lumbocostal arch) and to the twelfth rib by the lateral arcuate ligament.

A triangular gap, the vertebrocostal trigone often exists between the fibres attaching to the last rib and those arising from the bertebral column.

The central tendon gives attachment to the fibrous pericardium and is pierced by the inferior vena cava.

Apertures in the diaphragm transmit the inferior vena cava and the oesophagus. The opening for the inferior vena cava (caval opening) lies to the right of the midline, and the oesophageal opening (hiatus) is slightly to the left.

During quiet breathing these opening lie respectively at the levels of the eighth and tenth thoracic vertebrae. The caval opening pierces the central tendon and transmits the right phrenic nerve as well as thr vena cava . The oesophageal opening, which also transmits the vagal trunks and branches of the left gastric vessels, is surounded by muscle fibres of the right crus. The left phrenic nerve pierces the left dome adjacent to the apex of the heart while on each side the thoracic splanchnic nerves pass through the crus may also be prierced by the hemiazygos vein.

The aorta pierces the diaphragm and is accompanied by the thoracic duct and vein azygos. Besides, the subcostal nerves and vessels, (sympathetic trunks, superior epigastric vessels (branches of the internal thoracic vessels) and intercostal vessels and nerves pass between the muscular slips.

Movement

The diaphragm is an important muscle of inspiration and also assists the muscles of the abdominal walls and pelvic floor in rasing the pressure within the abdomen and pelvic.Thus, the diaphragm contracts during acts of lifting and straining (for exampel, defecation and childbirth).

The shape and position of the diaphragm vary according to body position and the phase of ventilation. During full inspiration the diaphragm contracts, pulling it,s central tendon to the level of the tenth thoracic vertebra. The descent of the diaphragm enlarges the thoracic cavity. When the diaphragm relaxes during expiration, its central tendon is pushed superiorly by intraabdominal pressure, compressing the thoracic contents.

Nerve supply.

The right and left phrenic nerves provide the main motor and sensory supply to the diaphragm. The phrenic nerves pierce the diaphragm and innervate it from the abdominal surface. Each phrenic nerve provides the motor supply to its own half of the diaphragm. The crus is innervated by the lower intercostals nerves. In addition, each phrenic nerve carries sensory fibres from the pericardium and from pleura and peritoneum covering the central portion of the diaphragm. Irritation of these sensory fibres may produse pain referred to the shoulder. Sensory fibres from the peritoneum and pleura covering the periphery of the diaphragm are conveyed by the lower intercostals nerves.

Blood supply.

The major blood supply is provided by the inferior phrenic arteries, which are usually direct branches of the aorta. The corresponding veins drain into the v. cava inferior. Also the musculophrenic vessels (the terminal branches of the internal thorasic vessels) and aa. intercostalis supplay the periphery of the diaphragm.

Relations.

The inferior surface of the diaphragm is in contact with abdominal organs including the liver, kidneys, spleen and stomach. Its thoracic surface is related to the heart and lungs and their associated pericardium and pleura upward and dounward excursions of the diaphragm cause corresponding movements of all the organs related to it.

Diaphragmatic hernias are the most widespread pathology of the diaphragm. The common symptom for all diaphragmatic hernias is the prolapse of the abdominal organs in the thoracic cavity through the congenital gaps (certebrocostal and sternocostal trigones) or through dilated natural apertures in the diaphragm and through traumatic opening.

Classification of the diaphragmatic hernias:

by the origin:

congenital

acquired

traumatic

non traumatic

by the localization:

hernias of the aponeurotic tendon

hernias of the muscular part of the diaphragm

hernias of the musculotendinous part of the diaphragm

hernias of the gaps and natural openings.

by the presence of the hernial sack

true

false

by the clinical course

acute

chronic

by the clinical picture

incarcerated

non-incarcerated

reducible

irreducible

by the hernia size

small

medium-sized

large

by the quantity

solitary

multiple

The main clinical symptoms are: gastrointestinal and cardio-respiratory.

Character, volum and the rate of the transferred organs filling and also, sizes, form and localization of the hernial opening influence the clinical symptoms evidence.

Cardio-respiratory abnormalities depend on the rate of the heart displacement and lungs compression. Transfer speed of the abdominal organs in the thoracic cavity has the big meaning, because the compensatory mechanism fails to develop. That’s why the more evident cardio-respiratory symptoms appear in case of acute traumatic hernias, which symptoms are the full-blown evident dyspnea, tachycardia, cyanosis and sometimes collaps, connected with the lung compression and dislocation of the mediastinum.

The localization of the hernia opening plays the important role. So, in case of congenital or acquired pericardial hernias the migration even of the small part of the bowel or omentum in the pericardial cavity can cause the symptoms of the heart compression or pericardial tamponade.

Gastrointestinal symptoms intensity depends on the organs, which dislocate in thoracic cavity. Stomach transfer is accompanied by symptoms of its acute or chronic torsion. Flexure of esophagus causes the dysphagy. Omentum transfer with the compression of the intestine leads to the development of the chronic or acute intestinal obstruction.

Farther, we will study the clinical pictures in case of different diaphragmatic hernias.

Traumatic diaphragmatic hernias

The cause of its development is open or closed damages of the diaphragm. Eventration of the organs through the opening in diaphragm happens in the moment of trauma or some time after trauma (sometimes months or years later).

Traumatic diaphragm hernias may be acute or chronic in case of blunt abdominal trauma, which brings on the increase of the intra-abdominal pressure, the diaphragm can’t stand the pressure and breaks. The left part of the diaphragm is damaged more often than the right one. The rupture of both diaphragm parts takes place very seldom. The rupture is formed on the border of the muscular and tendineos parts of the diaphragm.

In case of extensive diaphragm ruptures and dislocation of the abdominal organs in pleural cavity, the symptoms of the pleuropulmonalic shock, pain in abdomen and chest with the irradiation in the left arm and neck, cyanosis, dyspnea, tachycardia and arrhythnia are developed.

In this situation it is necessary to have a straight, oblique and lateral X-ray film taken. During the X-ray examination we can see higher position of the left or right dome of the diaphragm, limitation of the diaphragm mobility. In case of stomach prolapse in pleural cavity we can see the big horizontal fluid level in the left part of the chest. In case of intestine prolapse on the lungs fluid phone we can see shadows or air-fluid levels.

Dislocation of the liver or spleen gives the shadow in the appropriate part of the lung field. Sometimes we can see the diaphragm dome and abdominal organs situated higher of it.

The barrium swallow examination of the digestive tract gives the opportunity to determine the character of the organs, which were transfered to the thoracic cavity (parenchymatous or caval hollow) to specify the localization and size of the hernia opening.

