Diaphragmatic nhernia. Disease of mediastinum
Diaphragmatic nhernias
Diaphragmatic hernia nrepresents herniation of abdominal organs through natural openings of ndiaphragm, its weak places or ruptures.
A hiatal hernia occurs when a nportion of the stomach prolapses through the diaphragmatic esophageal hiatus. nAlthough the existence of hiatal hernia has been described in earlier medical nliterature, it has come under scrutiny only in the last century or so because nof its association with gastroesophageal reflux disease (GERD) and its ncomplications. There is also an association between obesity and the presence of nhiatal hernia. By far, most hiatal hernias are asymptomatic and are discovered nincidentally. On rare occasion, a life-threatening complication, such as ngastric volvulus or strangulation, may present acutely.
Etiology and pathogenesis
The cause of occurrence nof congenital hernia is the disturbance of embryogenesis with transformation ianomaly of diaphragm. The acquired diaphragmatic hernia more often arise owing nto age-dependent involution of diaphragm, its ptosis in the people with a nmainly sedentary mode of life, increase of intraperitoneal pressure, obesity, ncough, overfeeding, constipation, meteorism and pregnancy. The cause of sliding nhernias can be draw of esophagus upward in reflux esophagitis owing to nintensive contraction of its longitudinal musculature.
Predisposing factors include the nfollowing:
· nMuscle nweakening and loss of elasticity as people age is thought to predispose to nhiatus hernia, based on the increasing prevalence in older people. With ndecreasing tissue elasticity, the gastric cardia may not return to its normal nposition below the diaphragmatic hiatus following a normal swallow. Loss of nmuscle tone around the diaphragmatic opening also may make it more patulous.
· nHiatal nhernias are more common in women. This may relate to the intra-abdominal forces nexerted in pregnancy.
· nBurkitt net al suggest that the Western, fiber-depleted diet leads to a state of chronic nconstipation and straining during bowel movement, which might explain the nhigher incidence of this condition in Western countries.
· nObesity npredisposes to hiatus hernia because of increased abdominal pressure.
· nConditions nsuch as chronic esophagitis may cause shortening of the esophagus by causing nfibrosis of the longitudinal muscles and, therefore, predispose to hiatal nhernia. However, which comes first, the hiatal hernia worsening the reflux or nthe reflux-induced shortening of the esophagus, remains unknown.
· nThe npresence of abdominal ascites also is associated with hiatal hernias.
Diaphragmatic hernias may be ncongenital or acquired. Acquired hiatal hernias are divided further into nnontraumatic and traumatic hernias. The most common types of hernias are those nacquired in a nontraumatic fashion. Hernias acquired in a nontraumatic fashioare divided into 2 types, (1) sliding hiatal hernia and (2) paraesophageal nhiatal hernia. A mixed variety with coexisting sliding and paraesophageal ncomponents is possible.
· nSliding nhiatal hernia by far is the most common type of hiatal hernia. It occurs whethe gastroesophageal junction, along with a portion of the stomach, migrates ninto the mediastinum through the esophageal hiatus (see the image below). The nmajority of patients with demonstrated hiatal hernias are asymptomatic. This ntype of hernia interferes with the reflux barrier mechanism in several ways. As nthe LES moves into the chest, it no longer is exposed to positive nintra-abdominal pressure and, therefore, is less effective as a sphincter. Ifact, the sphincter moves into an area of low pressure, which interferes with nthe sphincter activity. In addition, the widening hiatus affects the competence nof the diaphragmatic crura. The angle of His is lost, making regurgitation of ngastric contents more likely. These changes not only predispose to reflux of ngastric contents into the esophagus, but also prolong the acid contact time nwith the epithelium of the esophagus.
· nIparaesophageal hernia, also called rolling-type hiatal hernia, the widened nhiatus permits the fundus of the stomach to protrude into the chest, anterior nand lateral to the body of the esophagus; however, the gastroesophageal njunction remains below the diaphragm (see Figure 3 of the image above). This ncauses the stomach to rotate in a counter-clockwise direction. As the hiatus nwidens, increasing amounts of the greater curvature of the stomach and, nsometimes, the gastric-colic omentum, follow. The fundus eventually comes to nlie above the gastroesophageal junction, with the pylorus being pulled towards nthe diaphragmatic hiatus. In this type of hernia, the anatomic relation of the nstomach to the lower end of the esophagus (angle of His) tends to remaiunchanged, so gross acid reflux does not occur.
1– norm, 2 – sliding hiatal hernia, n3 – paraesophageal hernia
Pathology
The esophagus passes through the ndiaphragmatic hiatus in the crural part of the diaphragm to reach the stomach. nThe diaphragmatic hiatus itself is approximately
The lower esophageal sphincter (LES) nis an area of smooth muscle approximately 2.5-
Any sudden increase iintra-abdominal pressure also acts on the portion of the LES below the ndiaphragm to increase the sphincter pressure. An acute angle, the angle of His, nis formed between the cardia of the stomach and the distal esophagus and nfunctions as a flap at the gastroesophageal junction and helps prevent reflux nof gastric contents into the esophagus (see the image below).
The gastroesophageal junction acts nas a barrier to prevent reflux of contents from the stomach into the esophagus nby a combination of mechanisms forming the antireflux barrier. The components nof this barrier include the diaphragmatic crura, the LES baseline pressure and nintra-abdominal segment, and the angle of His. The presence of a hiatal hernia ncompromises this reflux barrier not only in terms of reduced LES pressure but nalso reduced esophageal acid clearance. Patients with hiatal hernias also have nlonger transient LES relaxation episodes particularly at night time. These nfactors increase the esophageal mucosa acid contact time predisposing to nesophagitis and related complications.
Frequency
Hiatal hernias are more common in Western countries. The frequency of nhiatus hernia increases with age, from 10% in patients younger than 40 years to n70% in patients older than 70 years.
Paraesophageal hernias generally tend to enlarge with time, and nsometimes the entire stomach is found within the chest. The risk of these nhernias becoming incarcerated, leading to strangulation or perforation, is napproximately 5%. This complication is potentially lethal, and surgical nintervention is necessary. Because of the high mortality associated with this ncondition, elective repair often is advised wherever a paraesophageal hernia is nfound.
Classification
There are such types of hernia:
1) ncongenital;
2) nacquired;
3) nposttraumatic;
4) ntrue;
5) nfalse.
А. Diaphragmatic hernia.
I. Sliding (axial) diaphragmatic hernia:
1) nesophageal;
2) ncardial;
3) ncardiofundal.
ІІ. Diaphragmatic hernia of paraesophageal type:
1) nfundal;
2) nantral;
3) nintestinal (small and large intestine);
4) ncombined intestinal-gastric hernias;
5) nepiploic.
ІІІ. Huge diaphragmatic hernia:
1) nsubtotal gastric;
2) ntotal gastric.
ІV. A short esophagus:
1) nacquired short esophagus;
2) ncongenital short esophagus (thoracic stomach).
B. Parasternal hernias:
1) nretrosternal;
2) nretrocostosternal.
C. Lumbocostal diaphragmatic nhernias.
D. Hernia of atypical nlocalization.
Esophageal hernias:
Esophageal
Cardiofundal
Mixed paraesophageal
Paraesophageal fundal
Symptomatology and clinical course
The predominant nmanifestations resulting from sliding diaphragmatic hernia (about 90 % of ndiaphragmatic hernias) are the signs of gastroesophageal reflux. It is characterized by the pain behind breastbone or epigastric region. It more often appears nin supine position after meal or after intensive physical exertion.
