id
stringlengths 14
28
| title
stringclasses 18
values | content
stringlengths 2
999
| contents
stringlengths 19
1.02k
|
|---|---|---|---|
Surgery_Schwartz_7002 | Surgery_Schwartz | circular stapler to the current approach that uses a linear stapler creating a sta-pled wedge gastroplasty. Elements of importance in fashioning the fundoplication after Collis gastroplasty include placement of the initial suture of the fundoplication on the esophagus, immedi-ately above the GEJ to ensure that acid-secreting (gastric) mucosa does not reside above the fundoplication. A second element that ensures safety and avoids wrap deformation is to place the gastric portion of the staple line against the neoesophagus, such that the tip of the gastric staple line sits adjacent to the middle suture of the fundoplication on the right side of the esophagus.ResultsMost outcome studies report relief of symptoms following sur-gical repair of PEHs in more than 90% of patients. The current literature suggests that laparoscopic repair of a paraesophageal hiatal hernia can be successful. Most authors report symptom-atic improvement in 80% to 90% of patients, and <10% to 15% prevalence of | Surgery_Schwartz. circular stapler to the current approach that uses a linear stapler creating a sta-pled wedge gastroplasty. Elements of importance in fashioning the fundoplication after Collis gastroplasty include placement of the initial suture of the fundoplication on the esophagus, immedi-ately above the GEJ to ensure that acid-secreting (gastric) mucosa does not reside above the fundoplication. A second element that ensures safety and avoids wrap deformation is to place the gastric portion of the staple line against the neoesophagus, such that the tip of the gastric staple line sits adjacent to the middle suture of the fundoplication on the right side of the esophagus.ResultsMost outcome studies report relief of symptoms following sur-gical repair of PEHs in more than 90% of patients. The current literature suggests that laparoscopic repair of a paraesophageal hiatal hernia can be successful. Most authors report symptom-atic improvement in 80% to 90% of patients, and <10% to 15% prevalence of |
Surgery_Schwartz_7003 | Surgery_Schwartz | literature suggests that laparoscopic repair of a paraesophageal hiatal hernia can be successful. Most authors report symptom-atic improvement in 80% to 90% of patients, and <10% to 15% prevalence of recurrent symptomatic hernia. However, the problem of recurrent asymptomatic or minimally symp-tomatic hernia following PEH repair, open or laparoscopic, is Figure 25-41. Barium esophagogram showing Schatzki’s ring (i.e., a thin circumferential ring in the distal esophagus at the squa-mocolumnar junction). Below the ring is a hiatal hernia.becoming increasingly appreciated. Recurrent hiatal hernia is the most common cause of anatomic failure following laparoscopic Nissen fundoplication done for GERD (5–10%), but this risk is compounded for the giant hernia where radiologic recurrence is detected in 25% to 40% of patients. It appears that optimal results with open or laparoscopic giant hiatal hernia repair should include options for mesh buttressing of hiatal closure and selec-tive | Surgery_Schwartz. literature suggests that laparoscopic repair of a paraesophageal hiatal hernia can be successful. Most authors report symptom-atic improvement in 80% to 90% of patients, and <10% to 15% prevalence of recurrent symptomatic hernia. However, the problem of recurrent asymptomatic or minimally symp-tomatic hernia following PEH repair, open or laparoscopic, is Figure 25-41. Barium esophagogram showing Schatzki’s ring (i.e., a thin circumferential ring in the distal esophagus at the squa-mocolumnar junction). Below the ring is a hiatal hernia.becoming increasingly appreciated. Recurrent hiatal hernia is the most common cause of anatomic failure following laparoscopic Nissen fundoplication done for GERD (5–10%), but this risk is compounded for the giant hernia where radiologic recurrence is detected in 25% to 40% of patients. It appears that optimal results with open or laparoscopic giant hiatal hernia repair should include options for mesh buttressing of hiatal closure and selec-tive |
Surgery_Schwartz_7004 | Surgery_Schwartz | detected in 25% to 40% of patients. It appears that optimal results with open or laparoscopic giant hiatal hernia repair should include options for mesh buttressing of hiatal closure and selec-tive esophageal lengthening with one of the many techniques developed for the creation of a Collis gastroplasty. Despite this high incidence of radiologic recurrence, and the surgical pursuit of a remedy, it must be reinforced that asymptomatic recurrent hernias, like primary PEH, do not need to be repaired. The risk of incarceration, strangulation, or obstruction is minimal.SCHATZKI’S RINGSchatzki’s ring is a thin submucosal circumferential ring in the lower esophagus at the squamocolumnar junction, often associ-ated with a hiatal hernia. Its significance and pathogenesis are unclear (Fig. 25-41). The ring was first noted by Templeton, but Schatzki and Gary defined it as a distinct entity in 1953. Its prevalence varies from 0.2% to 14% in the general population, depending on the technique of | Surgery_Schwartz. detected in 25% to 40% of patients. It appears that optimal results with open or laparoscopic giant hiatal hernia repair should include options for mesh buttressing of hiatal closure and selec-tive esophageal lengthening with one of the many techniques developed for the creation of a Collis gastroplasty. Despite this high incidence of radiologic recurrence, and the surgical pursuit of a remedy, it must be reinforced that asymptomatic recurrent hernias, like primary PEH, do not need to be repaired. The risk of incarceration, strangulation, or obstruction is minimal.SCHATZKI’S RINGSchatzki’s ring is a thin submucosal circumferential ring in the lower esophagus at the squamocolumnar junction, often associ-ated with a hiatal hernia. Its significance and pathogenesis are unclear (Fig. 25-41). The ring was first noted by Templeton, but Schatzki and Gary defined it as a distinct entity in 1953. Its prevalence varies from 0.2% to 14% in the general population, depending on the technique of |
Surgery_Schwartz_7005 | Surgery_Schwartz | The ring was first noted by Templeton, but Schatzki and Gary defined it as a distinct entity in 1953. Its prevalence varies from 0.2% to 14% in the general population, depending on the technique of diagnosis and the criteria used. Stiennon believed the ring to be a pleat of mucosa formed by infolding of redundant esophageal mucosa due to shortening of the esophagus. Others believe the ring to be congenital, and still others suggest it is an early stricture resulting from inflamma-tion of the esophageal mucosa caused by chronic reflux.Schatzki’s ring is a distinct clinical entity having different symptoms, upper GI function studies, and response to treatment compared with patients with a hiatal hernia, but without a ring. Twenty-four-hour esophageal pH monitoring has shown that patients with a Schatzki’s ring have a lower incidence of reflux than hiatal hernia controls. They also have better LES function. This, together with the presence of a ring, could represent a pro-tective | Surgery_Schwartz. The ring was first noted by Templeton, but Schatzki and Gary defined it as a distinct entity in 1953. Its prevalence varies from 0.2% to 14% in the general population, depending on the technique of diagnosis and the criteria used. Stiennon believed the ring to be a pleat of mucosa formed by infolding of redundant esophageal mucosa due to shortening of the esophagus. Others believe the ring to be congenital, and still others suggest it is an early stricture resulting from inflamma-tion of the esophageal mucosa caused by chronic reflux.Schatzki’s ring is a distinct clinical entity having different symptoms, upper GI function studies, and response to treatment compared with patients with a hiatal hernia, but without a ring. Twenty-four-hour esophageal pH monitoring has shown that patients with a Schatzki’s ring have a lower incidence of reflux than hiatal hernia controls. They also have better LES function. This, together with the presence of a ring, could represent a pro-tective |
Surgery_Schwartz_7006 | Surgery_Schwartz | with a Schatzki’s ring have a lower incidence of reflux than hiatal hernia controls. They also have better LES function. This, together with the presence of a ring, could represent a pro-tective mechanism to prevent gastroesophageal reflux.Brunicardi_Ch25_p1009-p1098.indd 104901/03/19 6:04 PM 1050SPECIFIC CONSIDERATIONSPART IISymptoms associated with Schatzki’s ring are brief epi-sodes of dysphagia during hurried ingestion of solid foods. Its treatment has varied from dilation alone to dilation with antire-flux measures, antireflux procedure alone, incision, and even excision of the ring. Little is known about the natural progres-sion of Schatzki’s rings. Using radiologic techniques, Chen and colleagues showed progressive stenosis of rings in 59% of patients, whereas Schatzki found that the rings decreased in diameter in 29% of patients and remained unchanged in the rest.Symptoms in patients with a ring are caused more by the presence of the ring than by gastroesophageal reflux. | Surgery_Schwartz. with a Schatzki’s ring have a lower incidence of reflux than hiatal hernia controls. They also have better LES function. This, together with the presence of a ring, could represent a pro-tective mechanism to prevent gastroesophageal reflux.Brunicardi_Ch25_p1009-p1098.indd 104901/03/19 6:04 PM 1050SPECIFIC CONSIDERATIONSPART IISymptoms associated with Schatzki’s ring are brief epi-sodes of dysphagia during hurried ingestion of solid foods. Its treatment has varied from dilation alone to dilation with antire-flux measures, antireflux procedure alone, incision, and even excision of the ring. Little is known about the natural progres-sion of Schatzki’s rings. Using radiologic techniques, Chen and colleagues showed progressive stenosis of rings in 59% of patients, whereas Schatzki found that the rings decreased in diameter in 29% of patients and remained unchanged in the rest.Symptoms in patients with a ring are caused more by the presence of the ring than by gastroesophageal reflux. |
Surgery_Schwartz_7007 | Surgery_Schwartz | the rings decreased in diameter in 29% of patients and remained unchanged in the rest.Symptoms in patients with a ring are caused more by the presence of the ring than by gastroesophageal reflux. Most patients with a ring but without proven reflux respond to one dilation, while most patients with proven reflux require repeated dilations. In this regard, the majority of Schatzki’s ring patients without proven reflux have a history of ingestion of drugs known to be damaging to the esophageal mucosa. Bonavina and associates have suggested drug-induced injury as the cause of stenosis in patients with a ring, but without a history of reflux. Because rings also occur in patients with proven reflux, it is likely that gastroesophageal reflux also plays a part. This is supported by the fact that there is less drug ingestion in the history of these patients. Schatzki’s ring is prob-ably an acquired lesion that can lead to stenosis from chemical-induced injury by pill lodgment in the distal | Surgery_Schwartz. the rings decreased in diameter in 29% of patients and remained unchanged in the rest.Symptoms in patients with a ring are caused more by the presence of the ring than by gastroesophageal reflux. Most patients with a ring but without proven reflux respond to one dilation, while most patients with proven reflux require repeated dilations. In this regard, the majority of Schatzki’s ring patients without proven reflux have a history of ingestion of drugs known to be damaging to the esophageal mucosa. Bonavina and associates have suggested drug-induced injury as the cause of stenosis in patients with a ring, but without a history of reflux. Because rings also occur in patients with proven reflux, it is likely that gastroesophageal reflux also plays a part. This is supported by the fact that there is less drug ingestion in the history of these patients. Schatzki’s ring is prob-ably an acquired lesion that can lead to stenosis from chemical-induced injury by pill lodgment in the distal |
Surgery_Schwartz_7008 | Surgery_Schwartz | there is less drug ingestion in the history of these patients. Schatzki’s ring is prob-ably an acquired lesion that can lead to stenosis from chemical-induced injury by pill lodgment in the distal esophagus, or from reflux-induced injury to the lower esophageal mucosa.The best form of treatment of a symptomatic Schatzki’s ring in patients who do not have reflux consists of esophageal dilation for relief of the obstructive symptoms. In patients with a ring who have proven reflux and a mechanically defective sphincter, an antireflux procedure is necessary to obtain relief and avoid repeated dilation.SCLERODERMAScleroderma is a systemic disease accompanied by esophageal abnormalities in approximately 80% of patients. In most, the disease follows a prolonged course. Renal involvement occurs in a small percentage of patients and signals a poor prognosis. The onset of the disease is usually in the third or fourth decade of life, occurring twice as frequently in women as in men.Small vessel | Surgery_Schwartz. there is less drug ingestion in the history of these patients. Schatzki’s ring is prob-ably an acquired lesion that can lead to stenosis from chemical-induced injury by pill lodgment in the distal esophagus, or from reflux-induced injury to the lower esophageal mucosa.The best form of treatment of a symptomatic Schatzki’s ring in patients who do not have reflux consists of esophageal dilation for relief of the obstructive symptoms. In patients with a ring who have proven reflux and a mechanically defective sphincter, an antireflux procedure is necessary to obtain relief and avoid repeated dilation.SCLERODERMAScleroderma is a systemic disease accompanied by esophageal abnormalities in approximately 80% of patients. In most, the disease follows a prolonged course. Renal involvement occurs in a small percentage of patients and signals a poor prognosis. The onset of the disease is usually in the third or fourth decade of life, occurring twice as frequently in women as in men.Small vessel |
Surgery_Schwartz_7009 | Surgery_Schwartz | a small percentage of patients and signals a poor prognosis. The onset of the disease is usually in the third or fourth decade of life, occurring twice as frequently in women as in men.Small vessel inflammation appears to be an initiating event, with subsequent perivascular deposition of normal col-lagen, which may lead to vascular compromise. In the GI tract, the predominant feature is smooth muscle atrophy. Whether the atrophy in the esophageal musculature is a primary effect or occurs secondary to a neurogenic disorder is unknown. The results of pharmacologic and hormonal manipulation, with agents that act either indirectly via neural mechanisms or directly on the muscle, suggest that scleroderma is a pri-mary neurogenic disorder. Methacholine, which acts directly on smooth muscle receptors, causes a similar increase in LES pressure in normal controls and in patients with scleroderma. Edrophonium, a cholinesterase inhibitor that enhances the effect of acetylcholine when given to | Surgery_Schwartz. a small percentage of patients and signals a poor prognosis. The onset of the disease is usually in the third or fourth decade of life, occurring twice as frequently in women as in men.Small vessel inflammation appears to be an initiating event, with subsequent perivascular deposition of normal col-lagen, which may lead to vascular compromise. In the GI tract, the predominant feature is smooth muscle atrophy. Whether the atrophy in the esophageal musculature is a primary effect or occurs secondary to a neurogenic disorder is unknown. The results of pharmacologic and hormonal manipulation, with agents that act either indirectly via neural mechanisms or directly on the muscle, suggest that scleroderma is a pri-mary neurogenic disorder. Methacholine, which acts directly on smooth muscle receptors, causes a similar increase in LES pressure in normal controls and in patients with scleroderma. Edrophonium, a cholinesterase inhibitor that enhances the effect of acetylcholine when given to |
Surgery_Schwartz_7010 | Surgery_Schwartz | causes a similar increase in LES pressure in normal controls and in patients with scleroderma. Edrophonium, a cholinesterase inhibitor that enhances the effect of acetylcholine when given to patients with sclero-derma, causes an increase in LES pressure that is less marked in these patients than in normal controls, suggesting a neurogenic rather than myogenic etiology. Muscle ischemia due to peri-vascular compression has been suggested as a possible mecha-nism for the motility abnormality in scleroderma. Others have observed that in the early stage of the disease, the manomet-ric abnormalities may be reversed by reserpine, an agent that depletes catecholamines from the adrenergic system. This sug-gests that, in early scleroderma, an adrenergic overactivity may be present that causes a parasympathetic inhibition, supporting SclerodermammHg35 –0Esophagus25 cmEsophagus30 cmEsophagus35 cmSSSS35 –0035 –Figure 25-42. Esophageal motility record in a patient with sclero-derma showing | Surgery_Schwartz. causes a similar increase in LES pressure in normal controls and in patients with scleroderma. Edrophonium, a cholinesterase inhibitor that enhances the effect of acetylcholine when given to patients with sclero-derma, causes an increase in LES pressure that is less marked in these patients than in normal controls, suggesting a neurogenic rather than myogenic etiology. Muscle ischemia due to peri-vascular compression has been suggested as a possible mecha-nism for the motility abnormality in scleroderma. Others have observed that in the early stage of the disease, the manomet-ric abnormalities may be reversed by reserpine, an agent that depletes catecholamines from the adrenergic system. This sug-gests that, in early scleroderma, an adrenergic overactivity may be present that causes a parasympathetic inhibition, supporting SclerodermammHg35 –0Esophagus25 cmEsophagus30 cmEsophagus35 cmSSSS35 –0035 –Figure 25-42. Esophageal motility record in a patient with sclero-derma showing |
Surgery_Schwartz_7011 | Surgery_Schwartz | a parasympathetic inhibition, supporting SclerodermammHg35 –0Esophagus25 cmEsophagus30 cmEsophagus35 cmSSSS35 –0035 –Figure 25-42. Esophageal motility record in a patient with sclero-derma showing aperistalsis in the distal two-thirds of the esopha-geal body with peristalsis in the proximal portion. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)a neurogenic mechanism for the disease. In advanced disease manifested by smooth muscle atrophy and collagen deposition, reserpine no longer produces this reversal. Consequently, from a clinical perspective, the patient can be described as having a poor esophageal pump and a poor valve.The diagnosis of scleroderma can be made manometrically by the observation of normal peristalsis in the proximal striated esophagus, with absent peristalsis in the distal smooth muscle por-tion (Fig. 25-42). The LES pressure is progressively weakened as | Surgery_Schwartz. a parasympathetic inhibition, supporting SclerodermammHg35 –0Esophagus25 cmEsophagus30 cmEsophagus35 cmSSSS35 –0035 –Figure 25-42. Esophageal motility record in a patient with sclero-derma showing aperistalsis in the distal two-thirds of the esopha-geal body with peristalsis in the proximal portion. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)a neurogenic mechanism for the disease. In advanced disease manifested by smooth muscle atrophy and collagen deposition, reserpine no longer produces this reversal. Consequently, from a clinical perspective, the patient can be described as having a poor esophageal pump and a poor valve.The diagnosis of scleroderma can be made manometrically by the observation of normal peristalsis in the proximal striated esophagus, with absent peristalsis in the distal smooth muscle por-tion (Fig. 25-42). The LES pressure is progressively weakened as |
Surgery_Schwartz_7012 | Surgery_Schwartz | by the observation of normal peristalsis in the proximal striated esophagus, with absent peristalsis in the distal smooth muscle por-tion (Fig. 25-42). The LES pressure is progressively weakened as the disease advances. Because many of the systemic sequelae of the disease may be nondiagnostic, the motility pattern is fre-quently used as a specific diagnostic indicator. Gastroesophageal reflux commonly occurs in patients with scleroderma because they have both hypotensive sphincters and poor esophageal clearance. This combined defect can lead to severe esophagitis and stricture formation. The typical barium swallow shows a dilated, barium-filled esophagus, stomach, and duodenum, or a hiatal hernia with distal esophageal stricture and proximal dilatation (Fig. 25-43).Traditionally, esophageal symptoms have been treated with PPIs, antacids, elevation of the head of the bed, and multiple dilations for strictures, with generally unsatisfac-tory results. The degree of esophagitis is usually | Surgery_Schwartz. by the observation of normal peristalsis in the proximal striated esophagus, with absent peristalsis in the distal smooth muscle por-tion (Fig. 25-42). The LES pressure is progressively weakened as the disease advances. Because many of the systemic sequelae of the disease may be nondiagnostic, the motility pattern is fre-quently used as a specific diagnostic indicator. Gastroesophageal reflux commonly occurs in patients with scleroderma because they have both hypotensive sphincters and poor esophageal clearance. This combined defect can lead to severe esophagitis and stricture formation. The typical barium swallow shows a dilated, barium-filled esophagus, stomach, and duodenum, or a hiatal hernia with distal esophageal stricture and proximal dilatation (Fig. 25-43).Traditionally, esophageal symptoms have been treated with PPIs, antacids, elevation of the head of the bed, and multiple dilations for strictures, with generally unsatisfac-tory results. The degree of esophagitis is usually |
Surgery_Schwartz_7013 | Surgery_Schwartz | symptoms have been treated with PPIs, antacids, elevation of the head of the bed, and multiple dilations for strictures, with generally unsatisfac-tory results. The degree of esophagitis is usually severe and may lead to marked esophageal shortening as well as stric-ture. Scleroderma patients have frequently had numerous dilations before they are referred to the surgeon. The surgi-cal management is somewhat controversial, but the major-ity of opinion suggests that a partial fundoplication (anterior or posterior) performed laparoscopically is the procedure of choice. The need for a partial fundoplication is dictated by the likelihood of severe dysphagia if a total fundoplication is performed in the presence of aperistalsis. Esophageal short-ening may require a Collis gastroplasty in combination with a partial fundoplication. Surgery reduces esophageal acid exposure but does not return it to normal because of the poor Brunicardi_Ch25_p1009-p1098.indd 105001/03/19 6:04 PM | Surgery_Schwartz. symptoms have been treated with PPIs, antacids, elevation of the head of the bed, and multiple dilations for strictures, with generally unsatisfac-tory results. The degree of esophagitis is usually severe and may lead to marked esophageal shortening as well as stric-ture. Scleroderma patients have frequently had numerous dilations before they are referred to the surgeon. The surgi-cal management is somewhat controversial, but the major-ity of opinion suggests that a partial fundoplication (anterior or posterior) performed laparoscopically is the procedure of choice. The need for a partial fundoplication is dictated by the likelihood of severe dysphagia if a total fundoplication is performed in the presence of aperistalsis. Esophageal short-ening may require a Collis gastroplasty in combination with a partial fundoplication. Surgery reduces esophageal acid exposure but does not return it to normal because of the poor Brunicardi_Ch25_p1009-p1098.indd 105001/03/19 6:04 PM |