Sometimes diagnostical pneumoperitoneum is done to some patients. In case of false hernia the picture of the pneumothorax is determined during the X-ray examination. Sometimes the laparoscopy helps to confirm or make the final diagnosis. In case of prolonged hernia existence the dislocated organs become changed, for example in stomach in the place of strangulation ulcers with further perforation can be formed; in the bowel wall the fibrous scars can bring on the symptoms of the intestinal obstruction.

All traumatic hernias must be operated. The principle of surgery treatment is the suppression of the organs dislocation and suture of the diaphragm defect. Transpleural approach in fourth intercostal gap on the right or in the 7-8 intercostal gap on the left is usually used. In case of parasternal hernias laparotomy approach is used.

The opening in diaphragm is sutured with lavsan (catgut is not used). The duplication in the diaphragm opening is more reliable method. In case of suture tension the suture line can be strengthened by allograft. In case of strangulated diaphragm hernias the transthorocal approach must be used, because the transfer of incarcerated abdominal organs through narrow diaphragm opening from the direction of abdominal cavity is very dangerous and often impossible (especially if the perforation of the organ took place and its contents got into the pleural cavity). In this case there is high risk of abdonimal cavity infection. Defect suture in diaphragm is easier to fulfil through transthoracic approach. When the operation starts with laparotomy in case of acute abdomin and the diagnosis is defined during the operation, there can appear difficulties in transfer of dislocated organs, so the surgeon must fulfil thoracotomy. Operation volume depends on the kind of incarcerated organ and its damage rate. Defect suture in the diaphragm is fulfilled according to the methodics mentioned above. The mortality in this pathology amounts to 40%, which is very high.

HIATAL HERNIA AND GASTROESOPHAGEAL REFLUX

The subject оf hiatal hernia cannot Bе discussed separately from consideration оl gastroesophageal ref1ux and its соmрliсаtions. Each оf these entities has its own history, method оf evaluation, indications for treatment, and therapy; however, both conditions involve abnormalities at the gastroesophageal junction and mау coexist. Hiatal hernia has been recognized in autopsy studies for several centuries but was not diagnosed in а living human being until early in the twentieth century, following the development оf diagnostic radiographic methods. For almost 50 years thereafter, the herniation оf the stomach through the esophageal hiatus оf the diaphragm was thought to bе simply а hernial problem similar to other hernias through the abdorninal wall. Early surgical efforts to repair hiatal hemia emphasized anatomic correction bу obliteration оf the hernia sac and narrowing оl the diaphragmatic crura. Large experiences with these types of operation were reported by Harrington, Sweet, and others.

In 1951, Allison clearly described the clinical problem of gastroesophageal ref1ux with its symptoms and complications. Не noted the frequent association of ref1ux with hiatal hernia and emphasized the importance of phrenoesophageal membrane abnormalities in both conditions. Allison described а method of hiatal hernia repair involving reattachment of the phrenoesophageal membrane, which he hoped would correct the problem of gastroesophageal ref1ux as well. The Allison repair received wide trials; but before his death, Allison recognized that the incidence of persistence of reflux after repair was too high.2 It has not been the answer to the problem of gastroesophageal reflux.

Shortly after Allison's report, Belsey and Nissen independently and almost simultaneously developed more effective antireflux ореrаtiоns. They recognized the differences in symptoms caused by reflux, compared with those caused by hiatal hernia alone. Although surgical methods for effectively controlling reflux have been known for more than 35 years, the factors that control reflux in normal human beings are only recently being understood and still provoke controversy.

ANATOMY

А precise definition of the gastroesophageal junction is necessary to an understanding of this region, because it is described in several ways that influence clinical thinking. The distal esophagus is perhaps best defined as the nаrrоw-diаmеtеr swallowing tube, consisting of two muscle layers, that leads the normal peristaltic contraction to its conclusion. The presence of columnar epithelium within the most distal 2 сm of the esophagus is а common and normal finding but causes confusion аbоut the location of the gastroesophageal junction. А junction defined as the mucosal border between squamous and columnar epithelium is at а more cephalad level than the junction of the swallowing tube (as defined аbоvе) with the digestive pouch or stomach, which is of larger diameter, does not transmit the esophageal peristaltic wave, consists of three muscle layers, and has а serosal covering over а portion of its circumference. For an understanding of the mechanisms that control gastroesophageal reflux, the junction of the muscular swallowing tube with the gastric digestive pouch is а more useful definition of the gastroesophageal junction than the mucosal boundary.

The normal human distal esophagus passes through the diaphragm, and 2 to 4 сm. of distal esophagus lie within the abdomen. The abdomen is defined bу its inner boundary, consisting of the endoabdominal fascia. ln the region of the esophageal hiatus, this fascia comes off the underside of the diaphragm and bridges the hiatal opening. This fibroelastic fascial tissue inserts through the wall of the esophagus into the submucosa and thereby fixes the entry of the distal esophagus into the abdominal cavity (Fig. 1). The level of entry into the abdomen mау bе identified bу esophageal manometric studies. These demonstrate that intra-abdominal pressure increases with inspiration, whereas intrathoracic pressure decreases. This level of change in respiratory pressure dynamics occurs over а short distance in normal humans and confirms that 2 to 4 сm. of distal swallowing tube is located within the abdominal positive-pressure envirоnmеnt. Radiographic studies depend upon the air-tissue interface between lung and diaphragm to mark the level of the diaphragm. However, the hiatal opening through the diaphragm is in the posterior mediastinum; so the radiographic identification of the abdominal-thoracic barrier is not accurate for the hiatus. This causes further confusion in identifying а hiatal hernia and the gastroesophageal junction.

The distal esophagus itself differs only slight1y from the more proximal esophagus аbоvе the phrenoesophageal membrane. Although the muscles of the distal esophagus are similar to those located more proximаllу, the mucosa dеmоnstrаtеs а change from squamous to columnar epithelium within the lower 2 to 4 сm. of esophagus. Normally, nо parietal cells are seen in the mucosa аl this level. This zone of simple columnar epithelium resistant to acid digestion is an important protective transitional zone between the neutral рН of esophagus and the acid environment of the stomach.

In addition to the esophagus, the vagus nerve trunks pass through the phrenoesophageal membrane into the abdomen via the esophageal hiatus. No other structures of importance pass through this barrier. The arterial blood supply to the distal esophagus from the ascending branch of the left gastric artery enters the wall of the esophagus below the phrenoesophageal membrane. Аt the level of the membrane insertion, the vessels in the esophageal wall pass very close to the mucosa, whereas they are normally more deeply situated in the submucosa аt higher levels in the esophagus or lower оn the stomach. This observation mау bе responsible for the common location of а ruptured esophageal varix in the lowermost portion of the esophagus, where the veins are most superficial and where the abdominal thoracic pressure difference makes а large change in intraluminal tamponading pressure.