Heartburn is the second naccording to the frequency sign and caused by the injury of esophageal mucosa nby gastric juice as a result in turn of gastroesophageal reflux.
Belching by nair, as a rule, observed, which commonly results in pain relief and decrease nof arching feeling in epigastric region.
Regurgitation arises owing nto gastroesophageal reflux, which reaches pharynx and noral cavity. More often observed regurgitation by gastric acid or bitter liquid nor food.
The sign of n”lacing shoes“ is nexpressed when the patient bends down after liquid food, and the latter is npartially poured out into the mouth. It is caused by incompetence of the lower nesophageal sphincter (gastroesophageal junction).
Nausea and nvomiting are rare. The latter some patients cause by themselves to achieve some nrelief.
Dysphagia is rarely nobserved. More often it is the outcome of complications of diaphragmatic hernia n(esophageal stricture, malignancy).
Roentgenological nsigns: 1) the sign of “bell”; 2) blunt His angle; 3) lack of air bubble of the stomach.
Sliding ndiaphragmatic hernia
The clinical nmanifestations of paraesophageal, retrosternal or lumbocostal hernias basically depend on the character of organs, which nthe hernial sac contents, and their compressing by hernial ring. Sometimes the nclinical course even of major hernias is asymptomatic, and they are noccasionally found out during X-ray examinations. For the first time the ndisease can manifest under the influence of physical exertion, trauma, npregnancy, labors etc.
Paraesophageal nhernia
Variants of clinical course and complications
The sliding hiatal hernia ncommonly has typical clinical course and rather rich symptomatology, which nenable to establish the diagnosis with a great degree of probability. nNevertheless occasionally gastroesophageal reflux as the nsequel of a sliding hiatal hernia can result imisdiagnostics (stenocardia, acute cholelithiasis etc.).
The most oftecomplications of sliding diaphragmatic hernia are gastric bleeding, peptic nstricture of esophagus and malignancy.
The causes of the nbleeding can be erosion and ulcers of stomach, which result from compression of nthe organ in esophageal hiatus. More often observed small bleeding, but at nlong-stand recurrent course they result in chronic anemia. The profuse bleeding narise rarely. The strangulation of a sliding diaphragmatic hernia never occurs. n
Nevertheless for ndiaphragmatic hernias of other locations the most dangerous complication is nnaturally strangulation. Such pathology manifests by the signs of s nstrangulation intestinal obstruction. However nthe correct diagnosis frequently possible to establish only during operation.
The diagnostic program
1. Anamnesis and physical nfindings.
Hiatal hernias are relatively commoand, in themselves, do not cause symptoms. For this reason, most people with nhiatal hernias are asymptomatic. Hiatal hernias may predispose to reflux or nworsen existing reflux in a minority of individuals. Physicians should resist nthe temptation to label hiatal hernia as a disease.
Patients can have reflux without a ndemonstrable hiatal hernia. When a hernia is present in a patient with nsymptomatic GERD, the hernia may worsen symptoms for several reasons, including nthe hiatal hernia acting as a fluid trap for gastric reflux and increasing the nacid contact time in the esophagus. In addition, with a hiatal hernia, episodes nof transient relaxation of the LES are more frequent and the length of the nhigh-pressure zone is reduced. The main symptoms of a sliding hiatal hernia are nthose associated with reflux and its complications.
No clear correlation exists betweethe size of a hiatal hernia and the severity of the symptoms. A very large hiatal nhernia may be present with no symptoms at all. Some complications are specific nfor a hiatal hernia.
· nEsophageal ncomplications
o nBy nfar, the majority of hiatal hernias are asymptomatic.
o nOften, npatients are left with the impression that they have a disease when a hiatal nhernia is diagnosed.
o nIrare cases, however, a hiatal hernia may be responsible for intermittent nbleeding from associated esophagitis, erosions (Cameron ulcers), or a discrete nesophageal ulcer, leading to iron-deficiency anemia. The prevalence of large nhiatal hernias in patients with iron deficiency anemia is 6-7%. This particular ncomplication is more likely in patients who are bed-bound or those who take nnonsteroidal anti-inflammatory drugs. Massive bleeding is rare.
· nNonesophageal ncomplications
o nIncarceratioof a hiatal hernia is rare and is observed only with paraesophageal hernia.
o nWhethis occurs, it can present abruptly, with a sudden onset of vomiting and pain, nsometimes requiring immediate operative intervention.
2. X-radiography of chest nand abdomen.
Although a chest radiograph may nreveal a large hiatal hernia (see the first image below), and many incidentally ndiagnosed hiatal hernias are discovered in this manner, a barium study of the nesophagus helps establish the diagnosis with greater accuracy (see the second nimage below).
Typical findings include aoutpouching of barium at the lower end of the esophagus, a wide hiatus through nwhich gastric folds are seen in continuum with those in the stomach, and, noccasionally, free reflux of barium.
A barium study helps distinguish a nsliding from a paraesophageal hernia (see the images below).
In rare cases, the entire stomach nmay herniate into the chest
The stomach may then undergo nvolvulus (see the image below) and subsequent incarceration and strangulation.
3. Esophagogastroscopy nwith biopsy and histological investigation.
Hiatal hernia is diagnosed easily nusing upper gastrointestinal endoscopy.
The diagnosis of a hiatal hernia nactually is incidental, and endoscopy is used to diagnose complications such as nerosive esophagitis, ulcers in the hiatal hernia, Barrett esophagus, or tumor.
A hiatal hernia is confirmed whethe endoscope is about to enter the stomach or on retrograde view once inside nthe stomach (see the image below). If any doubt remains, the patient may be nasked to sniff through the nose, which causes the diaphragmatic crura to napproximate, seen as a pinch, closing the lumen.
Endoscopy also permits biopsy of any nabnormal or suspicious area.
Esophageal manometry has a low sensitivity for ndiagnosing hiatal hernia, as compared to endoscopy, and is therefore not nappropriate in helping to establish a diagnosis.
4. Contrast X-radiography nof esophagus and stomach in three positions: upward, supine and upside-dowposition.
5. General blood and nurine analyses.
6. Coagulogram.
Sliding nhernia
Paraesophageal nhernia
Mixed nhernia
Differential diagnostics
Stenocardia. Diaphragmatic nhernias frequently cause the pain, which character not only the patient, but nalso doctor can identify as anginal. However in diaphragmatic hernia the paimore often is vague, spread to the stomach region and depends on body position. nThe pain, as a rule, arises in supine position and disappears, if the patient nupward. More often it spreads to the right and anginal vice versa to the left. nIn diaphragmatic hernia the ECG can manifest the coronary failure, nevertheless nstanding up, owing to the stop of strangulation leads to disappearance of these npathological sings. The pain caused by diaphragmatic hernia does not relieve nafter nitroglycerin. In this case more effective and prompt is atropine.
Peptic ulcer. The pain igastric and duodenal ulcer frequently localized in epigastric region with nirradiation in the left or right hypochondrium. Nevertheless, it is ncharacterized by periodicity, which caused by meal and disappears after the nusage of soda.
Lung natelectasis, pleurisy, pneumonia are also nshould be differentiated with diaphragmatic hernia. Thus it is always necessary nto remember, that the extrapulmonary shadow of supradiaphragmatic disposed hernia on a plain roentgenogram caresemble intrapulmonary. For correct diagnosis it is possible to recommend npolypositional X-radiography, contrast roentgenography of esophagus and nstomach.