Surgery_Schwartz_7014 | Surgery_Schwartz | in combination with a partial fundoplication. Surgery reduces esophageal acid exposure but does not return it to normal because of the poor Brunicardi_Ch25_p1009-p1098.indd 105001/03/19 6:04 PM 1051ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-43. Barium esophagogram of a patient with sclero-derma and stricture. Note the markedly dilated esophagus and retained food material. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Figure 25-44. The esophagus on the left shows a stacking of rings, demonstrating eosinophilic esophagus. The esophagus on the right is a normal barium swallow.EOSINOPHILIC ESOPHAGITISEosinophilic esophagitis (EE) was first described in 1977, but it has become well known only in the last two decades. The condi-tion is characterized by a constellation of symptoms, endoscopic and radiologic findings, and distinctive pathology. The etiology of | Surgery_Schwartz. in combination with a partial fundoplication. Surgery reduces esophageal acid exposure but does not return it to normal because of the poor Brunicardi_Ch25_p1009-p1098.indd 105001/03/19 6:04 PM 1051ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-43. Barium esophagogram of a patient with sclero-derma and stricture. Note the markedly dilated esophagus and retained food material. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Figure 25-44. The esophagus on the left shows a stacking of rings, demonstrating eosinophilic esophagus. The esophagus on the right is a normal barium swallow.EOSINOPHILIC ESOPHAGITISEosinophilic esophagitis (EE) was first described in 1977, but it has become well known only in the last two decades. The condi-tion is characterized by a constellation of symptoms, endoscopic and radiologic findings, and distinctive pathology. The etiology of |
Surgery_Schwartz_7015 | Surgery_Schwartz | it has become well known only in the last two decades. The condi-tion is characterized by a constellation of symptoms, endoscopic and radiologic findings, and distinctive pathology. The etiology of eosinophilic esophagitis is not entirely known but its simi-larities, immunologically, to asthma suggest that it is a form of “allergic esophagitis.”SymptomsThe presentation of eosinophilic esophagitis is chest pain (often postprandial) and dysphagia. Dysphagia may occur with liquids or solids, but solid food dysphagia is most common. Because dysphagia and chest pain are characteristic of GERD, EE is often confused with GERD; however, EE does not respond to proton pump inhibitors. The evaluation of the patient with EE and dysphagia and chest pain with esophagram and endoscopy usually reveals the diagnosis.SignsA barium swallow should be the first test obtained in the patient with dysphagia. EE has a characteristic finding often called the “ringed esophagus” or the “feline esophagus,” as the | Surgery_Schwartz. it has become well known only in the last two decades. The condi-tion is characterized by a constellation of symptoms, endoscopic and radiologic findings, and distinctive pathology. The etiology of eosinophilic esophagitis is not entirely known but its simi-larities, immunologically, to asthma suggest that it is a form of “allergic esophagitis.”SymptomsThe presentation of eosinophilic esophagitis is chest pain (often postprandial) and dysphagia. Dysphagia may occur with liquids or solids, but solid food dysphagia is most common. Because dysphagia and chest pain are characteristic of GERD, EE is often confused with GERD; however, EE does not respond to proton pump inhibitors. The evaluation of the patient with EE and dysphagia and chest pain with esophagram and endoscopy usually reveals the diagnosis.SignsA barium swallow should be the first test obtained in the patient with dysphagia. EE has a characteristic finding often called the “ringed esophagus” or the “feline esophagus,” as the |
Surgery_Schwartz_7016 | Surgery_Schwartz | diagnosis.SignsA barium swallow should be the first test obtained in the patient with dysphagia. EE has a characteristic finding often called the “ringed esophagus” or the “feline esophagus,” as the esophageal rings are felt to look like the stripes on a housecat (Fig. 25-44). The endoscopic appearance of EE is also characteristic, and also appears as a series of rings (Fig. 25-45).PathologyEndoscopic biopsy specimens should be taken when eosin-ophilic esophagus is suspected. To make the diagnosis of EE, the pathologist should see a minimum of 15 eosinophils per high powered field, usually at the base of the epithelium (Fig. 25-46).TreatmentThe treatment of EE is largely symptomatic and includes test-ing for food allergies and elimination of identified items from the diet. Second-line therapy includes inhaled or ingested cor-ticosteroids, as would be used to treat asthma. If dysphagia is not relieved with steroids, it may be necessary to dilate the clearance function of the body of | Surgery_Schwartz. diagnosis.SignsA barium swallow should be the first test obtained in the patient with dysphagia. EE has a characteristic finding often called the “ringed esophagus” or the “feline esophagus,” as the esophageal rings are felt to look like the stripes on a housecat (Fig. 25-44). The endoscopic appearance of EE is also characteristic, and also appears as a series of rings (Fig. 25-45).PathologyEndoscopic biopsy specimens should be taken when eosin-ophilic esophagus is suspected. To make the diagnosis of EE, the pathologist should see a minimum of 15 eosinophils per high powered field, usually at the base of the epithelium (Fig. 25-46).TreatmentThe treatment of EE is largely symptomatic and includes test-ing for food allergies and elimination of identified items from the diet. Second-line therapy includes inhaled or ingested cor-ticosteroids, as would be used to treat asthma. If dysphagia is not relieved with steroids, it may be necessary to dilate the clearance function of the body of |
Surgery_Schwartz_7017 | Surgery_Schwartz | includes inhaled or ingested cor-ticosteroids, as would be used to treat asthma. If dysphagia is not relieved with steroids, it may be necessary to dilate the clearance function of the body of the esophagus. Only 50% of the patients have a good-to-excellent result. If the esopha-gitis is severe, or there has been a previous failed antireflux procedure and the disease is associated with delayed gastric emptying, a gastric resection with Roux-en-Y gastrojejunos-tomy has proved the best option.Brunicardi_Ch25_p1009-p1098.indd 105101/03/19 6:04 PM 1052SPECIFIC CONSIDERATIONSPART IIFigure 25-46. A cluster of eosinophils are visualized in the esophageal epithelium in a patient with EE.Figure 25-45. The endoscopic appearance of eosinophilic esopha-gitis is characteristically a series of stacked mucosal rings.esophagus. Because of the length of esophageal involvement, rigid dilators (Maloney or Savary) are often used. Great care must be exercised, as the inflamed EE is quite friable. The | Surgery_Schwartz. includes inhaled or ingested cor-ticosteroids, as would be used to treat asthma. If dysphagia is not relieved with steroids, it may be necessary to dilate the clearance function of the body of the esophagus. Only 50% of the patients have a good-to-excellent result. If the esopha-gitis is severe, or there has been a previous failed antireflux procedure and the disease is associated with delayed gastric emptying, a gastric resection with Roux-en-Y gastrojejunos-tomy has proved the best option.Brunicardi_Ch25_p1009-p1098.indd 105101/03/19 6:04 PM 1052SPECIFIC CONSIDERATIONSPART IIFigure 25-46. A cluster of eosinophils are visualized in the esophageal epithelium in a patient with EE.Figure 25-45. The endoscopic appearance of eosinophilic esopha-gitis is characteristically a series of stacked mucosal rings.esophagus. Because of the length of esophageal involvement, rigid dilators (Maloney or Savary) are often used. Great care must be exercised, as the inflamed EE is quite friable. The |
Surgery_Schwartz_7018 | Surgery_Schwartz | mucosal rings.esophagus. Because of the length of esophageal involvement, rigid dilators (Maloney or Savary) are often used. Great care must be exercised, as the inflamed EE is quite friable. The mucosal tears easily, and esophageal perforation (full thickness laceration) has been reported with EE dilation.MOTILITY DISORDERS OF THE PHARYNX AND ESOPHAGUSClinical ManifestationsDysphagia (i.e., difficulty in swallowing) is the primary symp-tom of esophageal motor disorders. Its perception by the patient is a balance between the severity of the underlying abnormality causing the dysphagia and the adjustment made by the patient in altering eating habits. Consequently, any complaint of dyspha-gia must include an assessment of the patient’s dietary history. It must be known whether the patient experiences pain, chokes, or vomits with eating; whether the patient requires liquids with the meal, is the last to finish, or is forced to interrupt or avoid a social meal; and whether he or she has | Surgery_Schwartz. mucosal rings.esophagus. Because of the length of esophageal involvement, rigid dilators (Maloney or Savary) are often used. Great care must be exercised, as the inflamed EE is quite friable. The mucosal tears easily, and esophageal perforation (full thickness laceration) has been reported with EE dilation.MOTILITY DISORDERS OF THE PHARYNX AND ESOPHAGUSClinical ManifestationsDysphagia (i.e., difficulty in swallowing) is the primary symp-tom of esophageal motor disorders. Its perception by the patient is a balance between the severity of the underlying abnormality causing the dysphagia and the adjustment made by the patient in altering eating habits. Consequently, any complaint of dyspha-gia must include an assessment of the patient’s dietary history. It must be known whether the patient experiences pain, chokes, or vomits with eating; whether the patient requires liquids with the meal, is the last to finish, or is forced to interrupt or avoid a social meal; and whether he or she has |
Surgery_Schwartz_7019 | Surgery_Schwartz | experiences pain, chokes, or vomits with eating; whether the patient requires liquids with the meal, is the last to finish, or is forced to interrupt or avoid a social meal; and whether he or she has been admitted to the hos-pital for food impaction. These assessments, plus an evaluation of the patient’s nutritional status, help to determine how severe the dysphagia is and judge the need for surgical intervention, rather than more conservative methods of treating dysphagia.Motility Disorders of the Pharynx and Upper Esophagus—Transit DysphagiaDisorders of the pharyngeal phase of swallowing result from a discoordination of the neuromuscular events involved in chew-ing, initiation of swallowing, and propulsion of the material from the oropharynx into the cervical esophagus. They can be categorized into one or a combination of the following abnor-malities: (a) inadequate oropharyngeal bolus transport; (b) inability to pressurize the pharynx; (c) inability to elevate the larynx; (d) | Surgery_Schwartz. experiences pain, chokes, or vomits with eating; whether the patient requires liquids with the meal, is the last to finish, or is forced to interrupt or avoid a social meal; and whether he or she has been admitted to the hos-pital for food impaction. These assessments, plus an evaluation of the patient’s nutritional status, help to determine how severe the dysphagia is and judge the need for surgical intervention, rather than more conservative methods of treating dysphagia.Motility Disorders of the Pharynx and Upper Esophagus—Transit DysphagiaDisorders of the pharyngeal phase of swallowing result from a discoordination of the neuromuscular events involved in chew-ing, initiation of swallowing, and propulsion of the material from the oropharynx into the cervical esophagus. They can be categorized into one or a combination of the following abnor-malities: (a) inadequate oropharyngeal bolus transport; (b) inability to pressurize the pharynx; (c) inability to elevate the larynx; (d) |
Surgery_Schwartz_7020 | Surgery_Schwartz | categorized into one or a combination of the following abnor-malities: (a) inadequate oropharyngeal bolus transport; (b) inability to pressurize the pharynx; (c) inability to elevate the larynx; (d) discoordination of pharyngeal contraction and cri-copharyngeal relaxation; and (e) decreased compliance of the pharyngoesophageal segment secondary to neuromuscular dis-ease. The latter may result in incomplete relaxation of the crico-pharyngeus and cervical esophagus during swallowing. Taken together, these disorders are termed transit dysphagia by many.Transit dysphagia is usually congenital or results from acquired disease involving the central and peripheral nervous system. This includes cerebrovascular accidents, brain stem tumors, poliomyelitis, multiple sclerosis, Parkinson’s disease, pseudobulbar palsy, peripheral neuropathy, and operative dam-age to the cranial nerves involved in swallowing. Pure muscular diseases such as radiation-induced myopathy, dermatomyositis, myotonic | Surgery_Schwartz. categorized into one or a combination of the following abnor-malities: (a) inadequate oropharyngeal bolus transport; (b) inability to pressurize the pharynx; (c) inability to elevate the larynx; (d) discoordination of pharyngeal contraction and cri-copharyngeal relaxation; and (e) decreased compliance of the pharyngoesophageal segment secondary to neuromuscular dis-ease. The latter may result in incomplete relaxation of the crico-pharyngeus and cervical esophagus during swallowing. Taken together, these disorders are termed transit dysphagia by many.Transit dysphagia is usually congenital or results from acquired disease involving the central and peripheral nervous system. This includes cerebrovascular accidents, brain stem tumors, poliomyelitis, multiple sclerosis, Parkinson’s disease, pseudobulbar palsy, peripheral neuropathy, and operative dam-age to the cranial nerves involved in swallowing. Pure muscular diseases such as radiation-induced myopathy, dermatomyositis, myotonic |
Surgery_Schwartz_7021 | Surgery_Schwartz | pseudobulbar palsy, peripheral neuropathy, and operative dam-age to the cranial nerves involved in swallowing. Pure muscular diseases such as radiation-induced myopathy, dermatomyositis, myotonic dystrophy, and myasthenia gravis are less common causes. Rarely, extrinsic compression of the cervical esophagus by thyromegaly, lymphadenopathy, or hyperostosis of the cervi-cal spine can cause transit dysphagia.Diagnostic Assessment of the Cricopharyngeal SegmentTransit dysphagia difficult to assess with standard manometric techniques because of the rapidity of the oropharyngeal phase of swallowing, the elevation of the larynx, and the asymmetry of the cricopharyngeus. Videoor cineradiography is currently the Brunicardi_Ch25_p1009-p1098.indd 105201/03/19 6:04 PM 1053ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25ABFigure 25-47. A. Zenker’s diverticulum, initially discovered 15 years ago and left untreated. B. Note its marked enlargement and evidence of laryngeal inlet aspiration on recent | Surgery_Schwartz. pseudobulbar palsy, peripheral neuropathy, and operative dam-age to the cranial nerves involved in swallowing. Pure muscular diseases such as radiation-induced myopathy, dermatomyositis, myotonic dystrophy, and myasthenia gravis are less common causes. Rarely, extrinsic compression of the cervical esophagus by thyromegaly, lymphadenopathy, or hyperostosis of the cervi-cal spine can cause transit dysphagia.Diagnostic Assessment of the Cricopharyngeal SegmentTransit dysphagia difficult to assess with standard manometric techniques because of the rapidity of the oropharyngeal phase of swallowing, the elevation of the larynx, and the asymmetry of the cricopharyngeus. Videoor cineradiography is currently the Brunicardi_Ch25_p1009-p1098.indd 105201/03/19 6:04 PM 1053ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25ABFigure 25-47. A. Zenker’s diverticulum, initially discovered 15 years ago and left untreated. B. Note its marked enlargement and evidence of laryngeal inlet aspiration on recent |
Surgery_Schwartz_7022 | Surgery_Schwartz | HERNIACHAPTER 25ABFigure 25-47. A. Zenker’s diverticulum, initially discovered 15 years ago and left untreated. B. Note its marked enlargement and evidence of laryngeal inlet aspiration on recent esophagogram. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Time 0Peak pharyngealpressureAtmosphericpressureABBolus pressureinitialMaximum residual(MaxR)contractionB0finalMinimum Residual(MinR)Subatomic pressureFigure 25-48. A. Schematic drawing of a pharyngeal pressure wave indicating the presence of the bolus pressure. B. Schematic drawing of the manometric recording typically seen during crico-pharyngeal sphincter relaxation.most objective test to evaluate oropharyngeal bolus transport, pharyngeal compression, relaxation of the pharyngoesophageal segment, and the dynamics of airway protection during swal-lowing. It readily identifies a diverticulum (Fig. 25-47), stasis of the | Surgery_Schwartz. HERNIACHAPTER 25ABFigure 25-47. A. Zenker’s diverticulum, initially discovered 15 years ago and left untreated. B. Note its marked enlargement and evidence of laryngeal inlet aspiration on recent esophagogram. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Time 0Peak pharyngealpressureAtmosphericpressureABBolus pressureinitialMaximum residual(MaxR)contractionB0finalMinimum Residual(MinR)Subatomic pressureFigure 25-48. A. Schematic drawing of a pharyngeal pressure wave indicating the presence of the bolus pressure. B. Schematic drawing of the manometric recording typically seen during crico-pharyngeal sphincter relaxation.most objective test to evaluate oropharyngeal bolus transport, pharyngeal compression, relaxation of the pharyngoesophageal segment, and the dynamics of airway protection during swal-lowing. It readily identifies a diverticulum (Fig. 25-47), stasis of the |
Surgery_Schwartz_7023 | Surgery_Schwartz | pharyngeal compression, relaxation of the pharyngoesophageal segment, and the dynamics of airway protection during swal-lowing. It readily identifies a diverticulum (Fig. 25-47), stasis of the contrast medium in the valleculae, a cricopharyngeal bar, and/or narrowing of the pharyngoesophageal segment. These are anatomic manifestations of neuromuscular disease, and they result from the loss of muscle compliance in portions of the pharynx and esophagus composed of skeletal muscle.Careful analysis of videoor cineradiographic studies com-bined with manometry using specially designed catheters can identify the cause of a pharyngoesophageal dysfunction in most sit-uations (Fig. 25-48). Motility studies may demonstrate inadequate pharyngeal pressurization, insufficient or lack of cricopharyngeal relaxation, marked discoordination of pharyngeal pressurization, cricopharyngeal relaxation and cervical esophageal contraction, or a hypopharyngeal bolus pressure suggesting decreased compli-ance of | Surgery_Schwartz. pharyngeal compression, relaxation of the pharyngoesophageal segment, and the dynamics of airway protection during swal-lowing. It readily identifies a diverticulum (Fig. 25-47), stasis of the contrast medium in the valleculae, a cricopharyngeal bar, and/or narrowing of the pharyngoesophageal segment. These are anatomic manifestations of neuromuscular disease, and they result from the loss of muscle compliance in portions of the pharynx and esophagus composed of skeletal muscle.Careful analysis of videoor cineradiographic studies com-bined with manometry using specially designed catheters can identify the cause of a pharyngoesophageal dysfunction in most sit-uations (Fig. 25-48). Motility studies may demonstrate inadequate pharyngeal pressurization, insufficient or lack of cricopharyngeal relaxation, marked discoordination of pharyngeal pressurization, cricopharyngeal relaxation and cervical esophageal contraction, or a hypopharyngeal bolus pressure suggesting decreased compli-ance of |
Surgery_Schwartz_7024 | Surgery_Schwartz | relaxation, marked discoordination of pharyngeal pressurization, cricopharyngeal relaxation and cervical esophageal contraction, or a hypopharyngeal bolus pressure suggesting decreased compli-ance of the skeletal portion of the cervical esophagus.In many patients with cricopharyngeal dysfunction, including those with Zenker’s diverticulum, it has been difficult to consistently demonstrate a motility abnormality or discoor-dination of pharyngoesophageal events. The abnormality most apt to be present is a loss of compliance in the pharyngoesopha-geal segment manifested by an increased bolus pressure. Cook and colleagues have demonstrated an increased resistance to the movement of a bolus through what appears on manometry to be a completely relaxed cricopharyngeal sphincter. Using simulta-neous manometry and videofluoroscopy, they showed that, in these patients, the cricopharyngeus is only partially relaxed; that is, the sphincter is relaxed enough to allow a drop of its pressure to | Surgery_Schwartz. relaxation, marked discoordination of pharyngeal pressurization, cricopharyngeal relaxation and cervical esophageal contraction, or a hypopharyngeal bolus pressure suggesting decreased compli-ance of the skeletal portion of the cervical esophagus.In many patients with cricopharyngeal dysfunction, including those with Zenker’s diverticulum, it has been difficult to consistently demonstrate a motility abnormality or discoor-dination of pharyngoesophageal events. The abnormality most apt to be present is a loss of compliance in the pharyngoesopha-geal segment manifested by an increased bolus pressure. Cook and colleagues have demonstrated an increased resistance to the movement of a bolus through what appears on manometry to be a completely relaxed cricopharyngeal sphincter. Using simulta-neous manometry and videofluoroscopy, they showed that, in these patients, the cricopharyngeus is only partially relaxed; that is, the sphincter is relaxed enough to allow a drop of its pressure to |
Surgery_Schwartz_7025 | Surgery_Schwartz | manometry and videofluoroscopy, they showed that, in these patients, the cricopharyngeus is only partially relaxed; that is, the sphincter is relaxed enough to allow a drop of its pressure to esophageal baseline on manometry, but insufficiently relaxed to allow unimpaired passage of the bolus into the esophagus. This incomplete relaxation is due to a loss of compliance of the muscle in the pharyngoesophageal segment, and may be associ-ated with a cricopharyngeal bar or Zenker’s diverticulum. This decreased compliance of the cricopharyngeal sphincter can be recognized on esophageal manometry by a “shoulder” on the pharyngeal pressure wave, the amplitude of which correlates directly with the degree of outflow obstruction (Fig. 25-49). Increasing the diameter of this noncompliant segment reduces the resistance imposed on the passage of a bolus. Consequently, patients with low pharyngeal pressure (i.e., poor piston function of the pharynx), or patients with increased resistance of the | Surgery_Schwartz. manometry and videofluoroscopy, they showed that, in these patients, the cricopharyngeus is only partially relaxed; that is, the sphincter is relaxed enough to allow a drop of its pressure to esophageal baseline on manometry, but insufficiently relaxed to allow unimpaired passage of the bolus into the esophagus. This incomplete relaxation is due to a loss of compliance of the muscle in the pharyngoesophageal segment, and may be associ-ated with a cricopharyngeal bar or Zenker’s diverticulum. This decreased compliance of the cricopharyngeal sphincter can be recognized on esophageal manometry by a “shoulder” on the pharyngeal pressure wave, the amplitude of which correlates directly with the degree of outflow obstruction (Fig. 25-49). Increasing the diameter of this noncompliant segment reduces the resistance imposed on the passage of a bolus. Consequently, patients with low pharyngeal pressure (i.e., poor piston function of the pharynx), or patients with increased resistance of the |
Surgery_Schwartz_7026 | Surgery_Schwartz | reduces the resistance imposed on the passage of a bolus. Consequently, patients with low pharyngeal pressure (i.e., poor piston function of the pharynx), or patients with increased resistance of the pha-ryngocervical esophageal segment from loss of skeletal muscle compliance, are improved by a cricopharyngeal myotomy. This enlarges the pharyngoesophageal segment and reduces outflow resistance. Esophageal muscle biopsy specimens from patients with Zenker’s diverticulum have shown histologic evidence of the restrictive myopathy in the cricophayngeous muscle. These findings correlate well with the observation of a decreased com-pliance of the upper esophagus demonstrated by videoradiog-raphy and the findings on detailed manometric studies of the pharynx and cervical esophagus. They suggest that the diver-ticulum develops as a consequence of the outflow resistance to bolus transport through the noncompliant muscle of the pharyn-goesophageal segment.The requirements for a successful | Surgery_Schwartz. reduces the resistance imposed on the passage of a bolus. Consequently, patients with low pharyngeal pressure (i.e., poor piston function of the pharynx), or patients with increased resistance of the pha-ryngocervical esophageal segment from loss of skeletal muscle compliance, are improved by a cricopharyngeal myotomy. This enlarges the pharyngoesophageal segment and reduces outflow resistance. Esophageal muscle biopsy specimens from patients with Zenker’s diverticulum have shown histologic evidence of the restrictive myopathy in the cricophayngeous muscle. These findings correlate well with the observation of a decreased com-pliance of the upper esophagus demonstrated by videoradiog-raphy and the findings on detailed manometric studies of the pharynx and cervical esophagus. They suggest that the diver-ticulum develops as a consequence of the outflow resistance to bolus transport through the noncompliant muscle of the pharyn-goesophageal segment.The requirements for a successful |