PHYSIOLOGY OF TНЕ ESOPHAGOGASTRIC JUNCTION

The distal esophagus has two irnportant physiologic functions: the transportation of an ingested bolus into the stomach and the prevention of reflux of gastric contents back into the esophagus. Measurements of pressure in the distal esophagus demonstrate а resting pressure between 10 and 20 mm. Hg greater in the distal esophagus than in adjacent stomach. This elevated pressure zone is evidence of the barrier to reflux. When а peristaltic wave occurs, (Fig. 2) the pressure in the distal esophageal segment drops to the level of gastric pressure. This prevents the distal esophageal segment from acting as an obstruction to passage of а bolus of food. The precise mechanism for this decrease in pressure with swallowing is uncertain. Some believe that this is an active muscular relaxation under neural control. Other evidence suggests that shortening of the longitudinal muscle of the esophagus puts tension оn the insertion of the phrenoesophageal membrane into the esophageal submucosallayer. Since this membrane enters the esophagus аt an angle, the effect of shortening the esophagus is to рull open the lumen of the distal segment and cause а "relaxation" in pressure. In achalasia, in which innervation is disturbed and longitudinal muscle shortening does not occur, the elevated pressure in the abdominal segment of esophagus does not relax after swallowing. This is thought to Bе а саusе of dysphagia in such patients.

The mechanism for the elevated pressure in the distal esophagus serving аs the barrier to ref1ux is also not completely understood. Some evidence suggests that specialized muscle in the distal esophagus acts аs а sphincter under neurohormonal соntrol. This theory of аn active intrinsic sphincter is challenged bу observations that the laws of physics governing tension in the walls of tubes of different diameter mау bе responsible for the barrier to rеf1uх. Аn abnormally low insertion of the phrenoesophageal membrane into the swallowing tube wou1d tend to рull the lumen ореn, with increases in abdominal pressure, and reduce the difference in diameter at the gastroesophageal junction. The theory that ref1ux is controlled Bу physical properties at the gastroesophageal junction depends ироn а normal insertion of the phrenoesophageal membrane 3 to 4 сm аbоvе the junction. Неnсе, pressure in the abdominal cavity does not tend to рull the junction ореn, and the distal abdominаl esophagus is subject to the sаmе external pressure аs the larger-diameter gastric tube. Аs а practical matter, creation of а 3- to 4-сm segment of intra-abdominal esophagus is а critical part of successful antiref1ux surgery. Fortunately, the relocation of the distal esophagus into the abdominal environment is much more readily accomplished than аn a1teration in the nеиrohormonal control of аn intrinsic sphincter if оnе is present.

Diaphragmatic hernias are the most widespread pathology of the diaphragm. The common symptom for all diaphragmatic hernias is the prolapse of the abdominal organs in the thoracic cavity through the congenital gaps (certebrocostal and sternocostal trigones) or through dilated natural apertures in the diaphragm and through traumatic opening.

Classification of the diaphragmatic hernias:

by the origin:

congenital

acquired

a) traumatic

b) non traumatic

by the localization:

hernias of the aponeurotic tendon

hernias of the muscular part of the diaphragm

hernias of the musculotendinous part of the diaphragm

hernias of the gaps and natural openings.

by the presence of the hernial sack

true

false

by the clinical course

acute

chronic

by the clinical picture

incarcerated

non-incarcerated

a) reducible

b) irreducible

by the hernia size

small

medium-sized

large

by the quantity

solitary

multiple

The main clinical symptoms are: gastrointestinal and cardio-respiratory.

Character, volum and the rate of the transferred organs filling and also, sizes, form and localization of the hernial opening influence the clinical symptoms evidence.

Cardio-respiratory abnormalities depend on the rate of the heart displacement and lungs compression. Transfer speed of the abdominal organs in the thoracic cavity has the big meaning, because the compensatory mechanism fails to develop. That’s why the more evident cardio-respiratory symptoms appear in case of acute traumatic hernias, which symptoms are the full-blown evident dyspnea, tachycardia, cyanosis and sometimes collaps, connected with the lung compression and dislocation of the mediastinum.

The localization of the hernia opening plays the important role. So, in case of congenital or acquired pericardial hernias the migration even of the small part of the bowel or omentum in the pericardial cavity can cause the symptoms of the heart compression or pericardial tamponade.

Gastrointestinal symptoms intensity depends on the organs, which dislocate in thoracic cavity. Stomach transfer is accompanied by symptoms of its acute or chronic torsion. Flexure of esophagus causes the dysphagy. Omentum transfer with the compression of the intestine leads to the development of the chronic or acute intestinal obstruction.

Farther, we will study the clinical pictures in case of different diaphragmatic hernias.

Traumatic diaphragmatic hernias

The cause of its development is open or closed damages of the diaphragm. Eventration of the organs through the opening in diaphragm happens in the moment of trauma or some time after trauma (sometimes months or years later).

Traumatic diaphragm hernias may be acute or chronic in case of blunt abdominal trauma, which brings on the increase of the intra-abdominal pressure, the diaphragm can’t stand the pressure and breaks. The left part of the diaphragm is damaged more often than the right one. The rupture of both diaphragm parts takes place very seldom. The rupture is formed on the border of the muscular and tendineos parts of the diaphragm.

In case of extensive diaphragm ruptures and dislocation of the abdominal organs in pleural cavity, the symptoms of the pleuropulmonalic shock, pain in abdomen and chest with the irradiation in the left arm and neck, cyanosis, dyspnea, tachycardia and arrhythnia are developed.

In this situation it is necessary to have a straight, oblique and lateral X-ray film taken. During the X-ray examination we can see higher position of the left or right dome of the diaphragm, limitation of the diaphragm mobility. In case of stomach prolapse in pleural cavity we can see the big horizontal fluid level in the left part of the chest. In case of intestine prolapse on the lungs fluid phone we can see shadows or air-fluid levels.

Dislocation of the liver or spleen gives the shadow in the appropriate part of the lung field. Sometimes we can see the diaphragm dome and abdominal organs situated higher of it.

The barrium swallow examination of the digestive tract gives the opportunity to determine the character of the organs, which were transfered to the thoracic cavity (parenchymatous or caval hollow) to specify the localization and size of the hernia opening.

Sometimes diagnostical pneumoperitoneum is done to some patients. In case of false hernia the picture of the pneumothorax is determined during the X-ray examination. Sometimes the laparoscopy helps to confirm or make the final diagnosis. In case of prolonged hernia existence the dislocated organs become changed, for example in stomach in the place of strangulation ulcers with further perforation can be formed; in the bowel wall the fibrous scars can bring on the symptoms of the intestinal obstruction.

All traumatic hernias must be operated. The principle of surgery treatment is the suppression of the organs dislocation and suture of the diaphragm defect. Transpleural approach in fourth intercostal gap on the right or in the 7-8 intercostal gap on the left is usually used. In case of parasternal hernias laparotomy approach is used.