Hypochromic anemia nfrequently associated due to repeated or permanent small bleedings. They are ncaused by a regional destruction a gastric mucosa. In the females of senior age nif it is fail to explain genesis of the revealed anemia, it is necessary to nthink about the opportunity of diaphragmatic hernia and carry out appropriate nX-ray examination.
Tactics and choice of treatment
The medical tactics ntoward diaphragmatic hernias of different localization essentially differs.
In case of sliding hiatal nhernia the method of a choice is the conservative ntherapy:
1) nthe diet the same, as in peptic ulcer;
An appropriate diet maintains aideal body mass index. Obesity predisposes to reflux disease. Burkitt et al nsuggest that the Western, fiber-depleted diet leads to a state of chronic nconstipation and straining during bowel movement, which would explain the nhigher incidence of this condition in Western countries.
2) nposition of the patient during sleeping – with elevated upside, nduring exacerbation – sedentary;
3) nsuppression of gastric secretion by administering of н2-blockers;
4) nneutralization of gastric acid;
5) nintensifying of evacuation of the food from stomach;
6) navoidance of constipation;
7) nanesthetics and sedative agents.
The indication for nsurgical treatment of sliding diaphragmatic hernia is the considerable nexpression of clinical signs, diminish of patient’s working capacity, fail of nconservative treatment, bleeding, peptic stricture, malignancy.
When hiatal hernias are symptomatic, nacid reflux usually produces the symptoms. If the hernia itself is causing nchest discomfort or other symptoms, surgery may be necessary.
· nWhesymptoms are due to GERD, the goals of treatment include prevention of reflux nof gastric contents, improved esophageal clearance, and reduction in acid nproduction. This is achieved in the majority of patients by a combination of nthe following:
o nModifying nlifestyle factors
o nNeutralizing nacid or inhibiting acid production
o nEnhancing nesophageal and gastric motility
· nThe ntreatment of GERD is beyond the scope of this article and is discussed iGastroesophageal Reflux Disease.
· nLarge nhiatal hernias may cause iron deficiency anemia regardless of whether Cameroulcers are present. This anemia responds well to PPI therapy with surgery noffering no clear advantage over medical therapy.
Surgical ntreatment. Upper median laparotomy is mainly used. Nevertheless some surgeons nprefer transthoracic accesses.
A patient with a large hiatal hernia nmay experience vague intermittent chest discomfort or pain. The paraesophageal nhernia may strangulate and frequently is operated on prophylactically to nprevent this complication. Paraesophageal hernias may present in infants or nadults as a potentially life-threatening complication of strangulation, and nprompt surgical repair is key. When found in asymptomatic individuals, nlaparoscopic repair is often undertaken, with large defects in the diaphragm nbeing closed with mesh.
Surgery is necessary only in the nminority of patients with complications of GERD despite aggressive treatment nwith proton pump inhibitors (PPIs). Because only a minority of patients with nhiatal hernia have any problems, this represents a very small proportion of npatients with sliding hiatal hernia; most patients with problems are managed nmedically.
By far, the majority of patients who nwould have undergone surgery in the past are managed successfully today with nPPIs. However, young patients with severe or recurrent complications of GERD, nsuch as strictures, ulcers, and bleeding, who cannot afford lifelong PPI ntreatment or would prefer to avoid taking medications long term, may be nsurgical candidates.
Another group of patients who are nsurgical candidates are those with pulmonary complications, in particular, nasthma, recurrent aspiration pneumonia, chronic cough, or hoarseness linked to nreflux disease.
Three major types of surgical nprocedures correct gastroesophageal reflux and repair the hernia in the nprocess. They can be performed by open laparotomy or with laparoscopic napproaches, which currently are being employed more frequently.
· nNissefundoplication
o nThe nNissen fundoplication performed laparoscopically has gained popularity because nof its lower morbidity and shorter hospital stay compared to the open procedure nperformed previously. Although a relatively high incidence of postoperative ncomplications, such as dysphagia and gas bloating, are reported, DeMeester and nPeters[7] have shown that placing a larger bougie in the esophagus during this nprocedure, along with a shorter wrap and more complete mobilization of the nstomach, have markedly reduced postoperative complications.[8, 9]
o nThis nprocedure involves a 360° fundic wrap around the gastroesophageal junction. The ndiaphragmatic hiatus also is repaired.
o nA ntransthoracic approach may be used in patients who have had a previous Nissewrap or those who have an irreducible hernia.
o nThe nToupet procedure is a variant of the Nissen wrap and involves a 180° wrap in aattempt to lessen the likelihood of postoperative dysphagia.
· nBelsey n(Mark IV) fundoplication: This operation involves a 270° wrap in an attempt to nreduce the incidence of gas bloating and postoperative dysphagia. It also is npreferred when minimal esophageal dysmotility is suspected. To complete this noperation, the left and right crura of the diaphragm are approximated.
· nHill nrepair: In this procedure, the cardia of the stomach is anchored to the nposterior abdominal areas, such as the medial arcuate ligament. This also has nthe effect of augmenting the angle of His and thus strengthening the antireflux nmechanism.
· nThe nantireflux procedures discussed above offer relief of symptoms in 80-90% of npatients. In most cases, the procedure of choice is the one with which the nsurgeon is most familiar. These procedures carry low mortality and morbidity nrates, lower than 15-20%. DeMeester et al found the Nissen procedure superior nto the Belsey and Hill repairs with regard to symptom relief and prevention of nreflux postoperatively (as judged by pH monitoring). Good long-term results nhave been reported for antireflux surgery, with adequate control of reflux ithe range of 80% at 10 years.
· nMost npatients with a paraesophageal hernia remain asymptomatic. In this type of nhernia, symptoms from acid reflux usually do not occur. Instead, the most ncommon symptom is epigastric or substernal pain. Some patients complain of nsubsternal fullness, nausea, and dysphagia.
o nA nsignificant proportion of patients with this type of hernia develop nincarceration of the hernia and possible gastric volvulus, which can lead to nperforation.
o nIf nperforation occurs, the mortality rate is high. Because of this, many surgeons nadvise elective repair when the diagnosis is made.
o nThe ngoal of surgery is to remove the hernia sac and close the abnormally wide nesophageal hiatus.
o nSome nsurgeons then tack the stomach down in the abdomen to prevent it from migrating nupwards again, or, they perform a temporary gastrostomy to help decompress the nstomach and anchor it in place in the abdominal cavity.
Stages of the operation:
1. nDrawing of the stomach into abdominal vacuity by ndisjunction of adhesions in the region of its cardial part, esophagus, excision of hernial sac.
2. nThe plastics of esophageal nhiatus of diaphragm (cruroplasty). The most widespread cruroplasty by Hill and nnarrowing of esophageal ring according to Garrington.
3. nElimination of valvular failure nof esophagocardial junction. The purpose of operation is to prevent ngastroesophageal reflux by means of formation of His angle and esophagocardial nvalve. Also Nissen fundoplication is applied.
4. nGastropexia – fixation of ngastric wall to parietal peritoneum.
Another tactics is napplied in the patients with paraesophageal, parasternal and lumbocostal hernias. The method of choice is the nsurgery. Such tactics is explained by the hazard of strangulation. The essence nof the operation consists of drawing down of hernial content (stomach, nintestine, omentum) into abdominal cavity, removing of hernial sac and nliquidation (suturing) of hernial ring.