Surgery_Schwartz_7027 | Surgery_Schwartz | that the diver-ticulum develops as a consequence of the outflow resistance to bolus transport through the noncompliant muscle of the pharyn-goesophageal segment.The requirements for a successful pharyngoesophageal myotomy are (a) adequate oropharyngeal bolus transport; (b) the presence of an intact swallowing reflex; (c) reasonable coordi-nation of pharyngeal pressurization with cricopharyngeal relax-ation; and (d) a cricopharyngeal bar, Zenker’s diverticulum, or a narrowed pharyngoesophageal segment on videoesophagogram and/or the presence of excessive pharyngoesophageal shoulder pressure on motility study.Zenker’s Diverticulum. In the past, the most common recog-nized sign of cricopharyngeal dysfunction was the presence of a Brunicardi_Ch25_p1009-p1098.indd 105301/03/19 6:04 PM 1054SPECIFIC CONSIDERATIONSPART IIZenker’s diverticulum, originally described by Ludlow in 1769. The eponym resulted from Zenker’s classic clinicopathologic descriptions of 34 cases published in 1878. | Surgery_Schwartz. that the diver-ticulum develops as a consequence of the outflow resistance to bolus transport through the noncompliant muscle of the pharyn-goesophageal segment.The requirements for a successful pharyngoesophageal myotomy are (a) adequate oropharyngeal bolus transport; (b) the presence of an intact swallowing reflex; (c) reasonable coordi-nation of pharyngeal pressurization with cricopharyngeal relax-ation; and (d) a cricopharyngeal bar, Zenker’s diverticulum, or a narrowed pharyngoesophageal segment on videoesophagogram and/or the presence of excessive pharyngoesophageal shoulder pressure on motility study.Zenker’s Diverticulum. In the past, the most common recog-nized sign of cricopharyngeal dysfunction was the presence of a Brunicardi_Ch25_p1009-p1098.indd 105301/03/19 6:04 PM 1054SPECIFIC CONSIDERATIONSPART IIZenker’s diverticulum, originally described by Ludlow in 1769. The eponym resulted from Zenker’s classic clinicopathologic descriptions of 34 cases published in 1878. |
Surgery_Schwartz_7028 | Surgery_Schwartz | CONSIDERATIONSPART IIZenker’s diverticulum, originally described by Ludlow in 1769. The eponym resulted from Zenker’s classic clinicopathologic descriptions of 34 cases published in 1878. Pharyngoesophageal diverticula have been reported to occur in 1 of 1000 routine barium examinations, and classically occur in elderly, white males. Zenker’s diverticula tend to enlarge progressively with time due to the decreased compliance of the skeletal portion of the cervical esophagus that occurs with aging.Presenting symptoms include dysphagia associated with the spontaneous regurgitation of undigested, bland material, often interrupting eating or drinking. On occasion, the dyspha-gia can be severe enough to cause debilitation and significant weight loss. Chronic aspiration and repetitive respiratory infec-tion are common associated complaints. Once suspected, the diagnosis is established by a barium swallow. Endoscopy is usually difficult in the presence of a cricopharyngeal diverticu-lum, and | Surgery_Schwartz. CONSIDERATIONSPART IIZenker’s diverticulum, originally described by Ludlow in 1769. The eponym resulted from Zenker’s classic clinicopathologic descriptions of 34 cases published in 1878. Pharyngoesophageal diverticula have been reported to occur in 1 of 1000 routine barium examinations, and classically occur in elderly, white males. Zenker’s diverticula tend to enlarge progressively with time due to the decreased compliance of the skeletal portion of the cervical esophagus that occurs with aging.Presenting symptoms include dysphagia associated with the spontaneous regurgitation of undigested, bland material, often interrupting eating or drinking. On occasion, the dyspha-gia can be severe enough to cause debilitation and significant weight loss. Chronic aspiration and repetitive respiratory infec-tion are common associated complaints. Once suspected, the diagnosis is established by a barium swallow. Endoscopy is usually difficult in the presence of a cricopharyngeal diverticu-lum, and |
Surgery_Schwartz_7029 | Surgery_Schwartz | infec-tion are common associated complaints. Once suspected, the diagnosis is established by a barium swallow. Endoscopy is usually difficult in the presence of a cricopharyngeal diverticu-lum, and potentially dangerous, owing to obstruction of the true esophageal lumen by the diverticulum and the attendant risk of diverticular perforation.Cricopharyngeal Myotomy. The low morbidity and mor-tality associated with cricopharyngeal and upper esophageal myotomy have encouraged a liberal approach toward its use for almost any problem in the oropharyngeal phase of swallowing. This attitude has resulted in an overall success rate in the relief of symptoms of only 64%. When patients are selected for sur-gery using radiographic or motility markers of disease, a much higher proportion will benefit. Two methods of cricopharyngo-esophageal myotomy are in common use, one using traditional surgical approaches, and one using rigid laryngoscopy and a linear cutting stapler.Open Cricopharyngeal | Surgery_Schwartz. infec-tion are common associated complaints. Once suspected, the diagnosis is established by a barium swallow. Endoscopy is usually difficult in the presence of a cricopharyngeal diverticu-lum, and potentially dangerous, owing to obstruction of the true esophageal lumen by the diverticulum and the attendant risk of diverticular perforation.Cricopharyngeal Myotomy. The low morbidity and mor-tality associated with cricopharyngeal and upper esophageal myotomy have encouraged a liberal approach toward its use for almost any problem in the oropharyngeal phase of swallowing. This attitude has resulted in an overall success rate in the relief of symptoms of only 64%. When patients are selected for sur-gery using radiographic or motility markers of disease, a much higher proportion will benefit. Two methods of cricopharyngo-esophageal myotomy are in common use, one using traditional surgical approaches, and one using rigid laryngoscopy and a linear cutting stapler.Open Cricopharyngeal |
Surgery_Schwartz_7030 | Surgery_Schwartz | Two methods of cricopharyngo-esophageal myotomy are in common use, one using traditional surgical approaches, and one using rigid laryngoscopy and a linear cutting stapler.Open Cricopharyngeal Myotomy, Diverticulopexy, and Diverticulectomy. The myotomy can be performed under local or general anesthesia through an incision along the anterior border of the left sternocleidomastoid muscle. The pharynx and cervi-cal esophagus are exposed by retracting the sternocleidomastoid muscle and carotid sheath laterally and the thyroid, trachea, and larynx medially (Fig. 25-50). When a pharyngoesophageal diverticulum is present, localization of the pharyngoesophageal segment is easy. The diverticulum is carefully freed from the overlying areolar tissue to expose its neck, just below the inferior pharyngeal constrictor and above the cricopharyngeus muscle. It can be difficult to identify the cricopharyngeus muscle in the absence of a diverticulum. A benefit of local anesthesia is that the patient | Surgery_Schwartz. Two methods of cricopharyngo-esophageal myotomy are in common use, one using traditional surgical approaches, and one using rigid laryngoscopy and a linear cutting stapler.Open Cricopharyngeal Myotomy, Diverticulopexy, and Diverticulectomy. The myotomy can be performed under local or general anesthesia through an incision along the anterior border of the left sternocleidomastoid muscle. The pharynx and cervi-cal esophagus are exposed by retracting the sternocleidomastoid muscle and carotid sheath laterally and the thyroid, trachea, and larynx medially (Fig. 25-50). When a pharyngoesophageal diverticulum is present, localization of the pharyngoesophageal segment is easy. The diverticulum is carefully freed from the overlying areolar tissue to expose its neck, just below the inferior pharyngeal constrictor and above the cricopharyngeus muscle. It can be difficult to identify the cricopharyngeus muscle in the absence of a diverticulum. A benefit of local anesthesia is that the patient |
Surgery_Schwartz_7031 | Surgery_Schwartz | constrictor and above the cricopharyngeus muscle. It can be difficult to identify the cricopharyngeus muscle in the absence of a diverticulum. A benefit of local anesthesia is that the patient can swallow and demonstrate an area of persistent nar-rowing at the pharyngoesophageal junction. Furthermore, before closing the incision, gelatin can be fed to the patient to ascertain whether the symptoms have been relieved, and to inspect the opening of the previously narrowed pharyngoesophageal seg-ment. Under general anesthesia, and in the absence of a diver-ticulum, the placement of a nasogastric tube to the level of the manometrically determined cricopharyngeal sphincter helps in localization of the structures. The myotomy is extended cephalad by dividing 1 to 2 cm of inferior constrictor muscle of the phar-ynx, and caudad by dividing the cricopharyngeal muscle and the cervical esophagus for a length of 4 to 5 cm. The cervical wound is closed only when all oozing of blood has ceased | Surgery_Schwartz. constrictor and above the cricopharyngeus muscle. It can be difficult to identify the cricopharyngeus muscle in the absence of a diverticulum. A benefit of local anesthesia is that the patient can swallow and demonstrate an area of persistent nar-rowing at the pharyngoesophageal junction. Furthermore, before closing the incision, gelatin can be fed to the patient to ascertain whether the symptoms have been relieved, and to inspect the opening of the previously narrowed pharyngoesophageal seg-ment. Under general anesthesia, and in the absence of a diver-ticulum, the placement of a nasogastric tube to the level of the manometrically determined cricopharyngeal sphincter helps in localization of the structures. The myotomy is extended cephalad by dividing 1 to 2 cm of inferior constrictor muscle of the phar-ynx, and caudad by dividing the cricopharyngeal muscle and the cervical esophagus for a length of 4 to 5 cm. The cervical wound is closed only when all oozing of blood has ceased |
Surgery_Schwartz_7032 | Surgery_Schwartz | muscle of the phar-ynx, and caudad by dividing the cricopharyngeal muscle and the cervical esophagus for a length of 4 to 5 cm. The cervical wound is closed only when all oozing of blood has ceased because a hematoma after this procedure is common and is often associated with temporary dysphagia while the hematoma absorbs. Oral ali-mentation is started the day after surgery. The patient is usually discharged on the first or second postoperative day.mm Hg40–0102030400HypopharynxCricopharyngeusFigure 25-50. Cross-section of the neck at the level of the thyroid isthmus that shows the sur-gical approach to the hypopharynx and cervical esophagus. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor dis-orders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Swallow volume010Pharyngeal shoulderpressure mmHgControlsZenker’s2030405101520200150100UES area mm25005101520Zenker’sControlsFigure 25-49. Pharyngeal shoulder pressures and diameter of the | Surgery_Schwartz. muscle of the phar-ynx, and caudad by dividing the cricopharyngeal muscle and the cervical esophagus for a length of 4 to 5 cm. The cervical wound is closed only when all oozing of blood has ceased because a hematoma after this procedure is common and is often associated with temporary dysphagia while the hematoma absorbs. Oral ali-mentation is started the day after surgery. The patient is usually discharged on the first or second postoperative day.mm Hg40–0102030400HypopharynxCricopharyngeusFigure 25-50. Cross-section of the neck at the level of the thyroid isthmus that shows the sur-gical approach to the hypopharynx and cervical esophagus. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor dis-orders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Swallow volume010Pharyngeal shoulderpressure mmHgControlsZenker’s2030405101520200150100UES area mm25005101520Zenker’sControlsFigure 25-49. Pharyngeal shoulder pressures and diameter of the |
Surgery_Schwartz_7033 | Surgery_Schwartz | volume010Pharyngeal shoulderpressure mmHgControlsZenker’s2030405101520200150100UES area mm25005101520Zenker’sControlsFigure 25-49. Pharyngeal shoulder pressures and diameter of the pharyngoesophageal segment in controls and patients with Zenker’s diverticulum. UES = upper esophageal sphincter. (Data from Cook IJ, et al. Zenker’s diverticu-lum: evidence for a restrictive cricopharyngeal myopathy. Gastroenterology. 1989;96:A98.)Brunicardi_Ch25_p1009-p1098.indd 105401/03/19 6:04 PM 1055ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Prevertebral fascia MyotomyZenker’sdiverticulumFigure 25-51. Posterior of the anatomy of the pharynx and cervical esophagus showing pharyngoesophageal myotomy and pexing of the diverticulum to the prevertebral fascia.If a diverticulum is present and is large enough to persist after a myotomy, it may be sutured in the inverted position to the prevertebral fascia using a permanent suture (i.e., diverticu-lopexy) (Fig. 25-51). If the diverticulum is | Surgery_Schwartz. volume010Pharyngeal shoulderpressure mmHgControlsZenker’s2030405101520200150100UES area mm25005101520Zenker’sControlsFigure 25-49. Pharyngeal shoulder pressures and diameter of the pharyngoesophageal segment in controls and patients with Zenker’s diverticulum. UES = upper esophageal sphincter. (Data from Cook IJ, et al. Zenker’s diverticu-lum: evidence for a restrictive cricopharyngeal myopathy. Gastroenterology. 1989;96:A98.)Brunicardi_Ch25_p1009-p1098.indd 105401/03/19 6:04 PM 1055ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Prevertebral fascia MyotomyZenker’sdiverticulumFigure 25-51. Posterior of the anatomy of the pharynx and cervical esophagus showing pharyngoesophageal myotomy and pexing of the diverticulum to the prevertebral fascia.If a diverticulum is present and is large enough to persist after a myotomy, it may be sutured in the inverted position to the prevertebral fascia using a permanent suture (i.e., diverticu-lopexy) (Fig. 25-51). If the diverticulum is |
Surgery_Schwartz_7034 | Surgery_Schwartz | large enough to persist after a myotomy, it may be sutured in the inverted position to the prevertebral fascia using a permanent suture (i.e., diverticu-lopexy) (Fig. 25-51). If the diverticulum is excessively large so that it would be redundant if suspended, or if its walls are thick-ened, a diverticulectomy should be performed. This is best per-formed under general anesthesia by placing a Maloney dilator (48F) in the esophagus, after controlling the neck of the diver-ticulum and after myotomy. A linear stapler is placed across the neck of the diverticulum, and the diverticulum is excised distal to the staple line. The security of this staple line and effective-ness of the myotomy may be tested before hospital discharge with a water-soluble contrast esophagogram. Postoperative complications include fistula formation, abscess, hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner’s syndrome. The incidence of the first two can be reduced by per-forming a | Surgery_Schwartz. large enough to persist after a myotomy, it may be sutured in the inverted position to the prevertebral fascia using a permanent suture (i.e., diverticu-lopexy) (Fig. 25-51). If the diverticulum is excessively large so that it would be redundant if suspended, or if its walls are thick-ened, a diverticulectomy should be performed. This is best per-formed under general anesthesia by placing a Maloney dilator (48F) in the esophagus, after controlling the neck of the diver-ticulum and after myotomy. A linear stapler is placed across the neck of the diverticulum, and the diverticulum is excised distal to the staple line. The security of this staple line and effective-ness of the myotomy may be tested before hospital discharge with a water-soluble contrast esophagogram. Postoperative complications include fistula formation, abscess, hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner’s syndrome. The incidence of the first two can be reduced by per-forming a |
Surgery_Schwartz_7035 | Surgery_Schwartz | complications include fistula formation, abscess, hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner’s syndrome. The incidence of the first two can be reduced by per-forming a diverticulopexy rather than diverticulectomy.Endoscopic Cricopharyngotomy. Endoscopic stapled crico-pharyngotomy and diverticulotomy recently has been described. This procedure is most effective for larger diverticula (>2 cm) and may be impossible to perform for the small diverticulum. The procedure uses a specialized “diverticuloscope” with two retractable valves passed into the hypopharynx. The lips of the diverticuloscope are positioned so that one lip lies in the esopha-geal lumen and the other in the diverticular lumen. The valves of the diverticuloscope are retracted appropriately so as to visu-alize the septum interposed between the diverticulum and the esophagus. An endoscopic linear stapler is introduced into the diverticuloscope and positioned against the common septum with the | Surgery_Schwartz. complications include fistula formation, abscess, hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner’s syndrome. The incidence of the first two can be reduced by per-forming a diverticulopexy rather than diverticulectomy.Endoscopic Cricopharyngotomy. Endoscopic stapled crico-pharyngotomy and diverticulotomy recently has been described. This procedure is most effective for larger diverticula (>2 cm) and may be impossible to perform for the small diverticulum. The procedure uses a specialized “diverticuloscope” with two retractable valves passed into the hypopharynx. The lips of the diverticuloscope are positioned so that one lip lies in the esopha-geal lumen and the other in the diverticular lumen. The valves of the diverticuloscope are retracted appropriately so as to visu-alize the septum interposed between the diverticulum and the esophagus. An endoscopic linear stapler is introduced into the diverticuloscope and positioned against the common septum with the |
Surgery_Schwartz_7036 | Surgery_Schwartz | to visu-alize the septum interposed between the diverticulum and the esophagus. An endoscopic linear stapler is introduced into the diverticuloscope and positioned against the common septum with the anvil in the diverticulum and the cartridge in the esoph-ageal lumen. Firing of the stapler divides the common septum between the posterior esophageal and the diverticular wall over a length of 30 mm, placing three rows of staples on each side. More than one stapler application may be needed, depending on the size of the diverticulum (Fig. 25-52). The patient is allowed to resume liquid feeds immediately and is usually discharged the day after surgery. Complications are rare and may include perforation at the apex of the diverticulum and failure to relieve dysphagia resulting from incomplete myotomy. The former complication can usually be treated with antibiotics, but it may, rarely, require neck drainage.Recurrence of a Zenker’s diverticulum may occur with long follow-up and is more | Surgery_Schwartz. to visu-alize the septum interposed between the diverticulum and the esophagus. An endoscopic linear stapler is introduced into the diverticuloscope and positioned against the common septum with the anvil in the diverticulum and the cartridge in the esoph-ageal lumen. Firing of the stapler divides the common septum between the posterior esophageal and the diverticular wall over a length of 30 mm, placing three rows of staples on each side. More than one stapler application may be needed, depending on the size of the diverticulum (Fig. 25-52). The patient is allowed to resume liquid feeds immediately and is usually discharged the day after surgery. Complications are rare and may include perforation at the apex of the diverticulum and failure to relieve dysphagia resulting from incomplete myotomy. The former complication can usually be treated with antibiotics, but it may, rarely, require neck drainage.Recurrence of a Zenker’s diverticulum may occur with long follow-up and is more |
Surgery_Schwartz_7037 | Surgery_Schwartz | myotomy. The former complication can usually be treated with antibiotics, but it may, rarely, require neck drainage.Recurrence of a Zenker’s diverticulum may occur with long follow-up and is more common after diverticulectomy without myotomy, presumably due to persistence of the under-lying loss of compliance of the cervical esophagus when a myot-omy is not performed. After endoscopic cricopharyngotomy Figure 25-52. The technique for transoral cricopharyngotomy and Zenker’s diverticulotomy.lateral residual “pouches” may be seen on radiographs, but they are rarely responsible for residual or recurrent symptoms if the myotomy has been complete.Postoperative motility studies have shown that the peak pharyngeal pressure generated on swallowing is not affected, the resting cricopharyngeal pressure is reduced but not elimi-nated, and the cricopharyngeal sphincter length is shortened. Consequently, after myotomy, there is protection against esoph-agopharyngeal regurgitation.Motility | Surgery_Schwartz. myotomy. The former complication can usually be treated with antibiotics, but it may, rarely, require neck drainage.Recurrence of a Zenker’s diverticulum may occur with long follow-up and is more common after diverticulectomy without myotomy, presumably due to persistence of the under-lying loss of compliance of the cervical esophagus when a myot-omy is not performed. After endoscopic cricopharyngotomy Figure 25-52. The technique for transoral cricopharyngotomy and Zenker’s diverticulotomy.lateral residual “pouches” may be seen on radiographs, but they are rarely responsible for residual or recurrent symptoms if the myotomy has been complete.Postoperative motility studies have shown that the peak pharyngeal pressure generated on swallowing is not affected, the resting cricopharyngeal pressure is reduced but not elimi-nated, and the cricopharyngeal sphincter length is shortened. Consequently, after myotomy, there is protection against esoph-agopharyngeal regurgitation.Motility |
Surgery_Schwartz_7038 | Surgery_Schwartz | pressure is reduced but not elimi-nated, and the cricopharyngeal sphincter length is shortened. Consequently, after myotomy, there is protection against esoph-agopharyngeal regurgitation.Motility Disorders of the Esophageal Body and Lower Esophageal SphincterDisorders of the esophageal phase of swallowing result from abnormalities in the propulsive pump action of the esophageal body or the relaxation of the LES. These disorders result from either primary esophageal abnormalities, or from generalized neural, muscular, or collagen vascular disease (Table 25-8). The use of standard and high-resolution esophageal manometry techniques has allowed specific primary esophageal motility disorders to be identified out of a pool of nonspecific motil-ity abnormalities. Primary esophageal motor disorders include achalasia, DES, nutcracker esophagus, and the hypertensive LES. The manometric characteristics of these disorders are shown in Table 25-9.The boundaries between the primary esophageal | Surgery_Schwartz. pressure is reduced but not elimi-nated, and the cricopharyngeal sphincter length is shortened. Consequently, after myotomy, there is protection against esoph-agopharyngeal regurgitation.Motility Disorders of the Esophageal Body and Lower Esophageal SphincterDisorders of the esophageal phase of swallowing result from abnormalities in the propulsive pump action of the esophageal body or the relaxation of the LES. These disorders result from either primary esophageal abnormalities, or from generalized neural, muscular, or collagen vascular disease (Table 25-8). The use of standard and high-resolution esophageal manometry techniques has allowed specific primary esophageal motility disorders to be identified out of a pool of nonspecific motil-ity abnormalities. Primary esophageal motor disorders include achalasia, DES, nutcracker esophagus, and the hypertensive LES. The manometric characteristics of these disorders are shown in Table 25-9.The boundaries between the primary esophageal |