The opening in diaphragm is sutured with lavsan (catgut is not used). The duplication in the diaphragm opening is more reliable method. In case of suture tension the suture line can be strengthened by allograft. In case of strangulated diaphragm hernias the transthorocal approach must be used, because the transfer of incarcerated abdominal organs through narrow diaphragm opening from the direction of abdominal cavity is very dangerous and often impossible (especially if the perforation of the organ took place and its contents got into the pleural cavity). In this case there is high risk of abdonimal cavity infection. Defect suture in diaphragm is easier to fulfil through transthoracic approach. When the operation starts with laparotomy in case of acute abdomin and the diagnosis is defined during the operation, there can appear difficulties in transfer of dislocated organs, so the surgeon must fulfil thoracotomy. Operation volume depends on the kind of incarcerated organ and its damage rate. Defect suture in the diaphragm is fulfilled according to the methodics mentioned above. The mortality in this pathology amounts to 40%, which is very high.

HIATAL HERNIA

Hiatal hemia is the herniation of аn abdominal organ, usuаllу the stomach, through the esophageal hiatus in the diaphragm. The diagnosis is usuаllу made bу radiographic contrast studies demonstrating аn abdominal organ higher than the level of the diaphragm. The diagnosis is confirmed bу surgical exploration or at autopsy. Весаusе the esophageal hiatus is located in the mediastinum and retroperitoneum, there is nо immediately adjacent air-tissue density contrast for radiographic observation. Accordingly, the radiologic diagnosis of hiatal hemia is based оn visualization of the lung-diaphragm interface near, but not at, the esophageal hiatus.

Confusion is increased bу failure to recognize that the endoabdominal fascia defines the inner boundary of the abdominаl cavity. When the fascia is intact, the significance of а protrusion through the esophageal hiatus is different from а defect in the fascia, allowing а true peritoneal sас to protrude through the endoabdominal lining. Tо emphasize thеsе important differеnсеs in the significance of herniation through the esophageal hiatus, hiatal hernias are classified into two major types (Fig. 3).

Tуре / Hiata/ Hernia

The Tуре 1 sliding, or axial, hiatal hemia is the result of an extension of the endoabdominal fascia through the hiatus, which allows а smаll portion of gastric cardia to slide uр into the esophageal hiatus. The phrenoesophageal membrane remains intact. There is nо true peritoneal hernia sас. If the phrenoesophageal membrane inserts normally into the esophagus 3 to 4 сm аbоvе the gastroesophageal junction, this type of hemia is generally asymptomatic and is аn incidental finding of nо consequence. The Tуре 1 hiatal hernia is extremely common and саn bе demonstrated in mаnу adu1t patients bу а radiologist using vigorous compression techniques. This type of hiatal hernia is of nо significance unless accompanied bу abnormal gastroesophageal ref1ux. There is nо indication for аnу medical or surgical treatment for а Tуре 1 hiatal hemia. If symptoms of ref1ux are associated with а Tуре 1 hiatal hemia, the diagnostic and treatment considerations are directed toward the ref1ux, rather than the hernia. For this reason, further discussion of this problem focuses ироn gastroesophageal ref1ux.

Tуре II Paraesophagea/ Hernia

The Tуре II hiatal hemia, also termed paraesophageal or rolling hernia, is uncommon and represents а true herniation of the stomach into а peritoneal sас in the mediastinum. The distal esophagus is located in its normal position, anchored bу the phrenoesophageal membrane. А defect in the membrane allows а peritoneal sac to protrude alongside the esophagus through the hiatus. This defect usually occurs at the left anterolateral portion of the esophageal hiatus where the greater peritoneal sac reflects off the gastroesophageal junction. А herniation mау occur posteriorly as well where the lesser sac peritoneum reflects off the junction. In а large Tуре 11 hernia, both greater and lesser peritoneal sacs are commonly present through two defects in the fascia. Because intrathoracic pressure is less than atmospheric and abdominal pressure is positive throughout the respiratory cycle, the natural history of this type of hemia is progressive enlargement. The entire stomach mау herniate completely upward into the sacs, so that the pylorus comes to lie near the cardia, which predisposes to gastric volvulus. This causes а giant Tуре 11 hernia with аn upside-down intrathoracic stomach.

[pic][pic]

Figuге 3. Diagrammatic representation of Type I and Tуре II hiatal hernias. In the Tуре I hernia the phrenoesophageal membrane is intact and there is nо true peritoneal sac extending into the thorax, In the Tуре II hiatal hemia there is а defect in the phrenoesophageal membrane, pemnitting а free peritoneal sac to enter the lower pressure thoracic cavity.

With progressive enlargement of the hernia through the hiatus, the remaining attachments of the phrenoesophageal membrane stretch; so it is common to find а combined, or Tуре lll, hernia in the advanced stages, with components of both sliding and paraesophageal types. With а large defect, other organs, such as the colon, spleen, pancreas, and small intestine, mayenter the hemia sac as well and cause а complicated Tуре lV hiatal hemia with symptoms attributable to the other organs involved.

The Tуре 11 hemia mау bе completely asymptomatic and reach а large size, so that the entire stomach is in аn intrathoracic location without the patient's awareness of disabling symptoms. If the distal esophageal segment maintains its intraabdominal location, there is usually nо associated gastroesophageal reflux, and therefore heartbum and regurgitation do not often occur.

When symptoms occur, the patient mау complain of fullness after meals, gurgling or splashing noises in the chest, slowness in food passing through the distal esophagus at the level where it is compressed bу the adjacent gastric роuсh, or early satiety and postprandial vomiting. Acute epigastric or chest раin after meals is аn ominous symptom, suggesting intermittent volvulus. Stases in the incarcerated gastric роuсh mау cause erosion of gastric mucosa. The result mау bе аn acute or chronic gastric ulcer in the роuсh or riding over the diaphragmatic margins ('а riding ulcer), which mау bleed or perforate. Occasionally, bleeding mау bе quite massive; but more оftеn а chronic unехplained anemia is noted in association with this type of hemia. Gastric volvulus causes gastric obstruction or strangulation, which mау cause sudden death.

May be the patients with large asymptomatic Tуре II hiatal hemias without symptoms but with а totally intrathoracic stomach. They can have оnе or more complications of the hemia, including gastric strangulation or infarction, bleeding, and acute intrathoracic gastric dilation causing respiratory insufficiency.

Anу patient who presents with symptoms of dysphagia should undergo а barium swallow examination or esophagoscopy. This is the most соmmоn sequence for the diagnosis of the paraesophageal hernia. Postprandial vomiting, early satiety, and other digestive disturbances mау also prompt а barium swallow examination. Radiography is the definitive test for the Tуре 11 hiatal hemia, although the diagnosis mау bе suspected if а chest film shows аn air-fluid level in the mediastinum behind the heart (Fig. 4).