Steps of cruroplastic
n
Diaphragmatic nrelaxation (Diaphragmatic Eventration)
The term n”diaphragmatic relaxation ” was used for the first time in 1906 by nWitting. It means a relaxation of diaphragm, its high standing and displacement nupward of abdominal organs.
The term n‘diaphragmatic eventration’ is used in common practice to describe a conditioof relaxation of the diaphragmatic dome. It may present at birth as a ncongenital condition due to a defect of diaphragmatic development or in a later nstage of life as an acquired condition (‘acquired diaphragmatic paralysis’ or n‘acquired diaphragmatic elevation’).
Etiology and pathogenesis
The cause of the disease nis the congenital or acquired decrease of diaphragmatic resistance, which nduring elevation of intraperitoneal pressure results in its outpouching. The ngreat importance in the development of acquired relaxation belongs to the ndamage of diaphragmatic nerve. The cause of the latter could be inflammatory nprocesses in chest and abdominal cavity, intoxication, poisoning, operations ochest organs and birth injury.
Pathology
In congenital form of a diaphragmatic relaxatiorevealed muscular aplasia, in acquired – atrophy of muscular fibers.
Classification
1) nComplete: left-side, right-side;
2) nIncomplete: anterior, posterior, restricted (partial).
Symptomatology and clinical course
Minor manifestation or nasymptomatic course characterizes diaphragmatic relaxation. Therefrom, it is always necessary to thoroughly nanalyze the occurrence of multiple signs from the organs of digestive, nrespiratory and cardiovascular system. The clinical symptomatology basically ndepends on dysfunction of the diaphragm by itself and organs, which adjoin to nit both in chest, and in abdominal cavity. In left-side diaphragmatic nrelaxation the asymptomatic course rarely occurs.
General nsymptomatology. The patients with diaphragmatic relaxation can feel a npain of different character, localization and intensity. The pain syndrome frequently nresults from gastric inflection or compression of vessels and nerves by filled nstomach. Inflection of vascular bundles nof pancreas, lien, kidneys, mesentery of small and large intestines as a result nof shift of abdominal organs also contribute to the development of paisyndrome. Frequently patients complain of general weakness and loss of weight.
Gastrointestinal nsymptomatology. Dysphagia almost always arises as a result of ninflection of abdominal part of esophagus. The heaviness after meal should be ncaused by atony of stomach and its evacuatiodysfunction. Ulceration and erosive gastritis, which occurs in some patients, nare the outcome of a regional ischemia from gastric inflection or torsion. nChronic constipation is basically caused by disturbance of massage influence of nthe diaphragm on intestine. Meanwhile heartburn, belching, nausea, vomiting and nmeteorism also observed.
A phrenocardiac nUden-Ramcheld’s syndrome represents cardiopulmonary nsigns. It is characterized by dyspnea, ndiscomfort in the region of heart, anginal pain, extrasystole and ECG changes n(elongation of Р wave, РQ interval and complex QRS).
Respiratory ndisturbances result from dynamic ndysfunction of the diaphragm. The high standing of the diaphragm leads to ncompression of lung on the side of lesion and disturbed ventilation of the nlower part. It causes the diminishing of vital capacity of the lungs and ndevelopment of dyspnea.
Roentgenologically nrevealed the high standing of diaphragmatic dome (to ІІ-ІІІ intercostal space), restriction of its excursioand reduce of the inferior pulmonary field. Frequently observed the mediastinal nshift to the opposite side. The contrast X-radiography of esophagogastric njunction can find out the inflection of abdominal part of esophagus. The X-ray nexamination enables to establish the diagnosis with a high degree of nreliability.
Diaphragmatic nrelaxation
Variants of clinical course and complications
Asymptomatic course of ndiaphragmatic relaxation in the majority of patients has caused interpretatioof this pathology as “innocent disease”. Nevertheless the shift and nrotation of heart can cause the heart failures, and the restriction of npulmonary excursion sometimes leads to chronic pneumonia. The gastric ninflection frequently may result in disturbance of the valvular mechanism of esophagogastric junction and occurrence of reflux nesophagitis.
The diagnostic program
1. nAnamnesis and physical findings.
2. nPlain chest X-radiography.
3. nEsophagogastroduodenoscopy.
4. nRoentgenoscopy of esophagus and gastrointestinal tract.
5. nGeneral blood and urine analyses.
Differential diagnostics
Diaphragmatic nelevation is the secondary high standing, nwhich can arise as a result of ascites, pregnancy, expressed meteorism, nperitonitis, tumours of abdomen, splenomegaly or megacolon.
Pneumothorax, npyopneumothorax, pleurisy. Such misdiagnostics in the patients with diaphragmatic nrelaxation frequently caused by chest pain, cough, dullness and tympanic sound revealed nat percussion, and weak breathing at auscultation. Chest X-radiography rather ncontributes to exact diagnostics.
Diaphragmatic nhernia. The differential diagnosis of diaphragmatic relaxation with this npathology is the most difficult. Nevertheless it has the important practical nvalue, because the threat of strangulation of diaphragmatic hernia requires aactive surgical tactics. During the establishment of the diagnosis it is always nnecessary to remember, that clinical manifestation of diaphragmatic hernia more nexpressed. However, the sharp inflection of abdominal organs in the patients nwith diaphragmatic relaxation also can associate with severe pain, which nresembles strangulation. Thereafter, a reliably differentiation of these ndiseases is possible only after a goal-oriented X-ray examination.
Cancer of nesophagus and cardial part of stomach. A sharp gastric shift upward with inflection of nabdominal part of esophagus can lead to dysphagia, substernal pain, disturbance nof digestion, considerable loss of weight etc. For differential diagnostics applied a contrast X-ray examination of nesophagus and stomach.
In difficult for ndifferential diagnostics cases a pneumoperitoneum with further X-ray nexamination is performed. This method allows with a major degree of reliability nto establish the diagnosis of diaphragmatic relaxation.
Tactics and choice of treatment
In most cases the nasymptomatic course of diaphragmatic relaxation requires no special treatment.
Conservative ntherapy applied at presence of symptomatology:
1) navoidance of physical exertions, which increases nintraperitoneal pressure;
2) ndiet – eating by small portions and exception of food, nwhich form waste and gases;
3) ntherapeutic gymnastics for improving of intestinal functioand decrease of the patient’s weight;
4) nsymptomatic therapy for regulation of cardiovascular and nrespiratory systems.
The indicatiofor operation: gastric torsion or severe cardiorespiratory ndysfunction. If clinical manifestations are absent, the surgical treatment cabe recommended only for women with further pregnancy and labors, because these nconditions cause a sharp increase of intraperitoneal pressure with further nshift of the diaphragm and abdominal organs.
Surgical treatment. By means of na lateral access in VІІ intercostal space a phrenoplasty is performed, which consist nof incision of diaphragm from costal edge to esophageal ring with following ndiaphragmatic duplication.
n
Acute nmediastinitis
Acute mediastinitis is a npurulent inflammation of mediastinum.
Etiology and pathogenesis
The penetration of pathogenic agents into mediastinum can result from nperforation and chemical burns of esophagus; injuries of trachea, bronchi, noperations on mediastinal organs and lungs. Also is possible the contaminatiofrom neck fat tissue and tracheobronchial lymph nodes.
Classificatioof mediastinitis
According to localization:
1) nanterior;
2) nposterior;
3) nsuperior;
4) nmedial;
5) ninferior.