Surgery_Schwartz_7039 | Surgery_Schwartz | include achalasia, DES, nutcracker esophagus, and the hypertensive LES. The manometric characteristics of these disorders are shown in Table 25-9.The boundaries between the primary esophageal motor disorders are vague, and intermediate types exist, some of which may combine more than one type of motility pattern. These findings indicate that esophageal motility disorders should be looked at as a spectrum of abnormalities that reflects various stages of destruction of esophageal motor function.Achalasia. The best known and best understood primary motil-ity disorder of the esophagus is achalasia, with an incidence of six Brunicardi_Ch25_p1009-p1098.indd 105501/03/19 6:04 PM 1056SPECIFIC CONSIDERATIONSPART IITable 25-9Manometric characteristics of the primary esophageal motility disordersAchalasiaIncomplete lower esophageal sphincter (LES) relaxation (<75% relaxation)Aperistalsis in the esophageal bodyElevated LES pressure ≤26 mmHgIncreased intraesophageal baseline pressures relative | Surgery_Schwartz. include achalasia, DES, nutcracker esophagus, and the hypertensive LES. The manometric characteristics of these disorders are shown in Table 25-9.The boundaries between the primary esophageal motor disorders are vague, and intermediate types exist, some of which may combine more than one type of motility pattern. These findings indicate that esophageal motility disorders should be looked at as a spectrum of abnormalities that reflects various stages of destruction of esophageal motor function.Achalasia. The best known and best understood primary motil-ity disorder of the esophagus is achalasia, with an incidence of six Brunicardi_Ch25_p1009-p1098.indd 105501/03/19 6:04 PM 1056SPECIFIC CONSIDERATIONSPART IITable 25-9Manometric characteristics of the primary esophageal motility disordersAchalasiaIncomplete lower esophageal sphincter (LES) relaxation (<75% relaxation)Aperistalsis in the esophageal bodyElevated LES pressure ≤26 mmHgIncreased intraesophageal baseline pressures relative |
Surgery_Schwartz_7040 | Surgery_Schwartz | lower esophageal sphincter (LES) relaxation (<75% relaxation)Aperistalsis in the esophageal bodyElevated LES pressure ≤26 mmHgIncreased intraesophageal baseline pressures relative to gastric baselineDiffuse esophageal spasm (DES)Simultaneous (nonperistaltic contractions) (>20% of wet swallows)Repetitive and multipeaked contractionsSpontaneous contractionsIntermittent normal peristalsisContractions may be of increased amplitude and durationNutcracker esophagusMean peristaltic amplitude (10 wet swallows) in distal esophagus ≥180 mmHgIncreased mean duration of contractions (>7.0 s)Normal peristaltic sequenceHypertensive lower esophageal sphincterElevated LES pressure (≥26 mmHg)Normal LES relaxationNormal peristalsis in the esophageal bodyIneffective esophageal motility disordersDecreased or absent amplitude of esophageal peristalsis (<30 mmHg)Increased number of nontransmitted contractionsReproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary | Surgery_Schwartz. lower esophageal sphincter (LES) relaxation (<75% relaxation)Aperistalsis in the esophageal bodyElevated LES pressure ≤26 mmHgIncreased intraesophageal baseline pressures relative to gastric baselineDiffuse esophageal spasm (DES)Simultaneous (nonperistaltic contractions) (>20% of wet swallows)Repetitive and multipeaked contractionsSpontaneous contractionsIntermittent normal peristalsisContractions may be of increased amplitude and durationNutcracker esophagusMean peristaltic amplitude (10 wet swallows) in distal esophagus ≥180 mmHgIncreased mean duration of contractions (>7.0 s)Normal peristaltic sequenceHypertensive lower esophageal sphincterElevated LES pressure (≥26 mmHg)Normal LES relaxationNormal peristalsis in the esophageal bodyIneffective esophageal motility disordersDecreased or absent amplitude of esophageal peristalsis (<30 mmHg)Increased number of nontransmitted contractionsReproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary |
Surgery_Schwartz_7041 | Surgery_Schwartz | absent amplitude of esophageal peristalsis (<30 mmHg)Increased number of nontransmitted contractionsReproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary Tract, 3rd ed. Vol 1. Philadelphia, PA: Elsevier/Saunders; 1991.Simultaneous esophageal waves develop as a result of the increased resistance to esophageal emptying caused by the nonre-laxing LES. This conclusion is supported by experimental studies in which a band placed loosely around the GEJ in experimental models did not change sphincter pressures but resulted in impaired relaxation of the LES and outflow resistance. This led to a mark-edly increased frequency of simultaneous waveforms and a decrease in contraction amplitude. The changes were associated with radiographic dilation of the esophagus and were reversible after removal of the band. Observations in patients with pseudo-achalasia due to tumor infiltration, a tight stricture in the distal esophagus, or an antireflux procedure | Surgery_Schwartz. absent amplitude of esophageal peristalsis (<30 mmHg)Increased number of nontransmitted contractionsReproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary Tract, 3rd ed. Vol 1. Philadelphia, PA: Elsevier/Saunders; 1991.Simultaneous esophageal waves develop as a result of the increased resistance to esophageal emptying caused by the nonre-laxing LES. This conclusion is supported by experimental studies in which a band placed loosely around the GEJ in experimental models did not change sphincter pressures but resulted in impaired relaxation of the LES and outflow resistance. This led to a mark-edly increased frequency of simultaneous waveforms and a decrease in contraction amplitude. The changes were associated with radiographic dilation of the esophagus and were reversible after removal of the band. Observations in patients with pseudo-achalasia due to tumor infiltration, a tight stricture in the distal esophagus, or an antireflux procedure |
Surgery_Schwartz_7042 | Surgery_Schwartz | and were reversible after removal of the band. Observations in patients with pseudo-achalasia due to tumor infiltration, a tight stricture in the distal esophagus, or an antireflux procedure that is too tight also provide evidence that dysfunction of the esophageal body can be caused by the increased outflow obstruction of a nonrelaxing LES. The observation that esophageal peristalsis can return in patients with classic achalasia following dilation or myotomy provides further support that achalasia is a primary disease of the LES.The pathogenesis of achalasia is presumed to be a neuro-genic degeneration, which is either idiopathic or due to infec-tion. In experimental animals, the disease has been reproduced by destruction of the nucleus ambiguus and the dorsal motor nucleus of the vagus nerve. In patients with the disease, degenerative changes have been shown in the vagus nerve and in the ganglia in the myenteric plexus of the esophagus itself. This degeneration results in | Surgery_Schwartz. and were reversible after removal of the band. Observations in patients with pseudo-achalasia due to tumor infiltration, a tight stricture in the distal esophagus, or an antireflux procedure that is too tight also provide evidence that dysfunction of the esophageal body can be caused by the increased outflow obstruction of a nonrelaxing LES. The observation that esophageal peristalsis can return in patients with classic achalasia following dilation or myotomy provides further support that achalasia is a primary disease of the LES.The pathogenesis of achalasia is presumed to be a neuro-genic degeneration, which is either idiopathic or due to infec-tion. In experimental animals, the disease has been reproduced by destruction of the nucleus ambiguus and the dorsal motor nucleus of the vagus nerve. In patients with the disease, degenerative changes have been shown in the vagus nerve and in the ganglia in the myenteric plexus of the esophagus itself. This degeneration results in |
Surgery_Schwartz_7043 | Surgery_Schwartz | the vagus nerve. In patients with the disease, degenerative changes have been shown in the vagus nerve and in the ganglia in the myenteric plexus of the esophagus itself. This degeneration results in hypertension of the LES, a failure of the sphincter to relax on swallowing, elevation of intraluminal esophageal pres-sure, esophageal dilatation, and a subsequent loss of progressive peristalsis in the body of the esophagus. The esophageal dilatation results from the combination of a nonrelaxing sphincter, which causes a functional retention of ingested material in the esopha-gus, and elevation of intraluminal pressure from repetitive pha-ryngeal air swallowing (Fig. 25-53). With time, the functional disorder results in anatomic alterations seen on radiographic stud-ies, such as a dilated esophagus with a tapering, “bird’s beak”-like narrowing of the distal end (Fig. 25-54). There is usually an air-fluid level in the esophagus from the retained food and saliva, the height of which | Surgery_Schwartz. the vagus nerve. In patients with the disease, degenerative changes have been shown in the vagus nerve and in the ganglia in the myenteric plexus of the esophagus itself. This degeneration results in hypertension of the LES, a failure of the sphincter to relax on swallowing, elevation of intraluminal esophageal pres-sure, esophageal dilatation, and a subsequent loss of progressive peristalsis in the body of the esophagus. The esophageal dilatation results from the combination of a nonrelaxing sphincter, which causes a functional retention of ingested material in the esopha-gus, and elevation of intraluminal pressure from repetitive pha-ryngeal air swallowing (Fig. 25-53). With time, the functional disorder results in anatomic alterations seen on radiographic stud-ies, such as a dilated esophagus with a tapering, “bird’s beak”-like narrowing of the distal end (Fig. 25-54). There is usually an air-fluid level in the esophagus from the retained food and saliva, the height of which |
Surgery_Schwartz_7044 | Surgery_Schwartz | esophagus with a tapering, “bird’s beak”-like narrowing of the distal end (Fig. 25-54). There is usually an air-fluid level in the esophagus from the retained food and saliva, the height of which reflects the degree of resistance imposed by the nonrelaxing sphincter. As the disease progresses, the esophagus becomes massively dilated and tortuous.A subgroup of patients with otherwise typical features of classic achalasia has simultaneous contractions of their esopha-geal body that can be of high amplitude. This manometric pattern has been termed vigorous achalasia, and chest pain episodes are a common finding in these patients. Since the development of high resolution esophageal manometry technology, the term vigorous achalasia has been replaced with Chicago type 3 achalasia. Dif-ferentiation of type 3 achalasia from DES can be difficult. In both diseases, videoradiographic examination may show a cork-screw deformity of the esophagus and diverticulum formation.Diffuse and Segmental | Surgery_Schwartz. esophagus with a tapering, “bird’s beak”-like narrowing of the distal end (Fig. 25-54). There is usually an air-fluid level in the esophagus from the retained food and saliva, the height of which reflects the degree of resistance imposed by the nonrelaxing sphincter. As the disease progresses, the esophagus becomes massively dilated and tortuous.A subgroup of patients with otherwise typical features of classic achalasia has simultaneous contractions of their esopha-geal body that can be of high amplitude. This manometric pattern has been termed vigorous achalasia, and chest pain episodes are a common finding in these patients. Since the development of high resolution esophageal manometry technology, the term vigorous achalasia has been replaced with Chicago type 3 achalasia. Dif-ferentiation of type 3 achalasia from DES can be difficult. In both diseases, videoradiographic examination may show a cork-screw deformity of the esophagus and diverticulum formation.Diffuse and Segmental |
Surgery_Schwartz_7045 | Surgery_Schwartz | of type 3 achalasia from DES can be difficult. In both diseases, videoradiographic examination may show a cork-screw deformity of the esophagus and diverticulum formation.Diffuse and Segmental Esophageal Spasm. DES is charac-terized by substernal chest pain and/or dysphagia. DES differs from classic achalasia in that it is primarily a disease of the esophageal body, produces a lesser degree of dysphagia, causes more chest pain, and has less effect on the patient’s general con-dition. Nonetheless, it is impossible to differentiate achalasia from DES on the basis of symptoms alone. Esophagogram and esophageal manometry are required to distinguish these two entities. True symptomatic DES is a rare condition, occurring about five times less frequently than achalasia.The causation and neuromuscular pathophysiology of DES are unclear. The basic motor abnormality is rapid wave progression down the esophagus secondary to an abnormality in Table 25-8Esophageal motility disordersPrimary | Surgery_Schwartz. of type 3 achalasia from DES can be difficult. In both diseases, videoradiographic examination may show a cork-screw deformity of the esophagus and diverticulum formation.Diffuse and Segmental Esophageal Spasm. DES is charac-terized by substernal chest pain and/or dysphagia. DES differs from classic achalasia in that it is primarily a disease of the esophageal body, produces a lesser degree of dysphagia, causes more chest pain, and has less effect on the patient’s general con-dition. Nonetheless, it is impossible to differentiate achalasia from DES on the basis of symptoms alone. Esophagogram and esophageal manometry are required to distinguish these two entities. True symptomatic DES is a rare condition, occurring about five times less frequently than achalasia.The causation and neuromuscular pathophysiology of DES are unclear. The basic motor abnormality is rapid wave progression down the esophagus secondary to an abnormality in Table 25-8Esophageal motility disordersPrimary |
Surgery_Schwartz_7046 | Surgery_Schwartz | pathophysiology of DES are unclear. The basic motor abnormality is rapid wave progression down the esophagus secondary to an abnormality in Table 25-8Esophageal motility disordersPrimary esophageal motility disordersAchalasia, “vigorous” achalasiaDiffuse and segmental esophageal spasmNutcracker esophagusHypertensive lower esophageal sphincterNonspecific esophageal motility disordersSecondary esophageal motility disordersCollagen vascular diseases: progressive systemic sclerosis, polymyositis and dermatomyositis, mixed connective tissue disease, systemic lupus erythematosus, etc.Chronic idiopathic intestinal pseudoobstructionNeuromuscular diseasesEndocrine and metastatic disordersper 100,000 population per year. Although complete absence of peristalsis in the esophageal body has been proposed as the major abnormality, present evidence indicates achalasia is a primary disorder of the LES. This is based on 24-hour outpatient esophageal motility monitoring, which shows that, even in | Surgery_Schwartz. pathophysiology of DES are unclear. The basic motor abnormality is rapid wave progression down the esophagus secondary to an abnormality in Table 25-8Esophageal motility disordersPrimary esophageal motility disordersAchalasia, “vigorous” achalasiaDiffuse and segmental esophageal spasmNutcracker esophagusHypertensive lower esophageal sphincterNonspecific esophageal motility disordersSecondary esophageal motility disordersCollagen vascular diseases: progressive systemic sclerosis, polymyositis and dermatomyositis, mixed connective tissue disease, systemic lupus erythematosus, etc.Chronic idiopathic intestinal pseudoobstructionNeuromuscular diseasesEndocrine and metastatic disordersper 100,000 population per year. Although complete absence of peristalsis in the esophageal body has been proposed as the major abnormality, present evidence indicates achalasia is a primary disorder of the LES. This is based on 24-hour outpatient esophageal motility monitoring, which shows that, even in |
Surgery_Schwartz_7047 | Surgery_Schwartz | proposed as the major abnormality, present evidence indicates achalasia is a primary disorder of the LES. This is based on 24-hour outpatient esophageal motility monitoring, which shows that, even in advanced disease, up to 5% of contractions can be peristaltic. 5Brunicardi_Ch25_p1009-p1098.indd 105601/03/19 6:04 PM 1057ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25A34140120100806050403020100–10–2056*60453525159–5–15–25–3550403020100–10–206040200–20100 mmHg10 mins10 secs100 mmHgB3*4*1501401201008060402001501401201008060402005*1501401201008060402006*1451251051008565455–15MealFigure 25-53. Pressurization of esophagus: ambulatory motility tracing of a patient with achalasia. A. Before esophageal myotomy. B. After esophageal myotomy. The tracings have been compressed to exaggerate the motility spikes and baseline elevations. Note the rise in esophageal baseline pressure during a meal represented by the rise off the baseline to the left of panel A. No such rise occurs postmyotomy | Surgery_Schwartz. proposed as the major abnormality, present evidence indicates achalasia is a primary disorder of the LES. This is based on 24-hour outpatient esophageal motility monitoring, which shows that, even in advanced disease, up to 5% of contractions can be peristaltic. 5Brunicardi_Ch25_p1009-p1098.indd 105601/03/19 6:04 PM 1057ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25A34140120100806050403020100–10–2056*60453525159–5–15–25–3550403020100–10–206040200–20100 mmHg10 mins10 secs100 mmHgB3*4*1501401201008060402001501401201008060402005*1501401201008060402006*1451251051008565455–15MealFigure 25-53. Pressurization of esophagus: ambulatory motility tracing of a patient with achalasia. A. Before esophageal myotomy. B. After esophageal myotomy. The tracings have been compressed to exaggerate the motility spikes and baseline elevations. Note the rise in esophageal baseline pressure during a meal represented by the rise off the baseline to the left of panel A. No such rise occurs postmyotomy |
Surgery_Schwartz_7048 | Surgery_Schwartz | motility spikes and baseline elevations. Note the rise in esophageal baseline pressure during a meal represented by the rise off the baseline to the left of panel A. No such rise occurs postmyotomy (B).Figure 25-54. Barium esophagogram showing a markedly dilated esophagus and characteristic “bird’s beak” in achalasia. (Repro-duced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)the latency gradient. Hypertrophy of the muscular layer of the esophageal wall and degeneration of the esophageal branches of the vagus nerve have been observed in this disease, although these are not constant findings. Manometric abnormalities in DES may be present over the total length of the esophageal body but usually are confined to the distal two-thirds. In segmental esophageal spasm, the manometric abnormalities are confined to a short segment of the esophagus.The classic manometric findings in these | Surgery_Schwartz. motility spikes and baseline elevations. Note the rise in esophageal baseline pressure during a meal represented by the rise off the baseline to the left of panel A. No such rise occurs postmyotomy (B).Figure 25-54. Barium esophagogram showing a markedly dilated esophagus and characteristic “bird’s beak” in achalasia. (Repro-duced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical management, Med Clin North Am. 1981 Nov;65(6):1235-1268.)the latency gradient. Hypertrophy of the muscular layer of the esophageal wall and degeneration of the esophageal branches of the vagus nerve have been observed in this disease, although these are not constant findings. Manometric abnormalities in DES may be present over the total length of the esophageal body but usually are confined to the distal two-thirds. In segmental esophageal spasm, the manometric abnormalities are confined to a short segment of the esophagus.The classic manometric findings in these |
Surgery_Schwartz_7049 | Surgery_Schwartz | usually are confined to the distal two-thirds. In segmental esophageal spasm, the manometric abnormalities are confined to a short segment of the esophagus.The classic manometric findings in these patients are characterized by the frequent occurrence of simultaneous wave-forms and multipeaked esophageal contractions, which may be of abnormally high amplitude or long duration. Key to the diag-nosis of DES is that there remain some peristaltic waveforms in excess of those seen in achalasia. A criterion of 30% or more peristaltic waveforms out of 10 wet swallows has been used to differentiate DES from vigorous achalasia. However, this figure is arbitrary and often debated.The LES in patients with DES usually shows a normal resting pressure and relaxation on swallowing. A hypertensive sphincter with poor relaxation may also be present. In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical and has been termed corkscrew esophagus or | Surgery_Schwartz. usually are confined to the distal two-thirds. In segmental esophageal spasm, the manometric abnormalities are confined to a short segment of the esophagus.The classic manometric findings in these patients are characterized by the frequent occurrence of simultaneous wave-forms and multipeaked esophageal contractions, which may be of abnormally high amplitude or long duration. Key to the diag-nosis of DES is that there remain some peristaltic waveforms in excess of those seen in achalasia. A criterion of 30% or more peristaltic waveforms out of 10 wet swallows has been used to differentiate DES from vigorous achalasia. However, this figure is arbitrary and often debated.The LES in patients with DES usually shows a normal resting pressure and relaxation on swallowing. A hypertensive sphincter with poor relaxation may also be present. In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical and has been termed corkscrew esophagus or |
Surgery_Schwartz_7050 | Surgery_Schwartz | sphincter with poor relaxation may also be present. In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical and has been termed corkscrew esophagus or pseudodiverticulosis (Fig. 25-55). Patients with segmental or diffuse esophageal spasm can compartmentalize the esophagus and develop an epiphrenic or midesophageal diverticulum between two areas of high pressure occurring simultaneously (Fig. 25-56).Nutcracker Esophagus. The disorder, termed nutcracker or supersqueezeresophagus, was recognized in the late 1970s. Other terms used to describe this entity are hypertensive peri-stalsis or high-amplitude peristaltic contractions. It is the most common of the primary esophageal motility disorders. By definition the so-called nutcracker esophagus is a manomet-ric abnormality in patients who are characterized by peristal-tic esophageal contractions with peak amplitudes greater than two SDs above the normal values in individual laboratories. | Surgery_Schwartz. sphincter with poor relaxation may also be present. In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical and has been termed corkscrew esophagus or pseudodiverticulosis (Fig. 25-55). Patients with segmental or diffuse esophageal spasm can compartmentalize the esophagus and develop an epiphrenic or midesophageal diverticulum between two areas of high pressure occurring simultaneously (Fig. 25-56).Nutcracker Esophagus. The disorder, termed nutcracker or supersqueezeresophagus, was recognized in the late 1970s. Other terms used to describe this entity are hypertensive peri-stalsis or high-amplitude peristaltic contractions. It is the most common of the primary esophageal motility disorders. By definition the so-called nutcracker esophagus is a manomet-ric abnormality in patients who are characterized by peristal-tic esophageal contractions with peak amplitudes greater than two SDs above the normal values in individual laboratories. |