When the diagnosis is established, the patient's general соndition is evaluated. Unless there is some other lifе-thrеаtеning i1lness, patients with а large Tуре 11 hiatal hemia are generally advised to hаvе surgical correction because of the risk of sudden catastrophic complications. Before operation, esophagogastroscopy is performed because the distortion of the anatomy makes it difficult for the radiologist to exclude other abnormalities of the esophagus or stomach that mау require attention or complicate operative management. The presence of the Tуре 11 hiatal hernia is аn indication for surgical therapy, because there is nо effective medical treatment for this condition.

Operative treatment mау bе performed through аn abdominal or thoracic incision. Because of the possibility of intrathoracic adhesions from а long-standing hemia, there is risk of being unаblе to reduce the hemia through аn abdominal арproach or of causing injury to the hernia contents within the thoracic sac. For these reasons, mаnу surgeons prefer а thoracic approach for the repair of а giant Tуре 11 hiatal hernia.

In principle, аll that must bе accomplished Bу the operation is reduction of the hemia, elimination of the sacs, and repair of the large opening in the hiatus. Although this mау Bе achievable in some patients, the dissection necessary to eliminate the hernial sacs often produces the potential for recurrence of а sliding hiatal hernia through the defect or the risk of gastroesophageal reflux. Preoperative esophageal function tests show that арproxirnately two thirds of patients with а Tуре 11 hernia also hаvе abnormal reflux as well. For this reason, аn antireflux repair is usually performed as part of the operative treatment. The operation consists of full mobilization of the hemia, resection of the redundant anterior and posterior hernia sacs if present, placement of sutures in the diaphragmatic crura posteriorly for narrowing the hiatus, and the creation of аn antireflux fundoplication between the stomach and esophagus for eliminating the risk of postoperative gastroesophageal reflux.

Operative treatment for this type of hernia has а mortality risk of approximately 1 per cent. No specific complications from the operation are anticipated, a1though the patient mау experiеnсе аn increased sensation оf abdominal fullness and tightness after the repair because оf the relocation оf the herniated organs back within the abdomen. Long-term recurrence оf а hiatal hemia in patients who have previously undergone repair оf а paraesophageal hemia occurs in approximately 15 per cent, а rate somewhat higher than that encountered with а repair оf а Tуре 1 sliding hiatal hemia. The higher rеcurrеnсе follows the attenuation оf tissues caused bу the very large hernia. These tissues are less suitable for holding permanent sutures than are the more normal diaphragmatic crura.

GASTROESOPHAGEAL REFLUX

Regurgitation оf gastric contents occurs normally in human beings, particularly after а large mеаl. Distention оf the stomach gradually effaces the intra-abdominal segment оf esophagus and shortens its length. The gradual conversion оf this segment to аn inverted-funnel shape permits postprandial reflux to occur normally. Belching, burping, and vomiting are normal experiences. It is only when reflux occurs with increased frequency and at times when the stomach is not distended that pathologic, gastroesophageal reflux is observed. An individual who overindulges at mealtimes generally accepts some symptoms оf reflux after the meal and does not consider this to bе аnillness. However, when symptomatic reflux occurs after every meal and between meals, medical advice is оftеn sought.

The precise abnormality causing pathologic gastroesophageal reflux is not completely understood. The study оf а population оf patients with frequent reflux indicate that the intraluminal tension оf the distal esophageal segment is generally reduced and the length оf the intra-abdominal esophagus is shorter than normal. The reasons for this loss оf intra-abdominal esophageal segment and its high-pressure barrier are not known.

Symptoms

The symptoms оf reflux are heartburn and regurgitation aggravated bу postural change such as stooping or lying flat and relieved bу standing upright. When heartbum is clearly related to postural change and the regurgitation indicates bу its sour or bitter taste that it is оf stomach origin, the diagnosis оf abnormal gastroesophageal reflux саn bе made оn the basis оf clinical features аlоnе. Other symptoms саn bе caused bу reflux or the complications оf reflux, such as dysphagia, bleeding, substernal chest pain, а sensation оf spasm or something sticking in the throat, and respiratory symptoms.

Dysphagia, or difficulty in swallowing, associated with аbnormal reflux mау occur through three mechanisms. Refluxed gastric contents mау serve as аn irritant to the esophagus, causing secondary muscle spasm. Direct injury to the esophagus from acid peptic regurgitation mау cause edema, inflammation, and spasm - and еуеn fibrosis and а stricture in advanced cases. When а large sliding hiatal hernia is present, the esophageal longitudinal muscle is not fixed at its distal end. As the esophagus contracts, the hernia is pulled ир, interfering with efficient progression оf peristalsis. The symptom оf dysphagia mау resu1t.

Bleeding from esophagitis usually presents as chronic anemia and stools positive for occult blood, rather than as frank hematemesis or melena. In а few patients, severe acute esophagitis mау cause massive upper gastrointestinal hеmоrrhаgе. This is diagnosed bу endoscopy. Such bleeding is best managed acutely bу intensive medical treatrnent, including а nasoesophageal antacid drip with the patient in аn upright position. Another source оf clinically severe bleeding mау bе an u1cer developing in аn esophagus lined with columnar epithelium. The ulcerations оn the squamous side оf the esophageal mисоsal junction are usually superficial. Ulcerations developing in columnar epithelium mау bесоmе quite deep, similar to gastric ulcers and mау cause rapid gastrointestinal bleeding.

The chest pain caused bу reflux is generally described bу the patient as heartburn or а burning substernal and epigastric раin. However, another type of раin caused bу reflux mау mimic the symptoms of аnginа pectoris, including radiation of the раin to the neck, shoulders, and аrms. This type of раin is thought to occur because of esophageal spasm, rather than mucosal irritation. It mау bе difficult to differentiate from true аnginа pectoris and ultimately must bе diagnosed bу objective testing for both reflux and coronary artery disease.

Respiratory symptoms, including productive cough, frequent respiratory infections, pneumonia, and chronie bronehitis, are соmmоn in the general population. Gastroesophageal reflux is also соmmоn. Without question, аbnоrшаl gastroesophageal reflux mау саusе chronic aspiration of gastric contents into the lung, with resulting respiratory disease. Recиrrent рnеumоniа, lung abscess, bronchieetasis-with symptoms similar to those of asthma, morning hoarseness, nосturnаl cough, and productive morning cough - have аll Bееn linked to abnormal reflux as а causative mechanism.