According to pathogenesis:
1) nprimary;
2) nsecondary.
According to the clinical course:
1) nacute: purulent, aseptic;
2) nchronic.
According to the character of infection:
1) nnonspecific;
2) nspecific.
Symptomatology and clinical course
The clinical manifestatioof acute mediastinitis is characterized by prompt progressing course, ndependence on extent of the process, gravity of infection and peculiarities of nunderlying disease.
Body temperature raises nup to 39-40°С and of hectic character, the npatients complain of dyspnea, cyanosis, fever and profuse sweating.
The local symptomatology nof the disease depends on location of the process and involvement of esophagus, ntrachea, heart, n. vagus, n. рhrеnісus, n. recurrens, tr. nsуmраtісus.
Also is possible ndysphagia, dyspnea, constant cough, hoarseness, change of cardiac rhythm.
On percussion revealed a nmediastinal widening, on auscultation – weak cardiac tones.
X-ray nexamination. The method of X-ray examination should be chosen according to the cause nof occurrence of acute mediastinitis. If the disease is caused by cervical nphlegmon the X-radiography examination should be restricted only by chest X-ray nfilm in three plains. In such situations observed widening of mediastinum, nshadowing of its anterior part and shift of trachea. Compression of esophagus nrevealed by barium swallow.
The contrast X-ray nexamination of esophagus after its iatrogenic perforation it is possible to see npenetration of barium into mediastinum, shadowing and widening of its nconsequent parts. Fiberesophagoscopy as the method of diagnostics of esophageal nperforation is not recommended due to pneumatic pressure during this nmanipulation.
Variants of clinical course and complications
According to the features nof clinical symptomatology, acute mediastinitis is divided into anterior and nposterior mediastinites.
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Anterior mediastinitis |
Posterior mediastinitis |
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Throbbing substernal pain |
Throbbing chest pain with irradiation in interscapular region |
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Intensifying of pain during percussion of breast bone |
Intensifying of pain during vertebral pressing |
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Intensifying of pain when head is unbent back |
Intensifying of pain at swallowing |
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Occurrence of swelling in the region of jugular fossa |
Swelling above clavicle |
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Signs of compression of superior vena cava |
Sig of compression of azygos and hemiazygos veins (distended intercostal veins, pleural effusion) |
The most oftecomplications of acute mediastinitis are: pyopneumothorax, which has ariseafter the abscess discharge into pleural space, pleural empyema, purulent npericarditis, erosive bleeding and lung abscesses.
The diagnostic program
1. nComplaint and history of the disease.
2. nPhysical findings.
3. nChest X-ray examination.
4. nContrast esophagography. n
5. nECG.
6. nFibrobronchoscopy.
Acute mediastinitis
Differential diagnostics
Acute mediastinitis nrequires express differential diagnostics.
Acute npneumonia, as a rule, is the outcome of catarrhal factor, which evidence is showed nby the patients. Besides, more long duration, high temperature, and cough with nexpectoration of mucopurulent sputum characterize the pneumonia; on auscultation –fine bubbling wet rales on the side of nlesion and infiltration of pulmonary tissue at chest X-ray examination. All nthese findings enable to confirm or to rule out pneumonia.
Exsudative npleurisy mostly arises as the result of complication of pleuropneumonia. The nprocess lasts, as a rule, 5-7 days. The most typical manifestations are cough nand chest pain on the side of lesion, which intensifies at deep breathing. nPercussion reveals a shortening of percussion sound. On auscultation – weak nbreathing sounds and pleural friction rub. The presence of intensive nhomogeneous shadow with oblique upper contour on chest X-radiography and also thoracentesis confirm the diagnosis of npleurisy.
Exsudative npericarditis. It most often results from rheumatic lesion of heart, acute myocardial ninfarction or polyserositis. Dyspnea, pain, heavy feeling behind breastbone, ngeneral malaise, forced sedentary patient’s position are the chief signs of pericarditis. On X-ray films observed a trapezoid shape nof heart, and on ECG – diminished waves. Puncture of the pericardium with nobtaining of exudate finally confirms the diagnosis.
Tactics and choice of treatment
The treatment of nmediastinitis is only surgical. Its character and volume significantly depend non the cause, location and extent of purulent process. Established perforatioof esophagus, trachea or bronchus requires an urgent operation. The foreigbodies thus removed, and operation ends by drainage. If the process located in anterosuperior mediastinum used a cervical nmediastinotomy.
Cervical mediastinotomy
Nevertheless cervical mediastinotomy is ninsufficient at low localization of the process. In such cases performed nanterior mediastinotomy. Meanwhile, isolated posterior mediastinitis is the indicatiofor drainage by means of posterior extrapleural mediastinotomy.
In postoperative period is necessary applicatioof intensive antibacterial, antiinflammatory and detoxycation therapy, and also ntreatment direct on the increase of immunological resistance of the organism. The mortality after such operative napproaches has been 26-36 %, and after conservative treatment – about 70 %.
n
Mediastinal tumors
The mediastinal tumors include true tumours, cyst nand masses.
Classificatioof tumours
1. Neurogenic tumours:
a) nganglioneuroma;
b) nneurinoma;
c) nneurogenic sarcoma;
d) nneuroblastoma;
e) nsympathoblastoma.
2. Mesenchymal tumours:
a) nfibroma;
b) nlipoma;
c) nhemangioma;
d) nfibrosarcoma;
e) nliposarcoma;
f) nangiosarcoma.
3. Tumours originated from reticular tissue of lymph nnodes:
a) nlymphosarcoma;
b) nreticulosarcoma;
c) nlymphogranulomatosis.
4. Tumour originated from thymus (thymoma), and nthyroid gland (substernal, intrathoracic ngoiter).
5. Germ cell tumours:
a) ndermoid cyst;
b) nteratoma;
c) nmediastinal seminoma;
d) nchoriocarcinoma.
6. True mediastinal cysts:
a) nmesothelial cyst;
b) npericardial diverticula;
c) nbronchogenic cyst;
d) nenteric cyst.
7. Parasitogenic (echinococcal) cysts.
Symptomatology and clinical course
On early stages of the ndevelopment the tumours are almost asymptomatic, and 40 % of mediastinal nneoplasms are revealed at preventive chest X-ray examination. The patients most noften complain of chest pain. The intensity of pain depends on degree of tumour ncompression or growth into nervous structures. In malignant growth the pain has nmore intensive character, than in benign. Frequently the pain precedes by feeling of heaviness, discomfort and foreigbody in chest. Sometimes observed dyspnea caused by compression of airways, and nmajor vessels both of anterior, and posterior mediastinum.
Owing to compression of nthe lumen of superior vena cava the syndrome of superior vena cava develops, nwhich manifest by cyanosis of face, neck and upper half of chest, distend ncervical veins, edema and dyspnea. Resulting from the rise of blood pressure nand disrupture of venous walls, the nasal, esophageal and pulmonary bleedings ndevelop. As the characteristic features considered headache, loss of nconsciousness and hallucinations. In overwhelming ncases superior vena cava syndrome results from malignant tumours of lungs and nmediastinum. Only in 5-7 % of patients they are benign.