Surgery_Schwartz_7051 | Surgery_Schwartz | is a manomet-ric abnormality in patients who are characterized by peristal-tic esophageal contractions with peak amplitudes greater than two SDs above the normal values in individual laboratories. Contraction amplitudes in these patients can easily be above 400 mmHg. At the lower end of peak pressure, it is unclear whether nutcracker esophagus causes any symptoms. In fact, chest pain symptoms in nutcracker esophagus patients may be related to GERD rather than intraluminal hypertension. Treatment in these patients should be aimed at the treatment of GERD. At the high end (peak pressures >300 mmHg) chest pain may be the result of the nutcracker physiology, as treatment directed at reducing intraluminal pressure is more effective than when used for those with lower peak pressures.Hypertensive Lower Esophageal Sphincter. Hyperten-sive lower esophageal sphincter (LES) in patients with chest pain or dysphagia was first described as a separate entity by Code and associates. This disorder is | Surgery_Schwartz. is a manomet-ric abnormality in patients who are characterized by peristal-tic esophageal contractions with peak amplitudes greater than two SDs above the normal values in individual laboratories. Contraction amplitudes in these patients can easily be above 400 mmHg. At the lower end of peak pressure, it is unclear whether nutcracker esophagus causes any symptoms. In fact, chest pain symptoms in nutcracker esophagus patients may be related to GERD rather than intraluminal hypertension. Treatment in these patients should be aimed at the treatment of GERD. At the high end (peak pressures >300 mmHg) chest pain may be the result of the nutcracker physiology, as treatment directed at reducing intraluminal pressure is more effective than when used for those with lower peak pressures.Hypertensive Lower Esophageal Sphincter. Hyperten-sive lower esophageal sphincter (LES) in patients with chest pain or dysphagia was first described as a separate entity by Code and associates. This disorder is |
Surgery_Schwartz_7052 | Surgery_Schwartz | Lower Esophageal Sphincter. Hyperten-sive lower esophageal sphincter (LES) in patients with chest pain or dysphagia was first described as a separate entity by Code and associates. This disorder is characterized by an ele-vated basal pressure of the LES with normal relaxation and Brunicardi_Ch25_p1009-p1098.indd 105701/03/19 6:04 PM 1058SPECIFIC CONSIDERATIONSPART IIFigure 25-56. Barium esophagogram showing a high epiphrenic diverticulum in a patient with diffuse esophageal spasm. (Repro-duced with permission from Castell DO: The Esophagus. Boston, MA: Little, Brown; 1992.)normal propulsion in the esophageal body. About one-half of these patients, however, have associated motility disorders of the esophageal body, particularly hypertensive peristalsis and simultaneous waveforms. In the remainder, the disorder exists as an isolated abnormality. Dysphagia in these patients may be caused by a lack of compliance of the sphincter, even in its relaxed state. Myotomy of the LES may be | Surgery_Schwartz. Lower Esophageal Sphincter. Hyperten-sive lower esophageal sphincter (LES) in patients with chest pain or dysphagia was first described as a separate entity by Code and associates. This disorder is characterized by an ele-vated basal pressure of the LES with normal relaxation and Brunicardi_Ch25_p1009-p1098.indd 105701/03/19 6:04 PM 1058SPECIFIC CONSIDERATIONSPART IIFigure 25-56. Barium esophagogram showing a high epiphrenic diverticulum in a patient with diffuse esophageal spasm. (Repro-duced with permission from Castell DO: The Esophagus. Boston, MA: Little, Brown; 1992.)normal propulsion in the esophageal body. About one-half of these patients, however, have associated motility disorders of the esophageal body, particularly hypertensive peristalsis and simultaneous waveforms. In the remainder, the disorder exists as an isolated abnormality. Dysphagia in these patients may be caused by a lack of compliance of the sphincter, even in its relaxed state. Myotomy of the LES may be |
Surgery_Schwartz_7053 | Surgery_Schwartz | the remainder, the disorder exists as an isolated abnormality. Dysphagia in these patients may be caused by a lack of compliance of the sphincter, even in its relaxed state. Myotomy of the LES may be indicated in patients not responding to medical therapy or dilation. When the symp-tom contribution of the hypertensive sphincter is in doubt, it is possible to inject the LES with botulinum toxin, endoscopically. If symptoms are relieved (temporarily) with this technique, then it is likely that myotomy will provide more permanent benefit.Secondary Esophageal Motility Disorders. Connective tissue disease, particularly scleroderma and the CREST syn-drome, exhibits severe esophageal motility disorders. Addi-tionally, patients treated as infants for esophageal atresia will often develop secondary motility disorders manifest later in life. Symptoms of these disorders are heartburn and dysphagia. The latter may be a result of a peptic stricture rather than the esophageal dysmotility. An | Surgery_Schwartz. the remainder, the disorder exists as an isolated abnormality. Dysphagia in these patients may be caused by a lack of compliance of the sphincter, even in its relaxed state. Myotomy of the LES may be indicated in patients not responding to medical therapy or dilation. When the symp-tom contribution of the hypertensive sphincter is in doubt, it is possible to inject the LES with botulinum toxin, endoscopically. If symptoms are relieved (temporarily) with this technique, then it is likely that myotomy will provide more permanent benefit.Secondary Esophageal Motility Disorders. Connective tissue disease, particularly scleroderma and the CREST syn-drome, exhibits severe esophageal motility disorders. Addi-tionally, patients treated as infants for esophageal atresia will often develop secondary motility disorders manifest later in life. Symptoms of these disorders are heartburn and dysphagia. The latter may be a result of a peptic stricture rather than the esophageal dysmotility. An |
Surgery_Schwartz_7054 | Surgery_Schwartz | motility disorders manifest later in life. Symptoms of these disorders are heartburn and dysphagia. The latter may be a result of a peptic stricture rather than the esophageal dysmotility. An esophageal motility study will usu-ally show severely reduced or absent peristalsis with severely reduced or absent LES pressure. The role of antireflux surgery under these conditions is controversial but, if performed, should be limited to partial fundoplication, as full (Nissen) fundoplica-tion may result in severe dysphagia.Nonspecific Esophageal Motor Disorders and Ineffective Esophageal Motility. Many patients complaining of dys-phagia or chest pain of noncardiac origin demonstrate a vari-ety of wave patterns and contraction amplitudes on esophageal manometry that are clearly out of the normal range, but do not meet the criteria of a primary esophageal motility disor-der. Esophageal motility in these patients frequently shows an increased number of multipeaked or repetitive contractions, | Surgery_Schwartz. motility disorders manifest later in life. Symptoms of these disorders are heartburn and dysphagia. The latter may be a result of a peptic stricture rather than the esophageal dysmotility. An esophageal motility study will usu-ally show severely reduced or absent peristalsis with severely reduced or absent LES pressure. The role of antireflux surgery under these conditions is controversial but, if performed, should be limited to partial fundoplication, as full (Nissen) fundoplica-tion may result in severe dysphagia.Nonspecific Esophageal Motor Disorders and Ineffective Esophageal Motility. Many patients complaining of dys-phagia or chest pain of noncardiac origin demonstrate a vari-ety of wave patterns and contraction amplitudes on esophageal manometry that are clearly out of the normal range, but do not meet the criteria of a primary esophageal motility disor-der. Esophageal motility in these patients frequently shows an increased number of multipeaked or repetitive contractions, |
Surgery_Schwartz_7055 | Surgery_Schwartz | range, but do not meet the criteria of a primary esophageal motility disor-der. Esophageal motility in these patients frequently shows an increased number of multipeaked or repetitive contractions, contractions of prolonged duration, nontransmitted contrac-tions, an interruption of a peristaltic wave at various levels of the esophagus, or contractions of low amplitude. These motility abnormalities have been termed nonspecific esophageal motility disorders. Their significance in the causation of chest pain or dysphagia is still unclear. Surgery plays no role in the treatment of these disorders unless there is an associated diverticulum.A clear distinction between primary esophageal motility disorders and nonspecific esophageal motility disorders is often not possible. Patients diagnosed as having nonspecific esophageal motility abnormalities on repeated studies will occasionally show abnormalities consistent with nutcracker esophagus. Similarly, progression from a nonspecific | Surgery_Schwartz. range, but do not meet the criteria of a primary esophageal motility disor-der. Esophageal motility in these patients frequently shows an increased number of multipeaked or repetitive contractions, contractions of prolonged duration, nontransmitted contrac-tions, an interruption of a peristaltic wave at various levels of the esophagus, or contractions of low amplitude. These motility abnormalities have been termed nonspecific esophageal motility disorders. Their significance in the causation of chest pain or dysphagia is still unclear. Surgery plays no role in the treatment of these disorders unless there is an associated diverticulum.A clear distinction between primary esophageal motility disorders and nonspecific esophageal motility disorders is often not possible. Patients diagnosed as having nonspecific esophageal motility abnormalities on repeated studies will occasionally show abnormalities consistent with nutcracker esophagus. Similarly, progression from a nonspecific |
Surgery_Schwartz_7056 | Surgery_Schwartz | as having nonspecific esophageal motility abnormalities on repeated studies will occasionally show abnormalities consistent with nutcracker esophagus. Similarly, progression from a nonspecific esophageal motility disorder to classic DES has been demonstrated. Therefore, the finding of a nonspecific esophageal motility disorder may represent only a manometric marker of an intermittent, more severe esophageal motor abnormality. Combined ambulatory 24-hour esophageal pH and motility monitoring has shown that an increased esopha-geal exposure to gastric juice is common in patients diagnosed as having a nonspecific esophageal motility disorder. In some situ-ations, the motor abnormalities may be induced by the irritation of refluxed gastric juice; in other situations, it may be a primary event unrelated to the presence of reflux. High-amplitude peristal-sis (nutcracker esophagus) and low-amplitude peristalsis (ineffec-tive esophageal motility) are frequently associated with | Surgery_Schwartz. as having nonspecific esophageal motility abnormalities on repeated studies will occasionally show abnormalities consistent with nutcracker esophagus. Similarly, progression from a nonspecific esophageal motility disorder to classic DES has been demonstrated. Therefore, the finding of a nonspecific esophageal motility disorder may represent only a manometric marker of an intermittent, more severe esophageal motor abnormality. Combined ambulatory 24-hour esophageal pH and motility monitoring has shown that an increased esopha-geal exposure to gastric juice is common in patients diagnosed as having a nonspecific esophageal motility disorder. In some situ-ations, the motor abnormalities may be induced by the irritation of refluxed gastric juice; in other situations, it may be a primary event unrelated to the presence of reflux. High-amplitude peristal-sis (nutcracker esophagus) and low-amplitude peristalsis (ineffec-tive esophageal motility) are frequently associated with |
Surgery_Schwartz_7057 | Surgery_Schwartz | a primary event unrelated to the presence of reflux. High-amplitude peristal-sis (nutcracker esophagus) and low-amplitude peristalsis (ineffec-tive esophageal motility) are frequently associated with GERD.Diverticula of the Esophageal Body. Diverticula of the esophagus may be characterized by their location in the esoph-agus (proximal, mid-, or distal esophagus), or by the nature of Figure 25-55. Barium esophagogram of patient with diffuse spasm showing the corkscrew deformity.Brunicardi_Ch25_p1009-p1098.indd 105801/03/19 6:04 PM 1059ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-57. Barium esophagogram showing a midesophageal diverticulum. Despite the anatomic distortion, the patient was asymptomatic. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical man-agement, Med Clin North Am. 1981 Nov;65(6):1235-1268.)InflamednodesTraction diverticulumFigure 25-58. Illustration of the pathophysiology of midesopha-geal diverticulum | Surgery_Schwartz. a primary event unrelated to the presence of reflux. High-amplitude peristal-sis (nutcracker esophagus) and low-amplitude peristalsis (ineffec-tive esophageal motility) are frequently associated with GERD.Diverticula of the Esophageal Body. Diverticula of the esophagus may be characterized by their location in the esoph-agus (proximal, mid-, or distal esophagus), or by the nature of Figure 25-55. Barium esophagogram of patient with diffuse spasm showing the corkscrew deformity.Brunicardi_Ch25_p1009-p1098.indd 105801/03/19 6:04 PM 1059ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-57. Barium esophagogram showing a midesophageal diverticulum. Despite the anatomic distortion, the patient was asymptomatic. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical man-agement, Med Clin North Am. 1981 Nov;65(6):1235-1268.)InflamednodesTraction diverticulumFigure 25-58. Illustration of the pathophysiology of midesopha-geal diverticulum |
Surgery_Schwartz_7058 | Surgery_Schwartz | and their surgical man-agement, Med Clin North Am. 1981 Nov;65(6):1235-1268.)InflamednodesTraction diverticulumFigure 25-58. Illustration of the pathophysiology of midesopha-geal diverticulum showing traction on the esophageal wall from adhesions to inflamed subcarinal lymph nodes.concomitant pathology. Diverticula associated with motor dis-orders are termed pulsion diverticula and those associated with inflammatory conditions are termed traction diverticula. Pulsion diverticula occur most commonly with nonspecific motility disor-ders, but they can occur with all of the primary motility disorders. In the latter situation, the motility disorder is usually diagnosed before the development of the diverticulum. When associated with achalasia, the development of a diverticulum may temporar-ily alleviate the symptom of dysphagia by becoming a receptacle for ingested food and substitute the symptom of dysphagia for postprandial pain and regurgitation of undigested food. If a motil-ity | Surgery_Schwartz. and their surgical man-agement, Med Clin North Am. 1981 Nov;65(6):1235-1268.)InflamednodesTraction diverticulumFigure 25-58. Illustration of the pathophysiology of midesopha-geal diverticulum showing traction on the esophageal wall from adhesions to inflamed subcarinal lymph nodes.concomitant pathology. Diverticula associated with motor dis-orders are termed pulsion diverticula and those associated with inflammatory conditions are termed traction diverticula. Pulsion diverticula occur most commonly with nonspecific motility disor-ders, but they can occur with all of the primary motility disorders. In the latter situation, the motility disorder is usually diagnosed before the development of the diverticulum. When associated with achalasia, the development of a diverticulum may temporar-ily alleviate the symptom of dysphagia by becoming a receptacle for ingested food and substitute the symptom of dysphagia for postprandial pain and regurgitation of undigested food. If a motil-ity |
Surgery_Schwartz_7059 | Surgery_Schwartz | alleviate the symptom of dysphagia by becoming a receptacle for ingested food and substitute the symptom of dysphagia for postprandial pain and regurgitation of undigested food. If a motil-ity abnormality of the esophageal body or LES cannot be identi-fied, a traction or congenital cause for the diverticulum should be considered.Because development in radiology preceded develop-ment in motility monitoring, diverticula of the esophagus were considered historically to be a primary abnormality, the cause, rather than the consequence, of motility disorders. Conse-quently, earlier texts focused on them as specific entities based upon their location.Epiphrenic diverticula arise from the terminal third of the thoracic esophagus and are usually found adjacent to the diaphragm. They have been associated with distal esophageal muscular hypertrophy, esophageal motility abnormalities, and increased luminal pressure. They are “pulsion” diverticula, and they are associated with diffuse spasm, | Surgery_Schwartz. alleviate the symptom of dysphagia by becoming a receptacle for ingested food and substitute the symptom of dysphagia for postprandial pain and regurgitation of undigested food. If a motil-ity abnormality of the esophageal body or LES cannot be identi-fied, a traction or congenital cause for the diverticulum should be considered.Because development in radiology preceded develop-ment in motility monitoring, diverticula of the esophagus were considered historically to be a primary abnormality, the cause, rather than the consequence, of motility disorders. Conse-quently, earlier texts focused on them as specific entities based upon their location.Epiphrenic diverticula arise from the terminal third of the thoracic esophagus and are usually found adjacent to the diaphragm. They have been associated with distal esophageal muscular hypertrophy, esophageal motility abnormalities, and increased luminal pressure. They are “pulsion” diverticula, and they are associated with diffuse spasm, |
Surgery_Schwartz_7060 | Surgery_Schwartz | associated with distal esophageal muscular hypertrophy, esophageal motility abnormalities, and increased luminal pressure. They are “pulsion” diverticula, and they are associated with diffuse spasm, achalasia, or nonspecific motor abnormalities in the body of the esophagus.Whether the diverticulum should be surgically resected or suspended depends on its size and proximity to the vertebral body. When diverticula are associated with esophageal motility disorders, esophageal myotomy from the proximal extent of the diverticulum to the stomach should be combined with diverticu-lectomy. If diverticulectomy alone is performed, one can expect a high incidence of suture line rupture due to the same intralu-minal pressure that initially gave rise to the diverticulum. If the diverticulum is suspended to the prevertebral fascia of the tho-racic vertebra, a myotomy is begun at the neck of the diverticu-lum and extended across the LES. If the diverticulum is excised by dividing the neck, the | Surgery_Schwartz. associated with distal esophageal muscular hypertrophy, esophageal motility abnormalities, and increased luminal pressure. They are “pulsion” diverticula, and they are associated with diffuse spasm, achalasia, or nonspecific motor abnormalities in the body of the esophagus.Whether the diverticulum should be surgically resected or suspended depends on its size and proximity to the vertebral body. When diverticula are associated with esophageal motility disorders, esophageal myotomy from the proximal extent of the diverticulum to the stomach should be combined with diverticu-lectomy. If diverticulectomy alone is performed, one can expect a high incidence of suture line rupture due to the same intralu-minal pressure that initially gave rise to the diverticulum. If the diverticulum is suspended to the prevertebral fascia of the tho-racic vertebra, a myotomy is begun at the neck of the diverticu-lum and extended across the LES. If the diverticulum is excised by dividing the neck, the |
Surgery_Schwartz_7061 | Surgery_Schwartz | to the prevertebral fascia of the tho-racic vertebra, a myotomy is begun at the neck of the diverticu-lum and extended across the LES. If the diverticulum is excised by dividing the neck, the muscle is closed over the excision site, and a myotomy is performed on the opposite esophageal wall, starting just above the level of the diverticulum or at the proximal extent of the spastic segment of the esophagus if high resolution motility is used. If complete, the myotomy will cross the LES, reducing distal esophageal peak pressure, and it will increase the likelihood that dysphagia will be replaced with GERD symp-toms. Increasingly, partial fundoplication (anterior or posterior) is performed after LES myotomy to decrease the frequency of disabling GERD developing after myotomy and diverticulec-tomy. When a large diverticulum is associated with a hiatal her-nia, then hiatal hernia repair is added. All these procedures may be performed with traditional or minimally invasive | Surgery_Schwartz. to the prevertebral fascia of the tho-racic vertebra, a myotomy is begun at the neck of the diverticu-lum and extended across the LES. If the diverticulum is excised by dividing the neck, the muscle is closed over the excision site, and a myotomy is performed on the opposite esophageal wall, starting just above the level of the diverticulum or at the proximal extent of the spastic segment of the esophagus if high resolution motility is used. If complete, the myotomy will cross the LES, reducing distal esophageal peak pressure, and it will increase the likelihood that dysphagia will be replaced with GERD symp-toms. Increasingly, partial fundoplication (anterior or posterior) is performed after LES myotomy to decrease the frequency of disabling GERD developing after myotomy and diverticulec-tomy. When a large diverticulum is associated with a hiatal her-nia, then hiatal hernia repair is added. All these procedures may be performed with traditional or minimally invasive |
Surgery_Schwartz_7062 | Surgery_Schwartz | and diverticulec-tomy. When a large diverticulum is associated with a hiatal her-nia, then hiatal hernia repair is added. All these procedures may be performed with traditional or minimally invasive techniques.Midesophageal or traction diverticula were first described in the 19th century (Fig. 25-57). At that time, they were fre-quently noted in patients who had mediastinal LN involve-ment with tuberculosis. It was theorized that adhesions formed between the inflamed mediastinal nodes and the esophagus. By contraction, the adhesions exerted traction on the esophageal wall and led to a localized diverticulum (Fig. 25-58). This theory was based on the findings of early dissections, where adhesions between diverticula and LNs were commonly found. Other con-ditions associated with mediastinal lymphadenopathy, such as pulmonary fungal infections (e.g., aspergillosis), lymphoma, or sarcoid, may create traction esophageal diverticula after success-ful treatment. Rarely, when no underlying | Surgery_Schwartz. and diverticulec-tomy. When a large diverticulum is associated with a hiatal her-nia, then hiatal hernia repair is added. All these procedures may be performed with traditional or minimally invasive techniques.Midesophageal or traction diverticula were first described in the 19th century (Fig. 25-57). At that time, they were fre-quently noted in patients who had mediastinal LN involve-ment with tuberculosis. It was theorized that adhesions formed between the inflamed mediastinal nodes and the esophagus. By contraction, the adhesions exerted traction on the esophageal wall and led to a localized diverticulum (Fig. 25-58). This theory was based on the findings of early dissections, where adhesions between diverticula and LNs were commonly found. Other con-ditions associated with mediastinal lymphadenopathy, such as pulmonary fungal infections (e.g., aspergillosis), lymphoma, or sarcoid, may create traction esophageal diverticula after success-ful treatment. Rarely, when no underlying |
Surgery_Schwartz_7063 | Surgery_Schwartz | lymphadenopathy, such as pulmonary fungal infections (e.g., aspergillosis), lymphoma, or sarcoid, may create traction esophageal diverticula after success-ful treatment. Rarely, when no underlying inflammatory pathol-ogy is identified, a motility disorder may be identified.Most midesophageal diverticula are asymptomatic and incidentally discovered during investigation for nonesophageal complaints. In such patients, the radiologic abnormality may Brunicardi_Ch25_p1009-p1098.indd 105901/03/19 6:04 PM 1060SPECIFIC CONSIDERATIONSPART II100%80%60%40%20%Normal volunteersPat, no dysphagiaPat, dysphagia0%Figure 25-59. Prevalence of effective contractions (i.e., peristaltic contractions with an amplitude >30 mmHg) during meal periods in individual normal volunteers, patients (Pat) without dysphagia, and patients with nonobstructive dysphagia.100%% Symptomatic10 cm5 cm0 cm80%60%40%20%0%Pre Rx17NEso. diameter% Retention0–24mo1725–48mo1649–72mo1473–120mo12Figure 25-60. Esophageal (Eso.) | Surgery_Schwartz. lymphadenopathy, such as pulmonary fungal infections (e.g., aspergillosis), lymphoma, or sarcoid, may create traction esophageal diverticula after success-ful treatment. Rarely, when no underlying inflammatory pathol-ogy is identified, a motility disorder may be identified.Most midesophageal diverticula are asymptomatic and incidentally discovered during investigation for nonesophageal complaints. In such patients, the radiologic abnormality may Brunicardi_Ch25_p1009-p1098.indd 105901/03/19 6:04 PM 1060SPECIFIC CONSIDERATIONSPART II100%80%60%40%20%Normal volunteersPat, no dysphagiaPat, dysphagia0%Figure 25-59. Prevalence of effective contractions (i.e., peristaltic contractions with an amplitude >30 mmHg) during meal periods in individual normal volunteers, patients (Pat) without dysphagia, and patients with nonobstructive dysphagia.100%% Symptomatic10 cm5 cm0 cm80%60%40%20%0%Pre Rx17NEso. diameter% Retention0–24mo1725–48mo1649–72mo1473–120mo12Figure 25-60. Esophageal (Eso.) |