Diagnostic Stиdies

RADIOGRAPHY. When symptoms suggestive of reflux саusе а patient to consult а physician, several stиdies are indicated to соnfirm or eliminate the diagnosis. As for аll esophageal disease, а barium swallow and upper gastrointestinal radiography are performed first. It is important to observe the whole esophagus and stomach as а unit, because disorders of the upper esophagus mау саusе symptoms that mау bе confused with reflux; and abnormalities of the stomaeh, including delayed gastric emptying, mау aggravate reflux or саusе symptoms similar to those of reflux. If the radiologist sees spontaneous free reflux, this alone is elear evidence of pathologic reflux, because it is usually difficult to demonstrate gastroesophageal reflux during the course of а barium swallow examination. Reflux is demonstrated spontaneously during а barium swallow examination in only approximately 40 per cent of patients who ultimately prove to have this disorder. А Tуре 1 axial hiatal hernia is а соmmоn finding during barium swallow ехаminаtion. The demonstration of hemia varies directly with the aggressiveness of the radiologic examination. The observation of аn axial hiatal hernia without free reflux does not establish the diagnosis of reflux as the саusе of the patient's symptoms. Several radiologic reports advocate the use of а "water-sipping" test accompanied bу abdorninal compression to demonstrate reflux. This is not аn accurate test, because swallowing of water is knоwn to саusе relaxation or opening of the distal esophagus. lf accompanied bу compression of the abdomen, this forces reflux to occиr in normal subjects. А positive water-sipping test alone should not bе considered as conclusive evidence of аn incompetent cardia. Because radiographic studies are usually nоt sufficient for diagnosing symptomatic gastroesophageal reflux, esophageal function tests using pressure and рН measurements in the esophagus are used for more precise diagnosis.

FUNCTION TESTS. For esophagitis to develop as а complication of reflux, two events are necessary. Thе patient must hаvе аbnоrmal frequency of reflux, but there must also bе prolonged contact bеtween the irritating gastric contents and the esophageal mucosa to permit penetration of the mucosa and the establishment of esophagitis. For this reason, аn acid-clearing test is helpful in identifying patients at risk for еsорhаgitis.

Symptoms caused bу reflux, including epigastric and substernа} рain, are sirniIar to those of а variety of other conditions, including gastric and duodenal ulcer, pancreatitis, biliary tract disease, and coronary artery disease. The alternate infusion of 0.1 N НСl and normal saline into the esophagus is а useful test for confirming esophageal origin of symptoms. If the patient's complaints are stimulated bу the infusion of hydrochloric acid into the esophagus for 10 minutes or more and are relieved bу the infusion of saline, а positive acid perfusion test is recorded. This does not prove that reflux is the cause of the symptoms, but it indicates а likely association.

The battery of esophageal function tests-manometry, the standard acid reflux test, the acid clearing test, and the acid perfusion test-are frequently performed together as аn outpatient screening procedure for functional disease of the esophagus. Coupled with analysis of radiographic findings and subsequent endoscopy, these tests enable аn accurate diagnosis of esophageal functional disease in nearly аll symptomatic раtients.

ESOPHAGOSCOPY. When abnormal reflux is diagnosed, esophagoscopy is indicated for assessing the degree of damage to the esophagus and observing other abnormalities that mау ассоmраnу pathologic reflux. Most important is the determination of whether esophagitis is present. Esophagitis is graded оn а scale of 0 to 4, depending оn the severity of the changes observed. Grade 1 esophagitis is recorded when reddening without ulceration is seen. А biopsy of such mucosa mау show proximity of the rete pegs to the surface, neovascularization of the squamous epithelium, and hyperplasia of the basallayer. No inflammation is seen in such biopsies; therefore, this is not true esophagitis. Grade 11 esophagitis is characterized bу frank ulcerations just above the gastroesophageal mucosal junction. At more advanced stages, or Grade III esophagitis, some stiffening of the wall is observed. When а frank stricture, which prevents passage of the esophagoscope into the stomach, is еncountered, Grade IV esophagitis is diagnosed. The presence of columnar epithelium more than 3 сm above the junction of the tubular esophagus with the gastric pouch establishes the diagnosis of Barrett's esophagus. Gastric ulceration in the columnar epithelium should bе carefully noted. When Barrett's epithelium is seen, multiple biopsies are obtained to exclude dysplasia or neoplasia. This complication, a1though most likely to bе caused bу chronic reflux, is а known precursor of adenocarcinоmа of the distal еsорhаgus. After endoscopic examination, sufficient information is available for deciding оn treatment for reflux.

TREATMENT. The indications for surgical treatment of gastroesophageal reflux are primarily the complications of reflux. Patients having ulcerative esophagitis (of Grade 11 or greater severity) despite medical therapy, stricture, bleeding documented as owing to esophagitis, or aspiration clearly following reflux and causing respiratory illness should bе treated bу surgical antireflux repair. Patients with less severe reflux are treated medically in аn effort to control symptoms. In а few patients whose symptoms cannot bе controlled satisfactorily bу medical measures, operation mау bе indicated. Repair should bе performed, however, only after the diagnosis is conclusively proved to bе abnormal reflux and after а sufficient trial of medical therapy, usually 6 months or more. As stated earlier, patients having а Tуре 11, Ш, or IV hiatal hernia are treated surgically, and аn anti-ref1ux repair is generally incorporated into the correction of the hiatal hernia.

The medical treatment of gastroesophageal reflux includes methods for reducing the amount of regurgitation Bу gravity, making the regurgitated gastric contents less damaging to the esophagus, and reducing gastric residual volume. Patients are instructed to sleep with the head of the bed elevated оn 6-inch blocks, to take small meals, to avoid eating before bedtime, to avoid lying down after meals, and to avoid stooping whenever possible. Antacids are prescribed to bе taken 1 hour after meals, before bedtime, and as necessary to relieve symptoms. If these measures are insufficient, а course of cimetidine or ranitidine is tried in order to reduce the acid content of the regurgitated gastric material. Omeprazole is аn a1ternative and highly effective drug for reducing acid secretion. Drugs such as metoclopramide, which mау increase gastric emptying and esophageal peristalsis, mау prove valuable. Tranquilizers, muscle relaxants, and anticholinergic drugs are not prescribed, because they interfere with effective esophageal peristalsis, аn important safeguard against the development of esophagitis. Weight loss is recommended but is very difficu1t for patients with chronic symptomatic reflux, because the ingestion of food is аn effective neutralizer for the regurgitated acid. With the newer medications for reducing acid, medical therapy generally is successfui in controlling symptomatic uncomplicated reflux.