The basic method of ndiagnostics is a complex X-ray examination: roentgenoscopy, polypositional nX-radiography, tomography, computer tomography. The examination should be start nfrom roentgenoscopy in different plains (multiaxial roentgenoscopy). It gives nthe possibility to find out a pathological shadow, its location, shape, size, nmobility, intensity, contours and to reveal the presence or lack of pulsatioof walls. Computer tomography is also a nhigh-grade method of diagnostics. It helps to receive the image of transversal nplain of chest at any level, to confirm the location of mediastinal tumour and nits communication with adjacent organs. In suspicion on a vascular nature of the process, angiography nis used. It enables to rule out aneurysm of heart, aorta and its branches, nreveal compression of superior vena cava and growth of the tumour into major arterial ntrunks.
If it is necessary to differentiate nthe tumour from cyst and reveal its different deposits, it is expedient to napply ultrasonic examination (sonography).
With the purpose of nimprovement of localization, size of mass, its communication with mediastinal norgans performed pneumomediastinography (X-radiography of mediastinum with nintroducing of oxygen or air). For pneumomediastinography, depending on tumour nlocating the gas is introduced through a puncture above jugular incissure of nbreastbone, under xyphoid process or parasternally. nThus gas at first is spread in anterior mediastinum, and in 45-60 min. npenetrates in posterior. The introduced gas achieves a good visualization of tumour contours and its growth into nadjacent organs. Sometimes an artificial pneumothorax is performed on the naffected side. In such patients collapse of lung gives the opportunity to ndifferentiate pulmonary tumour from mediastinal tumours and cysts.
For morphological nverification of the tumour applied such additional methods:
– nthoracoscopy, which allows to examine a pleural space, nto take biopsy from mediastinal lymph nodes or tumour;
– nmediastinoscopy (through a small incision above the nbreastbone exposed trachea, and along its position performed the canal ianterior mediastinum with following insertion of a special endoscope) enables nto examine anterior mediastinum, and take a biopsy from lymph nodes and tumour; n
– ntransthoracic aspiration biopsy is performed if tumour nis located near chest wall;
– ntransbronchial puncture of lymph nnodes is carried out during bronchoscopy.
During diagnostics of nmediastinal neoplasms applied according to indications bronchography, esophagography and pneumoperitoneum.
Variants of nclinical course and complications
Neurogenic tumours are the most commoeoplasms of mediastinum, which noccur in 20 % among the tumours of this location. There arise in any age and nmore often benign. Their predominant localization is the posterior mediastinum. nThe origin of such tumours could be nervous trunks, ganglions and other nervous nstructures of mediastinum. From the cells of sympathetic nervous trunk arise ganglioneuromas, neuroblastomas and sympathoblastomas. Slide
The tumours, which arise from peripheral nerves nare represent by neuromas and neurofibromas. The paragangliomas and mediastinal npheochromocytoma develop from chemoceptor cells of and according to the nstructure resemble the tumours of sinocarotid zone. They frequently produce hormones, and manifests by hypertension with noften crises. In half of patients these tumours are malignant.
Neurogenic sarcoma is a malignant tumour of nnervous sheath. It is usually solitary, or iassociation with von Recklinhausen’s disease.
The neurogenic tumours commonly manifest by backache, nhyperalgesia, pareses and paralyses at tumour ngrowth trough the spinal canal. The pain reaction varies from slight to severe nexpressed neuralgias. Frequently ganglioneuroma is asymptomatic for many years. nIn the clinical pattern of malignant neurogenic tumours prevail general nintoxication, loss of weight and pain syndrome.
Roentgenologically ieurogenic tumour of a nvertebrocostal angle observed characteristic intensive rounded shadow, with nvertebral and costal usuration, rib. Frequently revealed nhemorrhagic pleural effusion on the side of lesion by malignant tumour.
Ganglioneuroma
Mesenchymal tumours. According to nthe histological origin mesenchymal benign tumours are represented by:
– nfrom a fibrous connecting tissue – fibroma;
– nfrom a cartilaginous and osseous tissue – chondroma, nosteochondroma, osteoblastoclastoma;
– nfrom a spinal cord – chordoma;
– nfrom fat tissues – lipoma, hibernoma;
– nthe tumours, which originate from vessels – hemangioma, nlymphangioma;
– nfrom a muscular tissue – leiomyoma, rhabdomyoma.
Lipomas are the most frequent mesenchymal benigtumours with predominant location in cardiodiaphragmatic angle.
The clinical symptomatology of these tumours is natypical. At the small sizes they are usually asymptomatic. The malignant nneoplasms manifest much earlier as the result of prompt infiltrative growth of the tumour and intoxication of nthe organism. Nevertheless, despite the malignant character, liposarcoma cagrow rather slowly with late metastatic spread.
On roentgenogram such masses represented by homogeneous nformations, that applies to heart shadow.
The lymphomas occur in 3-5 n% of patients with mediastinal tumors and in 20-25 % with all malignant nneoplasms of mediastinum. The lymphomas arise from mediastinal lymph nodes. nTheir common localization – anterior mediastinum, nevertheless lymph nodes of nany part can be affected. There are three types of lymphomas: lymphosarcoma, nreticulosarcoma and lymphogranulomatosis. All of them are characterized by nmalignant course. The initial signs of this pathology mainly caused by nintoxication: malaise, subfebrile or febrile temperature with further remittent character, sweating and loss of weight. One of most typical manifestation of the disease should nbe considered itching of skin. Abnormally enlarged lymph nodes can compress nmediastinal organs, which lead to dry cough, chest pain, and dyspnea. Ilymphogranulomatosis, in contrast with other mediastinal tumours, the signs of ncompression are weakly expressed. It is characterized by bilateral lesion and nblood changes (leukocytosis or leukopenia and elevation of erythrocyte nsedimentation rate). Lymphosarcoma differs by more prompt course and nconsiderable progression of mediastinal compression syndrome. X-ray nexamination, mediastinoscopy and biopsy of lymph nodes are the most valuable nfor diagnostics.
The dermoid cysts and teratomas arise owing nto disturbance of embryogenesis and occur in 5-8 % of the patients with nmediastinal tumors. The origin of dermoid cysts is nthe ectoderm, which transforms to a fibrous connecting tissue. The cystic ncavity frequently contains similar to fat viscous mass of brown color with ndeposits of skin and hair. The teratomas arise from several germinal laminas nand contain different structural tissues. They are divided on mature and nimmature. All mature teratomas, as a rule, are characterized by well-defined ncapsule, irregular rounded or oval shape, different size, and look like a cyst non slit. Immature ones look like solitary nodes, sometimes with small cavities. nThe structure of teratomas can include parts of glands, teeth, bones and nsometimes even underdeveloped fetus. According to degree of cellular ndifferentiation teratoma divided on benign (80-90 %) and malignant (10-20 %). nAlthough this disease is always congenital, it diagnosed, mainly, in elderly nage at occurrence of pain and “compression syndrome”. 95 % of such ncysts are located in anterior mediastinum and frequently are accompanied with ncardiovascular disturbances (tachycardia, pressing pain in the region of nheart). The compression of major bronchi and trachea results in occurrence of ndyspnea, paroxysmal cough and hemoptysis. The infection of the tumour nfrequently leads to fever and increase of intoxication. The presence in sputum nof hair and other tissues is considered to be the sign of bronchial fistula.
In diagnostics of teratomas the major value has a ncomplex X-ray examination. It is possible to find out teeth, calcification of cystic capsule and its contents. Prompt ngrowth of the tumour, disappearance of its regular contours suspects the nmalignancy.