Surgery_Schwartz_7064 | Surgery_Schwartz | dysphagia, and patients with nonobstructive dysphagia.100%% Symptomatic10 cm5 cm0 cm80%60%40%20%0%Pre Rx17NEso. diameter% Retention0–24mo1725–48mo1649–72mo1473–120mo12Figure 25-60. Esophageal (Eso.) diameter, dysphagia, and esoph-ageal retention in patients with achalasia treated with myotomy and Nissen fundoplication, 10 years after treatment (Rx). (Data from Topart P, Deschamps C, Taillefer R, et al: Long-term effect of total fundoplication on the myotomized esophagus, Ann Thorac Surg. 1992 Dec;54(6):1046-1051.)be ignored. Patients with symptoms of dysphagia, regurgita-tion, chest pain, or aspiration, in whom a diverticulum is dis-covered, should be thoroughly investigated for an esophageal motor abnormality. Occasionally, a patient will present with a bronchoesophageal fistula manifested by a chronic cough on ingestion of meals. The diverticulum in such patients is most likely to have an inflammatory etiology.The indication for surgical intervention is dictated by the degree of | Surgery_Schwartz. dysphagia, and patients with nonobstructive dysphagia.100%% Symptomatic10 cm5 cm0 cm80%60%40%20%0%Pre Rx17NEso. diameter% Retention0–24mo1725–48mo1649–72mo1473–120mo12Figure 25-60. Esophageal (Eso.) diameter, dysphagia, and esoph-ageal retention in patients with achalasia treated with myotomy and Nissen fundoplication, 10 years after treatment (Rx). (Data from Topart P, Deschamps C, Taillefer R, et al: Long-term effect of total fundoplication on the myotomized esophagus, Ann Thorac Surg. 1992 Dec;54(6):1046-1051.)be ignored. Patients with symptoms of dysphagia, regurgita-tion, chest pain, or aspiration, in whom a diverticulum is dis-covered, should be thoroughly investigated for an esophageal motor abnormality. Occasionally, a patient will present with a bronchoesophageal fistula manifested by a chronic cough on ingestion of meals. The diverticulum in such patients is most likely to have an inflammatory etiology.The indication for surgical intervention is dictated by the degree of |
Surgery_Schwartz_7065 | Surgery_Schwartz | by a chronic cough on ingestion of meals. The diverticulum in such patients is most likely to have an inflammatory etiology.The indication for surgical intervention is dictated by the degree of symptomatic disability. Usually, midesophageal diverticula can be suspended due to their proximity to the spine. If a motor abnormality is documented, a myotomy should be performed as described for an epiphrenic diverticulum.OPERATIONS FOR ESOPHAGEAL MOTOR DISORDERS AND DIVERTICULALong Esophageal Myotomy for Motor Disorders of the Esophageal BodyA long esophageal myotomy is indicated for dysphagia caused by any motor disorder characterized by segmental or general-ized simultaneous waveforms in a patient whose symptoms are not relieved by medical therapy. Such disorders include diffuse and segmental esophageal spasm, vigorous or type 3 achalasia, and nonspecific motility disorders associated with a midor epiphrenic esophageal diverticulum. However, the decision to operate must be made by a | Surgery_Schwartz. by a chronic cough on ingestion of meals. The diverticulum in such patients is most likely to have an inflammatory etiology.The indication for surgical intervention is dictated by the degree of symptomatic disability. Usually, midesophageal diverticula can be suspended due to their proximity to the spine. If a motor abnormality is documented, a myotomy should be performed as described for an epiphrenic diverticulum.OPERATIONS FOR ESOPHAGEAL MOTOR DISORDERS AND DIVERTICULALong Esophageal Myotomy for Motor Disorders of the Esophageal BodyA long esophageal myotomy is indicated for dysphagia caused by any motor disorder characterized by segmental or general-ized simultaneous waveforms in a patient whose symptoms are not relieved by medical therapy. Such disorders include diffuse and segmental esophageal spasm, vigorous or type 3 achalasia, and nonspecific motility disorders associated with a midor epiphrenic esophageal diverticulum. However, the decision to operate must be made by a |
Surgery_Schwartz_7066 | Surgery_Schwartz | esophageal spasm, vigorous or type 3 achalasia, and nonspecific motility disorders associated with a midor epiphrenic esophageal diverticulum. However, the decision to operate must be made by a balanced evaluation of the patient’s symptoms, diet, lifestyle adjustments, and nutritional status, with the most important factor being the possibility of improv-ing the patient’s swallowing disability. The symptom of chest pain alone is not an indication for a surgical procedure.The identification of patients with symptoms of dyspha-gia and chest pain who might benefit from a surgical myotomy is difficult. Ambulatory motility studies have shown that when the prevalence of “effective contractions” (i.e., peristaltic waveforms consisting of contractions with an amplitude above 30 mmHg) drops below 50% during meals, the patient is likely to experience dysphagia (Fig. 25-59). This would suggest that relief from the symptom can be expected with an improvement of esophageal contraction amplitude | Surgery_Schwartz. esophageal spasm, vigorous or type 3 achalasia, and nonspecific motility disorders associated with a midor epiphrenic esophageal diverticulum. However, the decision to operate must be made by a balanced evaluation of the patient’s symptoms, diet, lifestyle adjustments, and nutritional status, with the most important factor being the possibility of improv-ing the patient’s swallowing disability. The symptom of chest pain alone is not an indication for a surgical procedure.The identification of patients with symptoms of dyspha-gia and chest pain who might benefit from a surgical myotomy is difficult. Ambulatory motility studies have shown that when the prevalence of “effective contractions” (i.e., peristaltic waveforms consisting of contractions with an amplitude above 30 mmHg) drops below 50% during meals, the patient is likely to experience dysphagia (Fig. 25-59). This would suggest that relief from the symptom can be expected with an improvement of esophageal contraction amplitude |
Surgery_Schwartz_7067 | Surgery_Schwartz | 50% during meals, the patient is likely to experience dysphagia (Fig. 25-59). This would suggest that relief from the symptom can be expected with an improvement of esophageal contraction amplitude or amelioration of non-peristaltic waveforms. Prokinetic agents may increase esopha-geal contraction amplitude, but they do not alter the prevalence of simultaneous waveforms. Patients in whom the efficacy of esophageal propulsion is severely compromised because of a high prevalence of simultaneous waveforms usually receive little benefit from medical therapy. In these patients, a surgi-cal myotomy of the esophageal body can improve the patients’ dysphagia, provided the loss of contraction amplitude in the remaining peristaltic waveforms, caused by the myotomy, has less effect on swallowing function than the presence of the excessive simultaneous contractions. This situation is reached when the prevalence of effective waveforms during meals drops below 30% (i.e., 70% of esophageal waveforms | Surgery_Schwartz. 50% during meals, the patient is likely to experience dysphagia (Fig. 25-59). This would suggest that relief from the symptom can be expected with an improvement of esophageal contraction amplitude or amelioration of non-peristaltic waveforms. Prokinetic agents may increase esopha-geal contraction amplitude, but they do not alter the prevalence of simultaneous waveforms. Patients in whom the efficacy of esophageal propulsion is severely compromised because of a high prevalence of simultaneous waveforms usually receive little benefit from medical therapy. In these patients, a surgi-cal myotomy of the esophageal body can improve the patients’ dysphagia, provided the loss of contraction amplitude in the remaining peristaltic waveforms, caused by the myotomy, has less effect on swallowing function than the presence of the excessive simultaneous contractions. This situation is reached when the prevalence of effective waveforms during meals drops below 30% (i.e., 70% of esophageal waveforms |
Surgery_Schwartz_7068 | Surgery_Schwartz | than the presence of the excessive simultaneous contractions. This situation is reached when the prevalence of effective waveforms during meals drops below 30% (i.e., 70% of esophageal waveforms are ineffective).In patients selected for surgery, preoperative high-resolution manometry is essential to determine the proximal extent of the esophageal myotomy. Most surgeons extend the myotomy distally across the LES to reduce outflow resistance. Consequently, some form of antireflux protection is needed to avoid gastroesophageal reflux if there has been extensive dissection of the cardia. In this situation, most authors prefer a partial, rather than a full, fundoplication, in order not to add back-resistance that will further interfere with the ability of the myotomized esophagus to empty (Fig. 25-60). If the symptoms of reflux are present preoperatively, 24-hour pH monitoring is required to confirm its presence.The procedure may be performed either open or via thoracoscopy. The open | Surgery_Schwartz. than the presence of the excessive simultaneous contractions. This situation is reached when the prevalence of effective waveforms during meals drops below 30% (i.e., 70% of esophageal waveforms are ineffective).In patients selected for surgery, preoperative high-resolution manometry is essential to determine the proximal extent of the esophageal myotomy. Most surgeons extend the myotomy distally across the LES to reduce outflow resistance. Consequently, some form of antireflux protection is needed to avoid gastroesophageal reflux if there has been extensive dissection of the cardia. In this situation, most authors prefer a partial, rather than a full, fundoplication, in order not to add back-resistance that will further interfere with the ability of the myotomized esophagus to empty (Fig. 25-60). If the symptoms of reflux are present preoperatively, 24-hour pH monitoring is required to confirm its presence.The procedure may be performed either open or via thoracoscopy. The open |
Surgery_Schwartz_7069 | Surgery_Schwartz | (Fig. 25-60). If the symptoms of reflux are present preoperatively, 24-hour pH monitoring is required to confirm its presence.The procedure may be performed either open or via thoracoscopy. The open technique is performed through a left thoracotomy in the sixth intercostal space (Fig. 25-61). An incision is made in the posterior mediastinal pleura over the esophagus, and the left lateral wall of the esophagus is exposed. The esophagus is not circumferentially dissected unless necessary. A 2-cm incision is made into the abdomen through the parietal peritoneum at the midportion of the left crus. A tongue of gastric fundus is pulled into the chest. This exposes the GEJ and its associated fat pad. The latter is excised to give a clear view of the junction. A myotomy is performed through all muscle layers, extending distally over the stomach 1 to 2 cm below the GEJ, and proximally on the esophagus over the distance of the manometric abnormality. The muscle layer is dissected from the | Surgery_Schwartz. (Fig. 25-60). If the symptoms of reflux are present preoperatively, 24-hour pH monitoring is required to confirm its presence.The procedure may be performed either open or via thoracoscopy. The open technique is performed through a left thoracotomy in the sixth intercostal space (Fig. 25-61). An incision is made in the posterior mediastinal pleura over the esophagus, and the left lateral wall of the esophagus is exposed. The esophagus is not circumferentially dissected unless necessary. A 2-cm incision is made into the abdomen through the parietal peritoneum at the midportion of the left crus. A tongue of gastric fundus is pulled into the chest. This exposes the GEJ and its associated fat pad. The latter is excised to give a clear view of the junction. A myotomy is performed through all muscle layers, extending distally over the stomach 1 to 2 cm below the GEJ, and proximally on the esophagus over the distance of the manometric abnormality. The muscle layer is dissected from the |
Surgery_Schwartz_7070 | Surgery_Schwartz | all muscle layers, extending distally over the stomach 1 to 2 cm below the GEJ, and proximally on the esophagus over the distance of the manometric abnormality. The muscle layer is dissected from the mucosa laterally for a distance of 1 cm. Care is taken to divide all minute muscle bands, particularly in the area of the GEJ. The gastric fundic tongue is sutured to the margins of the myotomy over a distance of 3 to 4 cm and replaced into the abdomen. This maintains separation of the muscle and acts as a partial fundoplication to prevent reflux.Brunicardi_Ch25_p1009-p1098.indd 106001/03/19 6:04 PM 1061ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-61. Technique of long myotomy: A. Exposure of the lower esophagus through the left sixth intercostal space and incision of the mediastinal pleura in preparation for surgical myotomy. B. Location of a 2-cm incision made through the phrenoesophageal mem-brane into the abdomen along the midlateral border of the left crus. C. Retraction | Surgery_Schwartz. all muscle layers, extending distally over the stomach 1 to 2 cm below the GEJ, and proximally on the esophagus over the distance of the manometric abnormality. The muscle layer is dissected from the mucosa laterally for a distance of 1 cm. Care is taken to divide all minute muscle bands, particularly in the area of the GEJ. The gastric fundic tongue is sutured to the margins of the myotomy over a distance of 3 to 4 cm and replaced into the abdomen. This maintains separation of the muscle and acts as a partial fundoplication to prevent reflux.Brunicardi_Ch25_p1009-p1098.indd 106001/03/19 6:04 PM 1061ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-61. Technique of long myotomy: A. Exposure of the lower esophagus through the left sixth intercostal space and incision of the mediastinal pleura in preparation for surgical myotomy. B. Location of a 2-cm incision made through the phrenoesophageal mem-brane into the abdomen along the midlateral border of the left crus. C. Retraction |
Surgery_Schwartz_7071 | Surgery_Schwartz | pleura in preparation for surgical myotomy. B. Location of a 2-cm incision made through the phrenoesophageal mem-brane into the abdomen along the midlateral border of the left crus. C. Retraction of tongue of gastric fundus into the chest through the previously made incision. D. Removal of the gastroesophageal fat pad to expose the gastroesophageal junction. E. A myotomy down to the mucosa is started on the esophageal body. F. Completed myotomy extending over the stomach for 1 cm. G. Reconstruction of the cardia after a myotomy, illustrating the position of the sutures used to stitch the gastric fundic flap to the margins of the myotomy. H. Reconstruction of the cardia after a myotomy, illustrating the intra-abdominal position of the gastric tongue covering the distal 4 cm of the myotomy.Brunicardi_Ch25_p1009-p1098.indd 106101/03/19 6:04 PM 1062SPECIFIC CONSIDERATIONSPART IIIf an epiphrenic diverticulum is present, it is excised by dividing the neck with a stapler sized for the | Surgery_Schwartz. pleura in preparation for surgical myotomy. B. Location of a 2-cm incision made through the phrenoesophageal mem-brane into the abdomen along the midlateral border of the left crus. C. Retraction of tongue of gastric fundus into the chest through the previously made incision. D. Removal of the gastroesophageal fat pad to expose the gastroesophageal junction. E. A myotomy down to the mucosa is started on the esophageal body. F. Completed myotomy extending over the stomach for 1 cm. G. Reconstruction of the cardia after a myotomy, illustrating the position of the sutures used to stitch the gastric fundic flap to the margins of the myotomy. H. Reconstruction of the cardia after a myotomy, illustrating the intra-abdominal position of the gastric tongue covering the distal 4 cm of the myotomy.Brunicardi_Ch25_p1009-p1098.indd 106101/03/19 6:04 PM 1062SPECIFIC CONSIDERATIONSPART IIIf an epiphrenic diverticulum is present, it is excised by dividing the neck with a stapler sized for the |
Surgery_Schwartz_7072 | Surgery_Schwartz | 106101/03/19 6:04 PM 1062SPECIFIC CONSIDERATIONSPART IIIf an epiphrenic diverticulum is present, it is excised by dividing the neck with a stapler sized for the thickness of the diverticulum (2.0to 4.8-mm staple leg length) followed by a closure of the muscle over the staple line, when possible. The myotomy is then performed on the opposite esophageal wall. If a midesophageal diverticulum is present, the myotomy is made so that it includes the muscle around the neck, and the diver-ticulum is suspended by attaching it to the paravertebral fascia of the thoracic vertebra above the level of the diverticular neck. Before performing any operation for an esophageal diverticu-lum, it is wise to endoscope the patient to wash all food and other debris from the diverticulum.The results of myotomy for motor disorders of the esopha-geal body have improved in parallel with the improved preop-erative diagnosis afforded by manometry. Previous published series report between 40% and 92% | Surgery_Schwartz. 106101/03/19 6:04 PM 1062SPECIFIC CONSIDERATIONSPART IIIf an epiphrenic diverticulum is present, it is excised by dividing the neck with a stapler sized for the thickness of the diverticulum (2.0to 4.8-mm staple leg length) followed by a closure of the muscle over the staple line, when possible. The myotomy is then performed on the opposite esophageal wall. If a midesophageal diverticulum is present, the myotomy is made so that it includes the muscle around the neck, and the diver-ticulum is suspended by attaching it to the paravertebral fascia of the thoracic vertebra above the level of the diverticular neck. Before performing any operation for an esophageal diverticu-lum, it is wise to endoscope the patient to wash all food and other debris from the diverticulum.The results of myotomy for motor disorders of the esopha-geal body have improved in parallel with the improved preop-erative diagnosis afforded by manometry. Previous published series report between 40% and 92% |
Surgery_Schwartz_7073 | Surgery_Schwartz | of myotomy for motor disorders of the esopha-geal body have improved in parallel with the improved preop-erative diagnosis afforded by manometry. Previous published series report between 40% and 92% improvement of symptoms, but interpretation is difficult due to the small number of patients involved and the varying criteria for diagnosis of the primary motor abnormality. When myotomy is accurately done, 93% of the patients have effective palliation of dysphagia after a mean follow-up of 5 years, and 89% would have the procedure again, if it was necessary. Most patients gain or maintain rather than lose weight after the operation. Postoperative motility studies show that the myotomy reduces the amplitude of esophageal contractions to near zero and eliminates simultaneous peristaltic waves. If the benefit of obliterating the simultaneous waves exceeds the adverse effect on bolus propulsion caused by the loss of peristaltic waveforms, the patient’s dysphagia is likely to be improved by | Surgery_Schwartz. of myotomy for motor disorders of the esopha-geal body have improved in parallel with the improved preop-erative diagnosis afforded by manometry. Previous published series report between 40% and 92% improvement of symptoms, but interpretation is difficult due to the small number of patients involved and the varying criteria for diagnosis of the primary motor abnormality. When myotomy is accurately done, 93% of the patients have effective palliation of dysphagia after a mean follow-up of 5 years, and 89% would have the procedure again, if it was necessary. Most patients gain or maintain rather than lose weight after the operation. Postoperative motility studies show that the myotomy reduces the amplitude of esophageal contractions to near zero and eliminates simultaneous peristaltic waves. If the benefit of obliterating the simultaneous waves exceeds the adverse effect on bolus propulsion caused by the loss of peristaltic waveforms, the patient’s dysphagia is likely to be improved by |
Surgery_Schwartz_7074 | Surgery_Schwartz | If the benefit of obliterating the simultaneous waves exceeds the adverse effect on bolus propulsion caused by the loss of peristaltic waveforms, the patient’s dysphagia is likely to be improved by the procedure. If not, the patient is likely to continue to complain of dysphagia and to have little improvement as a result of the operation.The thoracoscopic technique may be performed through the left or right chest. There has been little experience gained with doing adequate operations (as described previously with the open exposure) through left thoracoscopy, so most surgeons will combine a right thoracoscopic long myotomy with an abdominal approach for Heller myotomy and partial fundopli-cation. These two procedures may be done at the same setting, by double positioning the patient, or they may be done at two operations. If this is the case, it is best to do the abdominal com-ponent first, as the esophageal outflow obstruction is the source of most of the symptoms. Performing | Surgery_Schwartz. If the benefit of obliterating the simultaneous waves exceeds the adverse effect on bolus propulsion caused by the loss of peristaltic waveforms, the patient’s dysphagia is likely to be improved by the procedure. If not, the patient is likely to continue to complain of dysphagia and to have little improvement as a result of the operation.The thoracoscopic technique may be performed through the left or right chest. There has been little experience gained with doing adequate operations (as described previously with the open exposure) through left thoracoscopy, so most surgeons will combine a right thoracoscopic long myotomy with an abdominal approach for Heller myotomy and partial fundopli-cation. These two procedures may be done at the same setting, by double positioning the patient, or they may be done at two operations. If this is the case, it is best to do the abdominal com-ponent first, as the esophageal outflow obstruction is the source of most of the symptoms. Performing |
Surgery_Schwartz_7075 | Surgery_Schwartz | or they may be done at two operations. If this is the case, it is best to do the abdominal com-ponent first, as the esophageal outflow obstruction is the source of most of the symptoms. Performing abdominal myotomy (and diverticulectomy, if present) may be all that is required.Figure 25-61. (Continued )A new procedure, peroral endoscopic myotomy (POEM) allows a long myotomy to be performed from the lumen of the esophagus with an endoscope. This procedure is attractive for, at a minimum, those with type 3 achalasia (vigorous achalasia), where it is necessary to divide esopha-gogastric circular muscle on both sides of the diaphragm to the extent that might not be possible with laparoscopy or thoracoscopy alone. The POEM procedure is started by open-ing the esophageal mucosa several centimeters above the spastic segment with a needle–knife electrosurgery device passed through an endoscope. A long submucosal plane is developed with the endoscope, down to and below the LES. The circular | Surgery_Schwartz. or they may be done at two operations. If this is the case, it is best to do the abdominal com-ponent first, as the esophageal outflow obstruction is the source of most of the symptoms. Performing abdominal myotomy (and diverticulectomy, if present) may be all that is required.Figure 25-61. (Continued )A new procedure, peroral endoscopic myotomy (POEM) allows a long myotomy to be performed from the lumen of the esophagus with an endoscope. This procedure is attractive for, at a minimum, those with type 3 achalasia (vigorous achalasia), where it is necessary to divide esopha-gogastric circular muscle on both sides of the diaphragm to the extent that might not be possible with laparoscopy or thoracoscopy alone. The POEM procedure is started by open-ing the esophageal mucosa several centimeters above the spastic segment with a needle–knife electrosurgery device passed through an endoscope. A long submucosal plane is developed with the endoscope, down to and below the LES. The circular |