ANTIREFLUX SURGERY. When indications for surgical treatment are clear, the operation performed should bе аn antireflux repair and not а hiatal hernia repair, as advocated in the past. А number of operations are described to restore the intraabdominal segment of esophagus and to maintain the distal esophagus as а small-diameter tube. Аll such repairs generally involve mobilization of the cardia and lower esophagus, some type of plication of the stomach around the intraabdominal segment of esophagus, and narrowing of the esophageal hiatus to prevent the reconstituted abdominal esophagus from sliding back into the chest. Three types of antireflux repair have bееn extensively evaluated. Аll incorporate similar principles but vary considerably in technical details. Because this type of procedure is of recent origin, the operations саrrу the names of their developers, the Belsey Mark IV operation, the Nissen fundoplication, and the Нill posterior gastropexy and calibration of the cardia. There is nо conclusive evidence yet as to which is the best operation for the long-term control of gastroesophageal reflux.

The Belsey Mark IV operation was flrst performed bу Ronald Belsey in England in 1955. The term Mark IV indicates that this was the fourth modification of antireflux surgery from the originаl operation described bу Allison in 1951. The operation is performed оnlу through а thoracic аррrоасh. А sixth-interspace incision is preferred. The esophagus is mobilized fullу ир to the aortic arch to allow restoration of а long segment of intra-abdominal esophagus. The cardia is completely freed from its attachments to the diaphragm. The esophageal hiatus is nаrrоwеd bу the placement of sutures in the crura posteriorly. When eventually tied, these should permit only one finger of the operator tо pass through the narrowed hiatus (Fig. 5). The repair is achieved bу the plication of the stomach onto approximately 270 degrees of esophageal circumference, leaving the vagus nerves posteriorly.

The segment of the esophagus not included in the wrap is buttressed against the narrowed hiatus. Two rows of sutures are used, and three mattress sutures are placed in each layer. The first layer imbricates the adjacent gastric fundus onto the lower 2 сm. of esophagus. А second row of sutures, passing through the edge of the tendinous portion of the diaphragm, the fundus of the stomach, and the esophageal muscle 4 сm. above the gastroesophageal junction is then placed. The esophagus is then reduced manually through the hiatus. It should lie there without tension before the sutures are tied. А postoperative barium swallow should demonstrate а 4-сm segment of intra-abdominal esophagus. Long-term follow-up studies from some clinics indicate а recurrence rate of reflux or hiatal hernia after 10 years of approximately 15 per cent. Recurrence rates are higher in patients operated for а large Tуре 11 hiatal hernia and lower in those with the more соmmоn reflux indications without stricture. Recurrences most commonly are caused bу the sutures tearing out of the esophageal muscle or bу sutures cutting through the diaphragmatic crura posteriorly.

The fundoplication introduced bу Nissen in Switzerland in 1955 is performed through either an abdominal or а thoracic аррrоасh. In either case, the esophagus is fully detached from the margins of the hiatus. The thoracic approach is selected if more extensive mobilization of the esophagus is required to ensure an adequate intra-abdominal segment of esophagus. For facilitation of а full 360-degree plication of gastric fundus around the abdominal segment of esophagus without tension and without injury to the spleen, several short gastric arteries are ligated and divided. The fundus of the stomach is brought posteriorly around the esophagus. Sutures are placed through the anterior fundus and the wall of the esophagus, and the fundus is brought posteriorly. А 3- to 4-сm segment of intra-abdominal esophagus is wrapped bу the fundus in this manner (Fig. 6). If the fundus is not anchored securely to the intra-abdominal esophagus, the fundoplication mау slip down onto the body of the stomach and cause а double-chamber stomach, with obstruction to the proximal роисh, causing severe reflux. This is а serious complication that саn bе avoided bу adequate mobilization of the esophagus and bу placing the wrap around the esophagus above the intact gastrohepatic ligament and hepatic branch of the vagus nerve. The full 360-degree plication of stomach around the esophagus causes а somewhat higher luminal pressure in the abdominal segment of esophagus than does the Mark IV repair. Although this mау bе mechanically а more competent anti-reflux valve, it also introduces а greater risk of postoperative dysphagia as well as inability to belch and vomit. The danger of too tight а repair causing esophageal obstruction is real. Postoperative barium swal1ow should show the segment of abdominal esophagus and the pseudotumor effect of the fundoplication. Ten-year followир resu1ts in patients undergoing this repair are comparable to those achieved with the Mark IV repair.

The рroсеdurе of posterior gastropexy and calibration of the cardia has undergone several modifications since the operation was first introduced bу Нill in 1961. The resuIts achieved with this repair in recent years appear comparable to those achieved with the other two procedures. The operation is done through an abdominal incision. Afner extensive mobilization of the esophagus through the blatus, sutures are placed in the diаphragmatic crura to narrow the hiatus. The gastroesophageal junction is anchored to the arcuate ligament just cephalad to the celiac axis. Sutures are placed оn both the anterior and the posterior aspects of the gastroesophageal junction for the рurpose of causing а partial plication of stomach around the entrance of the esophagus into the stomach. The degree of narrowing of the abdominal esophagus is critical in this operation (Fig. 7); intraoperative manometry is therefore advocated as being essential to the success of this procedure. Postoperative barium swallow exarnination should demonstrate а narrow segment of abdominal esophagus entering the gastric pouch.

Each of these repairs provides excellent early resuIts in more than 90 per cent of patients. Published follow-up results for each, while not fully comparable, are so similar that it appears unlikely that one repair is clearly superior to the others. Reasons to choose а particular repair include the training and experience of the surgeon, whether an abdorninal or thoracic approach is preferred in а particular patient, and the advisability of avoiding а total fundoplication in patients with ineffective peristalsis and а motor disorder.

Side effects of the repair include inability to belch and vomit, symptomatic gaseous distention of the stomach and intestines from aerophagia unrelieved bу belching, the risk of dysphagia from too tight а repair, and the risk of injury to the esophagus or stomach owing to the placement of sutures.

ESOPHAGUS LINED WITH COLUMNAR EPITHELIUM

(ВАRRЕN'S ESOPHAGUS)

In 1950, Barrett described а condition in which columnar epithelium lining the esophagus was associated with either ulceration in the abnormal epithelium or esophagitis at the proximаllу located squamocolumnar junction. The cause of this condition is still undetermined. In some it mау bе of congenital origin. However, most patients with this condition have severe, chronic, long-standing reflux. It is known that the glandular epithelium mау migrate proximally and repopulate the denuded esophageal lining at the junction where the squamous epithelium is eroded bу chronic reflux. А stricture or severe esophagitis frequently occurs at the junction of columnar and squamous epithelium. This metaplastic epithelium mау undergo dysplasia or neoplastic change. Several types of glandular epithelium mау bе found in Barrett's esophagus, including cardiа type columnar, acid-secreting gastric fundic and metaplastic intestinal epithelium. А number of patients with adenocarcinоmа of the esophagus are seen in whom the cancer appears to arise from the columnar epithelium. When this condition is diagnosed, multiple biopsies must bе taken for exclusion of neoplastic change. If high-grade dysplasia or neoplasia is seen, an esophageal resection should bе performed. When complications of reflux accompany Barrett's esophagus, an antireflux repair should bе performed following dilation of the stricture if necessary. In such patients, long-term observation with repeated endoscopy and biopsy or brush cytology examination is essential to demonstrate that the mucosa is quiescent and not prone to neoplastic degeneration.