Cysts of pericardium are the ncavity thin-walled formations, which according to the structure resemble npericardium. They occur in 7-8 % of cases of all mediastinal tumors. Their most noften location is the right cardiodiaphragmatic angle, much nless often – left one. A true cyst may be single-, double- or multichamber, nconnected or non-connected with pericardium. The cases, when the cystic cavity ncommunicates with the cavity of pericardium, it should be considered as ndiverticulum. The disease, as a rule, asymptomatic and it is casually revealed nonly during prophylactic photoroentgenography. In cases of great size of cyst nthe patients complain of pain in the region of heart and cardiac arrhythmia. nDuring X-ray examination mesothelial cyst or pericardial diverticulum observed nas oval or semicircular homogeneous shadow with regular outline, which nintimately applies to the shadow of heart.
Cysts of npericardium. Computer tomography
Bronchogenic and enteric cysts of mediastinum arise in the period of intrauterine development and originated from dystopic ngerms of bronchial or intestinal epithelium.
Bronchogenic cysts, as a rule, are single chamber, nwith location either in mediastinum, or in pulmonary tissue. The neighborhood nof cyst with bifurcation of trachea can cause paroxysmal cough, dyspnea and respiratory disturbances. Paraesophageal nlocation of the cyst manifests by dysphagia. The clinical manifestations of nsuch pathology can be caused by inflammatory process in cyst or its suddedischarge into airways. If the cyst is communicated with airways, the nroentgenogram reveals a fluid level, and during bronchography a contrast agent nfills in the lumen of cyst. The diagnosis is possible to confirm by means of npneumomediastinography.
The enteric cyst (enterocystoma) arises from the dorsal parts of a primary intestinal tube, nlocated more often in lower parts of posterior mediastinum and applies to nesophagus. Depending on histology they are divided on esophageal, gastric and nintestinal cyst. In cases, when a cystic wall is covered by gastric epithelium, nwhich produces hydrochloric acid, an ulceration of wall, bleeding and its nperforation can develop.
Frequently enteric cyst suppurates with the hazard of discharge into pleural space or npericardium, esophagus and bronchi. The most often signs of the disease is ndyspnea and chest pain. Due to characteristic localization of the pathological nfocus in posterior mediastinum, to the right from median line, the nroentgenological diagnostics is usually not difficult. In order to determine nmutual relation of neoplasm to trachea, bronchi, and esophagus it is possible nto apply pneumomediastinography. As there is always a danger of the development nof complications, it is necessary to consider such pathology as absolute nindication for operative removal.
Echinococcosis of mediastinum noccurs rarely (1-2 % of all mediastinal tumors). If the parasite is of small nsize, the disease most often asymptomatic. The enlargement of echinococcal cyst ncauses pain, dyspnea, dysphagia and superior vena cava syndrome. Sometimes isuch patients the cyst can discharge into bronchus or trachea. The suppuratioof parasitogenic cysts is transformed into abscess and purulent mediastinitis. nRoentgenological method should be considered to be predominant in the ndiagnostics of echinococcosis of mediastinum. The presence of homogeneous, nround or oval shadow with regular outline (with further calcification) suggests nechinococcosis. For confirming of the diagnosis reaction of latex-agglutinatiois performed. Echinococcosis of mediastinum frequently associated with nanatomical lesion of lungs.
Principles of diagnostics in such situation are nsimilar to primary mediastinal tumors.
Tactics and choice of treatment
The presence of nmediastinal tumors requires surgical treatment. Expectant tactics and dynamic observation in such cases are unjustified.
In connection with a nconstant and substantial threat of infection, perforation and development of npurulent intrapleural complications, the pericardial, bronchogenic and enteric ncysts of mediastinum are the subjects to operative remove.
The operative treatment nof malignant mediastinal tumors should be applied on early stages of the ndisease. In advanced cases it is expedient to apply antineoplastic and nradiotherapy.
The benigeurogenic ntumours are removed in surgical way through thoracotomy incision. If the tumour grow like a ” sandglasses” na fragment of the tumour removed with following resection of vertebral arches. nThe malignant tumours are removed “іn mass”, with maximal excision of nthe tumour, affected ribs, paraaortic, esophageal and paratracheal lymph nodes. n
n
Superior vena cava (SVC) syndrome
Superior vena cava (SVC) syndrome n(SVCS) is characterized by gradual, insidious compression/obstruction of the nsuperior vena cava. Although the syndrome can be life threatening, its presentatiois often associated with a gradual increase in symptomatology. For this reason, ndiagnosis is often delayed until significant compression of the superior vena ncava has occurred.
Pathophysiology
Extrinsic compression of the nsuperior vena cava is possible because it has a thin wall coupled with a low nintravascular pressure. Because the superior vena cava is surrounded by rigid nstructures, it is relatively easy to compress. The low intravascular pressure nalso allows for the possibility of thrombus formation, such as catheter-induced nthrombus.
The subsequent obstruction to flow ncauses an increased venous pressure, which results in interstitial edema and nretrograde collateral flow.
Epidemiology
Superior vena cava syndrome is nchiefly associated with malignancy. Currently, more than 90% of patients with nsuperior vena cava syndrome have an associated malignancy as the cause. This ncontrasts with studies in the early 1950s in which a large proportion of cases nwere nonmalignant. Infectious causes (eg, syphilis, tuberculosis) have ndecreased because of improvements in antibiotic therapy. Of the nonmalignant ncauses of superior vena cava syndrome, thrombosis from central venous ninstrumentation (catheter, pacemaker, guidewire) is an increasingly commoevent, especially as these procedures become more common.
Causes
Today, the most common etiology of nsuperior vena cava syndrome is related to malignancy.
· nPrior nto modern antibiotics, infectious causes including syphilis, tuberculosis, and nfungi occurred with almost equal frequency.
· nThe nmost common cause of malignancy-related superior vena cava syndrome is nbronchogenic carcinoma, which accounts for nearly 80% of cases.
· nLymphoma naccounts for approximately 15% of cases.
· nOther ncases have various causes, including infectious and catheter-related netiologies. Increasingly, dialysis catheters and pacemaker leads are becoming nassociated with superior vena cava syndrome due to thrombosis.
Symptoms
The symptoms of SVCS are more severe nif the vein becomes blocked quickly. This is because the other veins in the narea do not have time to widen and take over the blood flow that cannot pass nthrough the superior vena cava.
The most common symptoms are:
· nTrouble nbreathing.
· nCoughing.
· nSwelling nin the face, neck, upper body, or arms.
Less common symptoms include the following:
· nHoarse nvoice.
· nTrouble nswallowing or talking.
· nCoughing nup blood.
· nSwolleveins in the chest or neck.
· nChest npain.
· nReddish nskin color.
Laboratory Studies
The diagnosis of superior vena cava nsyndrome (SVCS) is often made on clinical grounds alone, combining clinical npresentation with an often-obtained history of thoracic malignancy.
Imaging Studies
Plain radiography is often helpful nand reveals a mediastinal mass in most patients (as is seen in the image nbelow).
When in doubt, venography can aid ithe diagnosis, but this is usually not necessary.
scanning is helpful, but the histologic ndiagnosis is important in initiating therapy.
Treatment
Treatment for SCVS caused by cancer ndepends on the following:
· nThe ntype of cancer.
· nThe ncause of the blockage.
· nHow nsevere the symptoms are.
· nThe nprognosis (chance of recovery).
· nWhether ntreatment is to cure, control, or relieve the symptoms of cancer.
· nThe npatient’s wishes.
Treatment may include the following:
Watchful waiting
Watchful waiting is closely nmonitoring a patient’s condition without giving any treatment unless symptoms nappear or change. A patient who has good blood flow through smaller veins ithe area and mild symptoms may not need treatment.