Surgery_Schwartz_7076 | Surgery_Schwartz | above the spastic segment with a needle–knife electrosurgery device passed through an endoscope. A long submucosal plane is developed with the endoscope, down to and below the LES. The circular muscle of the LES and the esophagus is divided with endoscopic electrosurgery all the way back until normal (nonspastic) esophagus is reached. The submucosal entry site in the esophagus is then closed with endoscopic clips. While the results of POEM are still accumulating, the procedure is attractive because it is extremely minimally invasive and can be done on an outpatient basis.Epiphrenic diverticula cannot be treated with POEM and are most frequently addressed with laparoscopic access, in combination with a laparoscopic division of the LES (Heller myotomy) (Fig. 25-62). If the diverticulum can be completely mobilized through the hiatus, it may be safely excised from below. The neck of the diverticulum is transected with a GIA stapler after passage of a 48F dilator. Not infrequently, the | Surgery_Schwartz. above the spastic segment with a needle–knife electrosurgery device passed through an endoscope. A long submucosal plane is developed with the endoscope, down to and below the LES. The circular muscle of the LES and the esophagus is divided with endoscopic electrosurgery all the way back until normal (nonspastic) esophagus is reached. The submucosal entry site in the esophagus is then closed with endoscopic clips. While the results of POEM are still accumulating, the procedure is attractive because it is extremely minimally invasive and can be done on an outpatient basis.Epiphrenic diverticula cannot be treated with POEM and are most frequently addressed with laparoscopic access, in combination with a laparoscopic division of the LES (Heller myotomy) (Fig. 25-62). If the diverticulum can be completely mobilized through the hiatus, it may be safely excised from below. The neck of the diverticulum is transected with a GIA stapler after passage of a 48F dilator. Not infrequently, the |
Surgery_Schwartz_7077 | Surgery_Schwartz | be completely mobilized through the hiatus, it may be safely excised from below. The neck of the diverticulum is transected with a GIA stapler after passage of a 48F dilator. Not infrequently, the diverticulum is sufficiently large that access to the neck of the diverticulum across the hiatus is quite difficult. Addi-tionally, the inflammatory reaction to the diverticulum may further make the transhiatal dissection difficult. Under these circumstances, it is safer to perform the diverticulectomy through a right thoracoscopic approach either at the time of the initial procedure or at a later date, depending upon the frailty of the patient. Following diverticulectomy, it is critical that the esophageal staple line be treated with a great deal of care. Closure of the muscle over the staple line is preferable. Additionally, the patient is kept NPO or on clear liquids for 5 to 7 days, and a contrast study is obtained before advancing to a full liquid or “mushy food” diet. Solid foods are | Surgery_Schwartz. be completely mobilized through the hiatus, it may be safely excised from below. The neck of the diverticulum is transected with a GIA stapler after passage of a 48F dilator. Not infrequently, the diverticulum is sufficiently large that access to the neck of the diverticulum across the hiatus is quite difficult. Addi-tionally, the inflammatory reaction to the diverticulum may further make the transhiatal dissection difficult. Under these circumstances, it is safer to perform the diverticulectomy through a right thoracoscopic approach either at the time of the initial procedure or at a later date, depending upon the frailty of the patient. Following diverticulectomy, it is critical that the esophageal staple line be treated with a great deal of care. Closure of the muscle over the staple line is preferable. Additionally, the patient is kept NPO or on clear liquids for 5 to 7 days, and a contrast study is obtained before advancing to a full liquid or “mushy food” diet. Solid foods are |
Surgery_Schwartz_7078 | Surgery_Schwartz | is preferable. Additionally, the patient is kept NPO or on clear liquids for 5 to 7 days, and a contrast study is obtained before advancing to a full liquid or “mushy food” diet. Solid foods are withheld for 2 weeks to decrease the likelihood of staple line leak. But-tressing or sealing the staple line with fibrin glue is also an attractive option.Brunicardi_Ch25_p1009-p1098.indd 106201/03/19 6:04 PM 1063ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-62. A. Epiphrenic diverticula are situated above the lower esophageal sphincter on right side of esophagus. B. Stapler amputates neck of diverticulum. C. Muscle reapproximated over staple line, and Heller myotomy is performed.Myotomy of the Lower Esophageal Sphincter (Heller Myotomy)Second only to reflux disease, achalasia is the most common functional disorder of the esophagus to require surgical intervention. The goal of treatment is to relieve the functional outflow obstruction secondary to the loss of relaxation and | Surgery_Schwartz. is preferable. Additionally, the patient is kept NPO or on clear liquids for 5 to 7 days, and a contrast study is obtained before advancing to a full liquid or “mushy food” diet. Solid foods are withheld for 2 weeks to decrease the likelihood of staple line leak. But-tressing or sealing the staple line with fibrin glue is also an attractive option.Brunicardi_Ch25_p1009-p1098.indd 106201/03/19 6:04 PM 1063ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-62. A. Epiphrenic diverticula are situated above the lower esophageal sphincter on right side of esophagus. B. Stapler amputates neck of diverticulum. C. Muscle reapproximated over staple line, and Heller myotomy is performed.Myotomy of the Lower Esophageal Sphincter (Heller Myotomy)Second only to reflux disease, achalasia is the most common functional disorder of the esophagus to require surgical intervention. The goal of treatment is to relieve the functional outflow obstruction secondary to the loss of relaxation and |
Surgery_Schwartz_7079 | Surgery_Schwartz | the most common functional disorder of the esophagus to require surgical intervention. The goal of treatment is to relieve the functional outflow obstruction secondary to the loss of relaxation and compliance of the LES. This requires disrupting the LES muscle. When performed adequately (i.e., reducing sphincter pressure to <10 mmHg), and done early in the course of disease, LES myotomy results in symptomatic improvement with the occasional return of esophageal peristalsis. Reduction in LES resistance can be accomplished intraluminally by hydrostatic balloon dilation, which ruptures the sphincter muscle, by botulinum toxin injection, or by a surgical myotomy that cuts the sphincter. The difference between these three methods appears to be the greater likelihood of reducing sphincter pressure to <10 mmHg by surgical myotomy compared with hydrostatic balloon dilation. However, patients whose sphincter pressure has been reduced by hydrostatic balloon dilation to <10 mmHg have an outcome | Surgery_Schwartz. the most common functional disorder of the esophagus to require surgical intervention. The goal of treatment is to relieve the functional outflow obstruction secondary to the loss of relaxation and compliance of the LES. This requires disrupting the LES muscle. When performed adequately (i.e., reducing sphincter pressure to <10 mmHg), and done early in the course of disease, LES myotomy results in symptomatic improvement with the occasional return of esophageal peristalsis. Reduction in LES resistance can be accomplished intraluminally by hydrostatic balloon dilation, which ruptures the sphincter muscle, by botulinum toxin injection, or by a surgical myotomy that cuts the sphincter. The difference between these three methods appears to be the greater likelihood of reducing sphincter pressure to <10 mmHg by surgical myotomy compared with hydrostatic balloon dilation. However, patients whose sphincter pressure has been reduced by hydrostatic balloon dilation to <10 mmHg have an outcome |
Surgery_Schwartz_7080 | Surgery_Schwartz | to <10 mmHg by surgical myotomy compared with hydrostatic balloon dilation. However, patients whose sphincter pressure has been reduced by hydrostatic balloon dilation to <10 mmHg have an outcome similar to those after surgical myotomy (Fig. 25-63). Botulinum toxin injection may achieve similar results, but it has a longer duration of action that may be measured in weeks or months, rather than years. Botulinum toxin injection may best be used as a diagnostic tool, when it is not clear whether a hypertensive LES is the primary cause of dysphagia. Responsiveness to botulinum toxin injection may predict a good response to Heller myotomy.The therapeutic decisions regarding the treatment of patients with achalasia center on four issues. The first issue is the question of whether newly diagnosed patients should be treated with pneumatic dilation or a surgical myotomy. Long-term follow-up studies have shown that pneumatic dilation Brunicardi_Ch25_p1009-p1098.indd 106301/03/19 6:05 PM | Surgery_Schwartz. to <10 mmHg by surgical myotomy compared with hydrostatic balloon dilation. However, patients whose sphincter pressure has been reduced by hydrostatic balloon dilation to <10 mmHg have an outcome similar to those after surgical myotomy (Fig. 25-63). Botulinum toxin injection may achieve similar results, but it has a longer duration of action that may be measured in weeks or months, rather than years. Botulinum toxin injection may best be used as a diagnostic tool, when it is not clear whether a hypertensive LES is the primary cause of dysphagia. Responsiveness to botulinum toxin injection may predict a good response to Heller myotomy.The therapeutic decisions regarding the treatment of patients with achalasia center on four issues. The first issue is the question of whether newly diagnosed patients should be treated with pneumatic dilation or a surgical myotomy. Long-term follow-up studies have shown that pneumatic dilation Brunicardi_Ch25_p1009-p1098.indd 106301/03/19 6:05 PM |
Surgery_Schwartz_7081 | Surgery_Schwartz | patients should be treated with pneumatic dilation or a surgical myotomy. Long-term follow-up studies have shown that pneumatic dilation Brunicardi_Ch25_p1009-p1098.indd 106301/03/19 6:05 PM 1064SPECIFIC CONSIDERATIONSPART II10.80.60.40.200122426LES < 10 mmHg0.530.23LES > 10 mmHg48Months% in remission60728496Figure 25-63. Prevalence of clinical remission in 122 patients stratified according to postdilatation lower esophageal sphincter (LES) pressures greater than or <10 mmHg. (Reproduced with per-mission from Ponce J, Garrigues V, Pertejo V, et al: Individual pre-diction of response to pneumatic dilation in patients with achalasia, Dig Dis Sci. 1996 Nov;41(11):2135-2141.)achieves adequate relief of dysphagia and pharyngeal regurgi-tation in 50% to 60% of patients (Fig. 25-64). Close follow-up is required, and if dilation fails, myotomy is indicated. For those patients who have a dilated and tortuous esophagus or an associ-ated hiatal hernia, balloon dilation is dangerous and | Surgery_Schwartz. patients should be treated with pneumatic dilation or a surgical myotomy. Long-term follow-up studies have shown that pneumatic dilation Brunicardi_Ch25_p1009-p1098.indd 106301/03/19 6:05 PM 1064SPECIFIC CONSIDERATIONSPART II10.80.60.40.200122426LES < 10 mmHg0.530.23LES > 10 mmHg48Months% in remission60728496Figure 25-63. Prevalence of clinical remission in 122 patients stratified according to postdilatation lower esophageal sphincter (LES) pressures greater than or <10 mmHg. (Reproduced with per-mission from Ponce J, Garrigues V, Pertejo V, et al: Individual pre-diction of response to pneumatic dilation in patients with achalasia, Dig Dis Sci. 1996 Nov;41(11):2135-2141.)achieves adequate relief of dysphagia and pharyngeal regurgi-tation in 50% to 60% of patients (Fig. 25-64). Close follow-up is required, and if dilation fails, myotomy is indicated. For those patients who have a dilated and tortuous esophagus or an associ-ated hiatal hernia, balloon dilation is dangerous and |
Surgery_Schwartz_7082 | Surgery_Schwartz | follow-up is required, and if dilation fails, myotomy is indicated. For those patients who have a dilated and tortuous esophagus or an associ-ated hiatal hernia, balloon dilation is dangerous and surgery is the better option. The outcome of the one controlled random-ized study (38 patients) comparing the two modes of therapy suggests that surgical myotomy as a primary treatment gives better long-term results. Several randomized trials comparing laparoscopic cardiomyotomy with balloon dilation or botuli-num toxin injection have favored the surgical approach as well. 100908070605040%302010001234567Years89101112131415Pneumatic dilatation n = 122Pneumatic dilatation n = 54Myotomy + antireflux n = 22Myotomy n = 65Myotomy n = 81Figure 25-64. Summary of long-term studies reporting the proportion of patients with complete relief or minimal dysphagia (Stage 0–1) stratified according to type of treatment. (Data from: Ellis FH, Jr. Oesophagomyotomy for achalasia: a 22-year experience. Br J Surg. | Surgery_Schwartz. follow-up is required, and if dilation fails, myotomy is indicated. For those patients who have a dilated and tortuous esophagus or an associ-ated hiatal hernia, balloon dilation is dangerous and surgery is the better option. The outcome of the one controlled random-ized study (38 patients) comparing the two modes of therapy suggests that surgical myotomy as a primary treatment gives better long-term results. Several randomized trials comparing laparoscopic cardiomyotomy with balloon dilation or botuli-num toxin injection have favored the surgical approach as well. 100908070605040%302010001234567Years89101112131415Pneumatic dilatation n = 122Pneumatic dilatation n = 54Myotomy + antireflux n = 22Myotomy n = 65Myotomy n = 81Figure 25-64. Summary of long-term studies reporting the proportion of patients with complete relief or minimal dysphagia (Stage 0–1) stratified according to type of treatment. (Data from: Ellis FH, Jr. Oesophagomyotomy for achalasia: a 22-year experience. Br J Surg. |
Surgery_Schwartz_7083 | Surgery_Schwartz | of patients with complete relief or minimal dysphagia (Stage 0–1) stratified according to type of treatment. (Data from: Ellis FH, Jr. Oesophagomyotomy for achalasia: a 22-year experience. Br J Surg. 1993;80:882; Goulbourne IA, Walbaum PR. Long-term results of Heller’s operation for achalasia. J Royal Coll Surg. 1985;30:101; Malthaner RA, Todd TR, Miller L, et al. Long-term results in surgically managed esophageal achalasia. Ann Thorac Surg. 1994;58:1343; Ponce J, Garrigues V, Pertejo V, et al. Individual prediction of response to pneumatic dilation in patients with achalasia. Dig Dis Sci. 1996;41:2135; Eckardt V, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated by pneumatic dilation. Gastroenterology. 1992;103:1732.)Although it has been reported that a myotomy after previous balloon dilation is more difficult, this has not been the experi-ence of these authors unless the cardia has been ruptured in a sawtooth manner. In this situation, operative | Surgery_Schwartz. of patients with complete relief or minimal dysphagia (Stage 0–1) stratified according to type of treatment. (Data from: Ellis FH, Jr. Oesophagomyotomy for achalasia: a 22-year experience. Br J Surg. 1993;80:882; Goulbourne IA, Walbaum PR. Long-term results of Heller’s operation for achalasia. J Royal Coll Surg. 1985;30:101; Malthaner RA, Todd TR, Miller L, et al. Long-term results in surgically managed esophageal achalasia. Ann Thorac Surg. 1994;58:1343; Ponce J, Garrigues V, Pertejo V, et al. Individual prediction of response to pneumatic dilation in patients with achalasia. Dig Dis Sci. 1996;41:2135; Eckardt V, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated by pneumatic dilation. Gastroenterology. 1992;103:1732.)Although it has been reported that a myotomy after previous balloon dilation is more difficult, this has not been the experi-ence of these authors unless the cardia has been ruptured in a sawtooth manner. In this situation, operative |
Surgery_Schwartz_7084 | Surgery_Schwartz | a myotomy after previous balloon dilation is more difficult, this has not been the experi-ence of these authors unless the cardia has been ruptured in a sawtooth manner. In this situation, operative intervention, either immediately or after healing has occurred, can be difficult. Sim-ilarly, myotomy after botulinum toxin injection has reported to be more difficult, but this is largely a function of the submucosal inflammatory response, which may be a bit unpredictable, and is most intense in the first 6 to 12 weeks after injection. It is impor-tant to wait at least 3 months after botulinum toxin injection to perform cardiomyotomy to minimize the risk of encountering dense inflammation.The second issue is the question of whether a surgical myotomy should be performed through the abdomen or the chest. Myotomy of the LES can be accomplished via either an abdominal or thoracic approach. In the absence of a previous upper abdominal surgery, most surgeons prefer the abdominal approach to | Surgery_Schwartz. a myotomy after previous balloon dilation is more difficult, this has not been the experi-ence of these authors unless the cardia has been ruptured in a sawtooth manner. In this situation, operative intervention, either immediately or after healing has occurred, can be difficult. Sim-ilarly, myotomy after botulinum toxin injection has reported to be more difficult, but this is largely a function of the submucosal inflammatory response, which may be a bit unpredictable, and is most intense in the first 6 to 12 weeks after injection. It is impor-tant to wait at least 3 months after botulinum toxin injection to perform cardiomyotomy to minimize the risk of encountering dense inflammation.The second issue is the question of whether a surgical myotomy should be performed through the abdomen or the chest. Myotomy of the LES can be accomplished via either an abdominal or thoracic approach. In the absence of a previous upper abdominal surgery, most surgeons prefer the abdominal approach to |
Surgery_Schwartz_7085 | Surgery_Schwartz | or the chest. Myotomy of the LES can be accomplished via either an abdominal or thoracic approach. In the absence of a previous upper abdominal surgery, most surgeons prefer the abdominal approach to LES myotomy as laparoscopy results in less pain and a shorter length of stay than thoracoscopy. In addition, it is a bit easier to ensure a long gastric myotomy when the approach is transabdominal.The third issue—and one that has been long debated—is the question of whether an antireflux procedure should be added to a surgical myotomy. Excellent results have been reported fol-lowing meticulously performed myotomy without an antireflux component. Retrospective studies, with long-term follow-up of large cohorts of patients undergoing Heller myotomy demon-strated that, after 10 years, more than 50% of patients had reflux symptoms without a fundoplication. In a recent randomized clin-ical trial, 7% of patients undergoing Dor fundoplication follow-ing LES myotomy had abnormal 24-hour pH | Surgery_Schwartz. or the chest. Myotomy of the LES can be accomplished via either an abdominal or thoracic approach. In the absence of a previous upper abdominal surgery, most surgeons prefer the abdominal approach to LES myotomy as laparoscopy results in less pain and a shorter length of stay than thoracoscopy. In addition, it is a bit easier to ensure a long gastric myotomy when the approach is transabdominal.The third issue—and one that has been long debated—is the question of whether an antireflux procedure should be added to a surgical myotomy. Excellent results have been reported fol-lowing meticulously performed myotomy without an antireflux component. Retrospective studies, with long-term follow-up of large cohorts of patients undergoing Heller myotomy demon-strated that, after 10 years, more than 50% of patients had reflux symptoms without a fundoplication. In a recent randomized clin-ical trial, 7% of patients undergoing Dor fundoplication follow-ing LES myotomy had abnormal 24-hour pH |
Surgery_Schwartz_7086 | Surgery_Schwartz | than 50% of patients had reflux symptoms without a fundoplication. In a recent randomized clin-ical trial, 7% of patients undergoing Dor fundoplication follow-ing LES myotomy had abnormal 24-hour pH probes, and 42% of patients with a myotomy only had abnormal reflux profiles. If an antireflux procedure is used as an adjunct to esophageal myotomy, a complete 360° fundoplication should be avoided. Rather, a 270° Belsey fundoplication, a Toupet posterior 180° fundoplication, or a Dor anterior 180° fundoplication should be used to avoid the long-term esophageal dysfunction secondary to the outflow obstruction afforded by the fundoplication itself.The fourth issue centers on whether or not a cure of this disease is achievable. Long-term follow-up studies after surgical myotomy have shown that late deterioration in results occurs after this procedure, regardless of whether an antireflux pro-cedure is done, and also after balloon dilation, even when the sphincter pressure is reduced to below | Surgery_Schwartz. than 50% of patients had reflux symptoms without a fundoplication. In a recent randomized clin-ical trial, 7% of patients undergoing Dor fundoplication follow-ing LES myotomy had abnormal 24-hour pH probes, and 42% of patients with a myotomy only had abnormal reflux profiles. If an antireflux procedure is used as an adjunct to esophageal myotomy, a complete 360° fundoplication should be avoided. Rather, a 270° Belsey fundoplication, a Toupet posterior 180° fundoplication, or a Dor anterior 180° fundoplication should be used to avoid the long-term esophageal dysfunction secondary to the outflow obstruction afforded by the fundoplication itself.The fourth issue centers on whether or not a cure of this disease is achievable. Long-term follow-up studies after surgical myotomy have shown that late deterioration in results occurs after this procedure, regardless of whether an antireflux pro-cedure is done, and also after balloon dilation, even when the sphincter pressure is reduced to below |
Surgery_Schwartz_7087 | Surgery_Schwartz | deterioration in results occurs after this procedure, regardless of whether an antireflux pro-cedure is done, and also after balloon dilation, even when the sphincter pressure is reduced to below 10 mmHg. It may be that, even though a myotomy or balloon rupture of the LES muscle reduces the outflow obstruction at the cardia, the underlying motor disorder in the body of the esophagus persists and dete-riorates further with the passage of time, leading to increased impairment of esophageal emptying. The earlier an effective reduction in outflow resistance can be accomplished, the better the outcome will be, and the more likely some esophageal body function can be restored.In performing a surgical myotomy of the LES, there are four important principles: (a) complete division of all circular and collar-sling muscle fibers, (b) adequate distal myotomy to reduce outflow resistance, (c) “undermining” of the muscularis to allow wide separation of the esophageal muscle, and (d) pre-vention of | Surgery_Schwartz. deterioration in results occurs after this procedure, regardless of whether an antireflux pro-cedure is done, and also after balloon dilation, even when the sphincter pressure is reduced to below 10 mmHg. It may be that, even though a myotomy or balloon rupture of the LES muscle reduces the outflow obstruction at the cardia, the underlying motor disorder in the body of the esophagus persists and dete-riorates further with the passage of time, leading to increased impairment of esophageal emptying. The earlier an effective reduction in outflow resistance can be accomplished, the better the outcome will be, and the more likely some esophageal body function can be restored.In performing a surgical myotomy of the LES, there are four important principles: (a) complete division of all circular and collar-sling muscle fibers, (b) adequate distal myotomy to reduce outflow resistance, (c) “undermining” of the muscularis to allow wide separation of the esophageal muscle, and (d) pre-vention of |