REFLUX-INDUCED STRICTURES OF TНЕ ESOPHAGUS

At an advanced stage, reflux mау cause sufficient inflammation, ulceration, destruction, and scarring of the esophageallining to produce а frank stricture. These almost always consist of combinations of edema, inflammation, spasm, and fibrosis. The treatment of the reflux-induced stricture is more difficult and results are less successfuI than with management of straightforward reflux problems. Therefore, it is important to perform anti-reflux surgery before а stricture develops. For this reason, persistent Grade 2 ulcerative esophagitis is an indication for antireflux surgery, because this degree of esophagitis is а precursor of the eventual formation of а stricture if reflux persists.

Nearly аll patients with reflux-induced strictures, not previously treated surgically, respond to intensive mеdiсаl therapy and repeated dilatations prior to operation. This has the effect of reducing the inflammation, edema, and spasm and converting the stricture to а lesser degree of esophagitis. Esophageal length is restored. When dilatations to а No. 40 French bougie саn bе achieved easily prior to operation and the inflammation саn bе reduced bу intensive mеdiсаl therapy, an antireflux repair alone has а good likelihood of success. If the stricture cannot bе easily dilated or if extensive shortening of the esophagus is found at operation, additional operative measures mау bе necessary. Several approaches are advocated. These include lengthening the esophageal swallowing tube bу cutting а tube of stomach from the lesser curvature as а continuation of the esophagus. This procedure is termed а Collis gastroplasty. After the gastroplasty is performed, an antireflux repair. such as the Mark IV reconstruction or Nissen fundoplication is added to prevent further reflux into the gastric tube and distal esophagus. Postoperative dilatations of the stricture mау bе necessary in such cases. It is important that the gastric tube Bе made around а large-diameter bougie, at least а No. 40 French, to ensure that the tube is not too narrow.

Another approach to the management of а stricture that саnnot readily bе dilated preoperatively is the Thal fundic patch operation coupled with а fundoplication. Thal described а technique for cutting longitudinally across the stricture, allowing the opening in the esophagus to gape widely, applying а skin graft across the opening, and then plicating the adjacent fundus of stomach across the opening in the esophagus. This procedure alone does not prevent reflux; but when coupled with а full 360-degree fundoplication of the Nissen type (Fig. 9), satisfactory results are achieved in approximately three quarters of the patients, as reported bу Hollenbeck and Woodward.

Another method of treating the esophagus that cannot Bе reduced into the abdomen is intraoperative dilatation, coupled with а full fundoplication, but with the 360-degree fundoplicatiоn left in the chest. When this is done, the hiatus must bе opened widely, and the stomach serosa must bе carefully аnchored to the diaphragm. Despite this, there is а significant risk of progressive enlargement of the iatrogenic hiatal hernia, with further surgical therapy necessary at а later date. An incidence of gastric ulceration in the intrathoracic gastric роuсh is seen in these patients as well. None of these approaches, including antireflux surgery for stricture, Collis gastroplasty, Thal fundic patch operation, or intrathoracic Nissen fundoplication, is uniformly satisfactory in patients with stricture. Excellent results, including the relief of dysphagia and long-term control of reflux, are reported in approximately three quarters of the patients after аnу of these procedures.

When а recurrence develops after previous surgical therapy for а stricture, it is unlikely that further attempts at repair will bе successful. In such complicated reoperative cases, а resection of the damaged esophagus with аn intestinal interposition using either left colon or jejunum is highly satisfactory. The use of stomach to reconstitute the esophagus after resection is not advocated for bеnign disease, because the incidence of reflux fоllowing esophagogastrostomy is too high. The risk of rеcurrеnt esophagitis and stricture is minimized bу the interposition of an intestinal segment from the esophageal remnant through the diaphragm and into the stomach. Although this operation yields excellent results, it is а procedure of greater magnitude than аnу of the others and so should bе reserved for those patients who have recurrent strictures after failure of previous operative attempts.

Literature.

1. Short Practice of Surgery by Charles V. Mann and all.

2. Textbook of surgery by Sabiston

3. Lectures

Approximate actions base.

1. Introduction /5 min/. Teacher short characterizes topic actuality, meets students with main aims of the study and plan.

2. Initial knowledge’s control /15 min/.

3. Individual students work with patients /30 min/. The teacher explains some more difficult and important parts of problem. The choice is realized by asking of students and their answers correction.

4. Clinical analyses of topical patients /100 min/. Students observe topical patients under teaches control. After it finishing, the students report about receiving results.

5. Work in dressing-room and operation theater. Teacher and students change the dressings of patients after different surgical procedures on esophagus.

6. Study of X-ray pictures.

7. Final knowledge control. Solution of test-questions /25 min/.

8. Conclusion /5 min/. The teacher concludes the session and gives new task for the next once.

Test questions.

1. Choose the most accurate diagnostic method of gastro-esophageal reflux.

a) X-ray examination

b) esophagoscopy/

c) US-scanning

d) CT-scanning

2. Clinical picture of gastro-esophageal reflux includes the following:

a) heartburn/

b) regurgitation/

c) substernal chest pain/

d) dysphagia/

e) vomiting

f) abdominal pain

3. Note the main complications of the types II, III and IV hiatal hernia:

a) gastric volvulus/

b) bowel strangulation/

c) ulcerative bleeding/

d) respiratory insufficiency/

e) coronary insufficiency

f) malaise

4. How many severity grades does esophagitis have?

a) 2

b) 4/

c) 5

5. Enumerate the arteries, which supply the diaphragm by blood.

a) inferior phrenic arteries/

b) musculophrenic arteries/

c) aa. Intercostals/

d) a. gastrica sinistra

e) aa. bronchialis

6. What part of the diaphragm is ruptured more often in case of blunt abdominal trauma?

a) the right part

b) the left part/

c) both parts

7. Note the main principles of the anti-reflux surgery:

a) mobilization of the cardia and lower esophagus/

b) plication of the stomach around the intra-abdominal segment of esophagus/

c) narrowing of the esophageal hiatus/

8. Choose the drugs for medical treatment of the gastro-esophageal reflux:

a) Antacids/

b) H2-receptor antagonists/

c) tranquilizers

d) muscle relaxants

e) anticholingergic drugs

9. What should the patient avoid in case of gastro-esophageal reflux?

a) lying down after meals/

b) sleeping in a semirecumbent position/

c) lying on the left side at night

d) heavy work/

e) excessive bending/

f) eating small meals

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