The following may be used to relieve nsymptoms and keep the patient comfortable:
· nKeeping nthe upper body raised higher than the lower body.
· nCorticosteroids n(drugs that reduce swelling).
· nDiuretics n(drugs that make excess fluid pass from the body in urine). Patients taking ndiuretics are closely watched because these drugs can cause dehydration (loss nof too much fluid from the body).
Chemotherapy
Chemotherapy is the usual treatment nfor tumors that respond to anticancer drugs, including small cell lung cancer nand lymphoma. Chemotherapy uses drugs to stop the growth of cancer cells, neither by killing the cells or by stopping them from dividing. Whechemotherapy is taken by mouth or injected into a vein or muscle, the drugs nenter the bloodstream and can reach cancer cells throughout the body (systemic nchemotherapy). When chemotherapy is placed directly into the cerebrospinal nfluid, an organ, or a body cavity such as the abdomen, the drugs mainly affect ncancer cells in those areas (regional chemotherapy). The way the chemotherapy nis given depends on the type and stage of the cancer being treated.
Radiation therapy
If the blockage of the superior vena ncava is caused by a tumor that does not usually respond to chemotherapy, nradiation therapy may be given. Radiation therapy is a cancer treatment that nuses high-energy x-rays or other types of radiation to kill cancer cells. nExternal radiation therapy uses a machine outside the body to send radiatiotoward the cancer. The way the radiation therapy is given depends on the type nand stage of the cancer being treated.
Thrombolysis
SVCS may occur when a thrombus n(blood clot) forms in a partly blocked vein. Thrombolysis is a way to break up nand remove blood clots. This may done by a thrombectomy. Thrombectomy is nsurgery to remove the blood clot or the use of a device inserted into the veito remove the blood clot. This may be done with or without the use of drugs to nbreak up the clot.
Stent placement
If the superior vena cava is partly nblocked by the tumor, an expandable stent (tube) may be placed inside the nsuperior vena cava to help keep it open and allow blood to pass through. This nhelps most patients. Drugs to keep more blood clots from forming may also be nused.
Surgery
Surgery to bypass (go around) the nblocked part of the vein is sometimes used for cancer patients, but is used nmore often for patients without cancer.
Palliative ncare may be given to nrelieve symptoms in patients with SVCS.
Superior vena cava syndrome is nserious and the symptoms can be upsetting for the patient and family. It is nimportant that patients and family members ask questions about superior vena ncava syndrome and how to treat it. This can help relieve anxiety about symptoms nsuch as swelling, trouble swallowing, coughing, and hoarseness.
Patients with advanced cancer nsometimes decide not to have any serious treatment. Palliative treatment cahelp keep patients comfortable by relieving symptoms to improve their quality of nlife.
n
Gastroesophageal nreflux disease
Gastroesophageal reflux disease n(GERD) is a condition in which the stomach contents (food or liquid) leak nbackwards from the stomach into the esophagus (the tube from the mouth to the nstomach). This action can irritate the esophagus, causing heartburn and other nsymptoms.
Causes
When you eat, food passes from the nthroat to the stomach through the esophagus (also called the food pipe or nswallowing tube). Once food is in the stomach, a ring of muscle fibers prevents nfood from moving backward into the esophagus. These muscle fibers are called nthe lower esophageal sphincter, or LES.
If this sphincter muscle doesn’t nclose well, food, liquid, and stomach acid can leak back into the esophagus. nThis is called reflux or gastroesophageal reflux. Reflux may cause symptoms, or nit can even damage the esophagus.
The risk factors for reflux include:
· nAlcohol n(possibly)
· nHiatal nhernia (a condition in which part of the stomach moves above the diaphragm, nwhich is the muscle that separates the chest and abdominal cavities)
· nObesity
· nPregnancy
· nScleroderma
· nSmoking
Heartburn and gastroesophageal nreflux can be brought on or made worse by pregnancy and many different nmedications. Such drugs include:
· nAnticholinergics n(e.g., for seasickness)
· nBeta-blockers nfor high blood pressure or heart disease
· nBronchodilators nfor asthma
· nCalcium nchannel blockers for high blood pressure
· nDopamine-active ndrugs for Parkinson’s disease
· nProgestifor abnormal menstrual bleeding or birth control
· nSedatives nfor insomnia or anxiety
· nTricyclic nantidepressants
If you suspect that one of your nmedications may be causing heartburn, talk to your doctor. Never change or stop na medication you take regularly without talking to your doctor.
Symptoms
More common symptoms are:
· nFeeling nthat food is stuck behind the breastbone
· nHeartburor a burning pain in the chest (under the breastbone)
· nIncreased nby bending, stooping, lying down, or eating
· nMore nlikely or worse at night
· nRelieved nby antacids
· nNausea nafter eating
Less common symptoms are:
· nBringing nfood back up (regurgitation)
· nCough nor wheezing
· nDifficulty nswallowing
· nHiccups
· nHoarseness nor change in voice
· nSore nthroat
Exams and Tests
You may not need any tests if your nsymptoms are not severe.
If your symptoms are severe or they ncome back after you have been treated, one or more tests may help diagnose nreflux or any complications:
· nEsophagogastroduodenoscopy n(EGD) is often used to find the cause and examine the esophagus (swallowing ntube) for damage. The doctor inserts a thin tube with a camera on the end nthrough your mouth. The tube is then passed into your esophagus, stomach, and nsmall intestine.
· nBarium nswallow
· nContinuous nesophageal pH monitoring
· nEsophageal nmanometry
A positive stool occult blood test nmay diagnose bleeding that is coming from the irritation in the esophagus, nstomach, or intestines.
Treatment
You can make many lifestyle changes nto help treat your symptoms. Avoid foods that cause problems for you. Making nchanges to your routine before you go to sleep may also help.
Avoid drugs such as aspirin, nibuprofen (Advil, Motrin), or naproxen (Aleve, Naprosyn). Take acetaminophe(Tylenol) to relieve pain. Take your medicines with plenty of water. When your ndoctor gives you a new medicine, remember to ask whether it will make your nheartburn worse.
You may use over-the-counter nantacids after meals and at bedtime, although they do not last very long. nCommon side effects of antacids include diarrhea or constipation.
Other over-the-counter and prescriptiodrugs can treat GERD. They work more slowly than antacids but give you longer nrelief. Your pharmacist, doctor, or nurse can tell you how to take these drugs.
· nProtopump inhibitors (PPIs) decrease the amount of acid produced in your stomach
· nH2 nblockers (antagonists) lower the amount of acid released in the stomach
Anti-reflux operations n(fundoplication and others) may be an option for patients whose symptoms do not ngo away with lifestyle changes and drugs. Heartburn and other symptoms should nimprove after surgery, but you may still need to take drugs for your heartburn.
There are also new therapies for nreflux that can be performed through an endoscope (a flexible tube passed nthrough the mouth into the stomach).
Outlook (Prognosis)
Most people respond to lifestyle nchanges and medications. However, many patients need to continue taking drugs nto control their symptoms.
Possible Complications
· nAsthma
· nBarrett’s nesophagus (a change in the lining of the esophagus that can increase the risk nof cancer)
· nBronchospasm n(irritation and spasm of the airways due to acid)
· nChronic ncough or hoarseness
· nDental nproblems
· nEsophageal nulcer
· nStricture n(a narrowing of the esophagus due to scarring)