Surgery_Schwartz_7088 | Surgery_Schwartz | and collar-sling muscle fibers, (b) adequate distal myotomy to reduce outflow resistance, (c) “undermining” of the muscularis to allow wide separation of the esophageal muscle, and (d) pre-vention of postoperative reflux. In the past, the drawback of a surgical myotomy was the need for an open procedure, which often deterred patients from choosing the best treatment option for achalasia. With the advent of minimally invasive surgi-cal techniques two decades ago, laparoscopic cardiomyotomy Brunicardi_Ch25_p1009-p1098.indd 106401/03/19 6:05 PM 1065ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25(Heller myotomy) has become the treatment of choice for most patients with achalasia.Open Esophageal MyotomyOpen techniques of distal esophageal myotomy are rarely used outside reoperations. In fact, primary procedures can almost always be successfully completed via laparoscopy. A modified Heller myotomy can be performed through a left thoracotomy incision in the sixth intercostal space along the | Surgery_Schwartz. and collar-sling muscle fibers, (b) adequate distal myotomy to reduce outflow resistance, (c) “undermining” of the muscularis to allow wide separation of the esophageal muscle, and (d) pre-vention of postoperative reflux. In the past, the drawback of a surgical myotomy was the need for an open procedure, which often deterred patients from choosing the best treatment option for achalasia. With the advent of minimally invasive surgi-cal techniques two decades ago, laparoscopic cardiomyotomy Brunicardi_Ch25_p1009-p1098.indd 106401/03/19 6:05 PM 1065ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25(Heller myotomy) has become the treatment of choice for most patients with achalasia.Open Esophageal MyotomyOpen techniques of distal esophageal myotomy are rarely used outside reoperations. In fact, primary procedures can almost always be successfully completed via laparoscopy. A modified Heller myotomy can be performed through a left thoracotomy incision in the sixth intercostal space along the |
Surgery_Schwartz_7089 | Surgery_Schwartz | primary procedures can almost always be successfully completed via laparoscopy. A modified Heller myotomy can be performed through a left thoracotomy incision in the sixth intercostal space along the upper border of the seventh rib. The esophagus and a tongue of gastric fun-dus are exposed as described for a long myotomy. A myotomy through all muscle layers is performed, extending distally over the stomach to 1 to 2 cm below the junction, and proximally on the esophagus for 4 to 5 cm. The cardia is reconstructed by suturing the tongue of gastric fundus to the margins of the myotomy to prevent rehealing of the myotomy site and to pro-vide reflux protection in the area of the divided sphincter. If an extensive dissection of the cardia has been done, a more for-mal Belsey repair is performed. The tongue of gastric fundus is allowed to retract into the abdomen. Traditionally, nasogastric drainage is maintained for 6 days to prevent distention of the stomach during healing. An oral diet is | Surgery_Schwartz. primary procedures can almost always be successfully completed via laparoscopy. A modified Heller myotomy can be performed through a left thoracotomy incision in the sixth intercostal space along the upper border of the seventh rib. The esophagus and a tongue of gastric fun-dus are exposed as described for a long myotomy. A myotomy through all muscle layers is performed, extending distally over the stomach to 1 to 2 cm below the junction, and proximally on the esophagus for 4 to 5 cm. The cardia is reconstructed by suturing the tongue of gastric fundus to the margins of the myotomy to prevent rehealing of the myotomy site and to pro-vide reflux protection in the area of the divided sphincter. If an extensive dissection of the cardia has been done, a more for-mal Belsey repair is performed. The tongue of gastric fundus is allowed to retract into the abdomen. Traditionally, nasogastric drainage is maintained for 6 days to prevent distention of the stomach during healing. An oral diet is |
Surgery_Schwartz_7090 | Surgery_Schwartz | The tongue of gastric fundus is allowed to retract into the abdomen. Traditionally, nasogastric drainage is maintained for 6 days to prevent distention of the stomach during healing. An oral diet is resumed on the seventh day, after a barium swallow study shows unobstructed passage of the bolus into the stomach without extravasation.In a randomized, long-term follow-up by Csendes and colleagues of 81 patients treated for achalasia, either by forceful dilation or by surgical myotomy, myotomy was associated with a significant increase in the diameter at the GEJ and a decrease in the diameter at the middle third of the esophagus on follow-up radiographic studies. There was a greater reduction in sphincter pressure and improvement in the amplitude of esophageal contractions after myotomy. After dilation, 13% of patients regained some peristalsis, compared with 28% after surgery. These findings were shown to persist over a 5-year follow-up period, at which time 95% of those treated with | Surgery_Schwartz. The tongue of gastric fundus is allowed to retract into the abdomen. Traditionally, nasogastric drainage is maintained for 6 days to prevent distention of the stomach during healing. An oral diet is resumed on the seventh day, after a barium swallow study shows unobstructed passage of the bolus into the stomach without extravasation.In a randomized, long-term follow-up by Csendes and colleagues of 81 patients treated for achalasia, either by forceful dilation or by surgical myotomy, myotomy was associated with a significant increase in the diameter at the GEJ and a decrease in the diameter at the middle third of the esophagus on follow-up radiographic studies. There was a greater reduction in sphincter pressure and improvement in the amplitude of esophageal contractions after myotomy. After dilation, 13% of patients regained some peristalsis, compared with 28% after surgery. These findings were shown to persist over a 5-year follow-up period, at which time 95% of those treated with |
Surgery_Schwartz_7091 | Surgery_Schwartz | dilation, 13% of patients regained some peristalsis, compared with 28% after surgery. These findings were shown to persist over a 5-year follow-up period, at which time 95% of those treated with surgical myotomy were doing well. Of those who were treated with dilation, only 54% were doing well, while 16% required redilation, and 22% eventually required surgical myotomy to obtain relief.If simultaneous esophageal contractions are associated with the sphincter abnormality, the so-called vigorous achala-sia, then the myotomy should extend over the distance of the abnormal motility as mapped by the preoperative motility study. Failure to do this will result in continuing dysphagia and a dis-satisfied patient. The best objective evaluation of improvement in the patient following either balloon dilation or myotomy is a scintigraphic measurement of esophageal emptying time. A good therapeutic response improves esophageal emptying toward normal. However, some degree of dysphagia may per-sist | Surgery_Schwartz. dilation, 13% of patients regained some peristalsis, compared with 28% after surgery. These findings were shown to persist over a 5-year follow-up period, at which time 95% of those treated with surgical myotomy were doing well. Of those who were treated with dilation, only 54% were doing well, while 16% required redilation, and 22% eventually required surgical myotomy to obtain relief.If simultaneous esophageal contractions are associated with the sphincter abnormality, the so-called vigorous achala-sia, then the myotomy should extend over the distance of the abnormal motility as mapped by the preoperative motility study. Failure to do this will result in continuing dysphagia and a dis-satisfied patient. The best objective evaluation of improvement in the patient following either balloon dilation or myotomy is a scintigraphic measurement of esophageal emptying time. A good therapeutic response improves esophageal emptying toward normal. However, some degree of dysphagia may per-sist |
Surgery_Schwartz_7092 | Surgery_Schwartz | dilation or myotomy is a scintigraphic measurement of esophageal emptying time. A good therapeutic response improves esophageal emptying toward normal. However, some degree of dysphagia may per-sist despite improved esophageal emptying, due to disturbances in esophageal body function. When an antireflux procedure is added to the myotomy, it should be a partial fundoplication. A 360° fundoplication is associated with progressive retention of swallowed food, regurgitation, and aspiration to a degree that exceeds the patient’s preoperative symptoms.Laparoscopic CardiomyotomyMore commonly known as a laparoscopic Heller myotomy, after Ernst Heller, a German surgeon who described a “dou-ble myotomy” in 1913, the laparoscopic approach is similar to the Nissen fundoplication in terms of the trocar placement and exposure and dissection of the esophageal hiatus (Fig. 25-65). The procedure begins by division of the short gastric vessels in preparation for fundoplication. Exposure of the GEJ via | Surgery_Schwartz. dilation or myotomy is a scintigraphic measurement of esophageal emptying time. A good therapeutic response improves esophageal emptying toward normal. However, some degree of dysphagia may per-sist despite improved esophageal emptying, due to disturbances in esophageal body function. When an antireflux procedure is added to the myotomy, it should be a partial fundoplication. A 360° fundoplication is associated with progressive retention of swallowed food, regurgitation, and aspiration to a degree that exceeds the patient’s preoperative symptoms.Laparoscopic CardiomyotomyMore commonly known as a laparoscopic Heller myotomy, after Ernst Heller, a German surgeon who described a “dou-ble myotomy” in 1913, the laparoscopic approach is similar to the Nissen fundoplication in terms of the trocar placement and exposure and dissection of the esophageal hiatus (Fig. 25-65). The procedure begins by division of the short gastric vessels in preparation for fundoplication. Exposure of the GEJ via |
Surgery_Schwartz_7093 | Surgery_Schwartz | placement and exposure and dissection of the esophageal hiatus (Fig. 25-65). The procedure begins by division of the short gastric vessels in preparation for fundoplication. Exposure of the GEJ via removal of the gastroesophageal fat pad follows. The anterior vagus nerve is swept right laterally along with the fat pad. Once completed, the GEJ and distal 4 to 5 cm of esophagus should be bared of any overlying tissue, and generally follows dissection of the GEJ. A distal esophageal myotomy is performed. It is generally easiest to begin the myotomy 1 to 2 cm above the GEJ, in an area above that of previous botulinum toxin injections or balloon dilation. Either scissors or a hook-type electrocautery can be used to initiate the incision in the longitudinal and circu-lar muscle. Distally, the myotomy is carried across the GEJ and onto the proximal stomach for approximately 2 to 3 cm. After completion, the muscle edges are separated bluntly from the esophageal mucosa for approximately 50% of | Surgery_Schwartz. placement and exposure and dissection of the esophageal hiatus (Fig. 25-65). The procedure begins by division of the short gastric vessels in preparation for fundoplication. Exposure of the GEJ via removal of the gastroesophageal fat pad follows. The anterior vagus nerve is swept right laterally along with the fat pad. Once completed, the GEJ and distal 4 to 5 cm of esophagus should be bared of any overlying tissue, and generally follows dissection of the GEJ. A distal esophageal myotomy is performed. It is generally easiest to begin the myotomy 1 to 2 cm above the GEJ, in an area above that of previous botulinum toxin injections or balloon dilation. Either scissors or a hook-type electrocautery can be used to initiate the incision in the longitudinal and circu-lar muscle. Distally, the myotomy is carried across the GEJ and onto the proximal stomach for approximately 2 to 3 cm. After completion, the muscle edges are separated bluntly from the esophageal mucosa for approximately 50% of |
Surgery_Schwartz_7094 | Surgery_Schwartz | is carried across the GEJ and onto the proximal stomach for approximately 2 to 3 cm. After completion, the muscle edges are separated bluntly from the esophageal mucosa for approximately 50% of the esophageal circumference. An antireflux procedure follows completion of the myotomy. Either an anterior hemifundoplication augment-ing the angle of His (Dor) or posterior partial fundoplication (Toupet) can be performed. The Dor type fundoplication is slightly easier to perform, and it does not require disruption of the normal posterior gastroesophageal attachments (a theoretical advantage in preventing postoperative reflux).Per Oral Endoscopic Myotomy (POEM)The POEM procedure was developed in Japan. It is the ultimate minimally invasive myotomy as it requires no incisions through the skin. With the POEM procedure, a very effective myotomy is performed entirely from the lumen of the esophagus. The POEM procedure is started by opening the esophageal mucosa 10 cm above the lower esophageal | Surgery_Schwartz. is carried across the GEJ and onto the proximal stomach for approximately 2 to 3 cm. After completion, the muscle edges are separated bluntly from the esophageal mucosa for approximately 50% of the esophageal circumference. An antireflux procedure follows completion of the myotomy. Either an anterior hemifundoplication augment-ing the angle of His (Dor) or posterior partial fundoplication (Toupet) can be performed. The Dor type fundoplication is slightly easier to perform, and it does not require disruption of the normal posterior gastroesophageal attachments (a theoretical advantage in preventing postoperative reflux).Per Oral Endoscopic Myotomy (POEM)The POEM procedure was developed in Japan. It is the ultimate minimally invasive myotomy as it requires no incisions through the skin. With the POEM procedure, a very effective myotomy is performed entirely from the lumen of the esophagus. The POEM procedure is started by opening the esophageal mucosa 10 cm above the lower esophageal |
Surgery_Schwartz_7095 | Surgery_Schwartz | the POEM procedure, a very effective myotomy is performed entirely from the lumen of the esophagus. The POEM procedure is started by opening the esophageal mucosa 10 cm above the lower esophageal sphincter with a needle–knife electrosurgery device passed through an endoscope. A long submucosal plane is developed with the endoscope, down to and below the LES. The circular muscle of the LES, above and below the gastroesophageal junction, is divided with endoscopic electrosurgery. The submucosal entry site in the esophagus is then closed with endoscopic clips. While the results of POEM are still accumulating, the procedure is attractive because it is extremely minimally invasive, and can be done on an outpatient basis. The major downside of POEM is that an effective antire-flux valve cannot be created, exposing the patient to a 40% to 50% risk of GERD post procedure.Outcome Assessment of the Therapy for AchalasiaCritical analysis of the results of therapy for motor disor-ders of the | Surgery_Schwartz. the POEM procedure, a very effective myotomy is performed entirely from the lumen of the esophagus. The POEM procedure is started by opening the esophageal mucosa 10 cm above the lower esophageal sphincter with a needle–knife electrosurgery device passed through an endoscope. A long submucosal plane is developed with the endoscope, down to and below the LES. The circular muscle of the LES, above and below the gastroesophageal junction, is divided with endoscopic electrosurgery. The submucosal entry site in the esophagus is then closed with endoscopic clips. While the results of POEM are still accumulating, the procedure is attractive because it is extremely minimally invasive, and can be done on an outpatient basis. The major downside of POEM is that an effective antire-flux valve cannot be created, exposing the patient to a 40% to 50% risk of GERD post procedure.Outcome Assessment of the Therapy for AchalasiaCritical analysis of the results of therapy for motor disor-ders of the |
Surgery_Schwartz_7096 | Surgery_Schwartz | be created, exposing the patient to a 40% to 50% risk of GERD post procedure.Outcome Assessment of the Therapy for AchalasiaCritical analysis of the results of therapy for motor disor-ders of the esophagus requires objective measurement. The use of symptoms alone as an endpoint to evaluate therapy for achalasia may be misleading. The propensity for patients to unconsciously modify their diet to avoid difficulty swallowing is underestimated, making an assessment of results based on symptoms unreliable. Insufficient reduction in outflow resis-tance may allow progressive esophageal dilation to develop slowly, giving the impression of improvement because the volume of food able to be ingested with comfort increases. A variety of objective measurements may be used to assess success, including LES pressure, esophageal baseline pressure, and scintigraphic assessment of esophageal emptying time. Esophageal baseline pressure is usually negative compared to gastric pressure. Given that the | Surgery_Schwartz. be created, exposing the patient to a 40% to 50% risk of GERD post procedure.Outcome Assessment of the Therapy for AchalasiaCritical analysis of the results of therapy for motor disor-ders of the esophagus requires objective measurement. The use of symptoms alone as an endpoint to evaluate therapy for achalasia may be misleading. The propensity for patients to unconsciously modify their diet to avoid difficulty swallowing is underestimated, making an assessment of results based on symptoms unreliable. Insufficient reduction in outflow resis-tance may allow progressive esophageal dilation to develop slowly, giving the impression of improvement because the volume of food able to be ingested with comfort increases. A variety of objective measurements may be used to assess success, including LES pressure, esophageal baseline pressure, and scintigraphic assessment of esophageal emptying time. Esophageal baseline pressure is usually negative compared to gastric pressure. Given that the |
Surgery_Schwartz_7097 | Surgery_Schwartz | LES pressure, esophageal baseline pressure, and scintigraphic assessment of esophageal emptying time. Esophageal baseline pressure is usually negative compared to gastric pressure. Given that the goal of therapy is to eliminate the outflow resistance of a nonrelaxing sphincter, measure-ments of improvements in esophageal baseline pressure and scintigraphic transit time may be better indicators of success, but these are rarely reported.Brunicardi_Ch25_p1009-p1098.indd 106501/03/19 6:05 PM 1066SPECIFIC CONSIDERATIONSPART IIFigure 25-65. A. Longitudinal muscle is divided. B. Mechanical disruption of lower esophageal sphincter muscle fibers. C. Myotomy must be carried across gastroesophageal junction. D. Gastric extension should equal 2 to 3 cm. E. Anterior (Dor) fundoplication is sutured to the diaphragmatic arch. F. Posterior (Toupet) fundoplication is sutured to cut edges of myotomy. EG jct = esophagogastric junction.Eckardt and associates investigated whether the outcome of | Surgery_Schwartz. LES pressure, esophageal baseline pressure, and scintigraphic assessment of esophageal emptying time. Esophageal baseline pressure is usually negative compared to gastric pressure. Given that the goal of therapy is to eliminate the outflow resistance of a nonrelaxing sphincter, measure-ments of improvements in esophageal baseline pressure and scintigraphic transit time may be better indicators of success, but these are rarely reported.Brunicardi_Ch25_p1009-p1098.indd 106501/03/19 6:05 PM 1066SPECIFIC CONSIDERATIONSPART IIFigure 25-65. A. Longitudinal muscle is divided. B. Mechanical disruption of lower esophageal sphincter muscle fibers. C. Myotomy must be carried across gastroesophageal junction. D. Gastric extension should equal 2 to 3 cm. E. Anterior (Dor) fundoplication is sutured to the diaphragmatic arch. F. Posterior (Toupet) fundoplication is sutured to cut edges of myotomy. EG jct = esophagogastric junction.Eckardt and associates investigated whether the outcome of |
Surgery_Schwartz_7098 | Surgery_Schwartz | to the diaphragmatic arch. F. Posterior (Toupet) fundoplication is sutured to cut edges of myotomy. EG jct = esophagogastric junction.Eckardt and associates investigated whether the outcome of pneumatic dilation in patients with achalasia could be pre-dicted on the basis of objective measurements. Postdilation LES pressure was the most valuable measurement for predict-ing long-term clinical response. A postdilatation sphincter pres-sure <10 mmHg predicted a good response. Approximately 50% of the patients studied had postdilatation sphincter pressures between 10 and 20 mmHg, with a 2-year remission rate of 71%. More important, 16 of 46 patients were left with a postdilatation sphincter pressure of >20 mmHg and had an unacceptable out-come. Overall, only 30% of patients dilated remained in symp-tomatic remission at 5 years.Bonavina and colleagues reported good to excellent results with transabdominal myotomy and Dor fundoplication in 94% of patients after a mean follow-up of 5.4 years. | Surgery_Schwartz. to the diaphragmatic arch. F. Posterior (Toupet) fundoplication is sutured to cut edges of myotomy. EG jct = esophagogastric junction.Eckardt and associates investigated whether the outcome of pneumatic dilation in patients with achalasia could be pre-dicted on the basis of objective measurements. Postdilation LES pressure was the most valuable measurement for predict-ing long-term clinical response. A postdilatation sphincter pres-sure <10 mmHg predicted a good response. Approximately 50% of the patients studied had postdilatation sphincter pressures between 10 and 20 mmHg, with a 2-year remission rate of 71%. More important, 16 of 46 patients were left with a postdilatation sphincter pressure of >20 mmHg and had an unacceptable out-come. Overall, only 30% of patients dilated remained in symp-tomatic remission at 5 years.Bonavina and colleagues reported good to excellent results with transabdominal myotomy and Dor fundoplication in 94% of patients after a mean follow-up of 5.4 years. |
Surgery_Schwartz_7099 | Surgery_Schwartz | symp-tomatic remission at 5 years.Bonavina and colleagues reported good to excellent results with transabdominal myotomy and Dor fundoplication in 94% of patients after a mean follow-up of 5.4 years. No operative mortality occurred in either of these series, attesting to the safety of the procedure. Malthaner and Pearson reported the long-term clinical results in 35 patients with achalasia, having a minimum follow-up of 10 years (Table 25-10). Twenty-two of these patients underwent primary esophageal myotomy and Belsey hemifundoplication at the Toronto General Hospital. Excellent to good results were noted in 95% of patients at 1 year, declining to 68%, 69%, and 67% at 10, 15, and 20 years, respectively. Two patients underwent early reoperation for an incomplete myotomy, and three underwent an esophagectomy for progressive disease. They concluded that there was a deterioration of the initially good results after surgical myotomy and hiatal repair for achalasia, which is due to late | Surgery_Schwartz. symp-tomatic remission at 5 years.Bonavina and colleagues reported good to excellent results with transabdominal myotomy and Dor fundoplication in 94% of patients after a mean follow-up of 5.4 years. No operative mortality occurred in either of these series, attesting to the safety of the procedure. Malthaner and Pearson reported the long-term clinical results in 35 patients with achalasia, having a minimum follow-up of 10 years (Table 25-10). Twenty-two of these patients underwent primary esophageal myotomy and Belsey hemifundoplication at the Toronto General Hospital. Excellent to good results were noted in 95% of patients at 1 year, declining to 68%, 69%, and 67% at 10, 15, and 20 years, respectively. Two patients underwent early reoperation for an incomplete myotomy, and three underwent an esophagectomy for progressive disease. They concluded that there was a deterioration of the initially good results after surgical myotomy and hiatal repair for achalasia, which is due to late |
Surgery_Schwartz_7100 | Surgery_Schwartz | an esophagectomy for progressive disease. They concluded that there was a deterioration of the initially good results after surgical myotomy and hiatal repair for achalasia, which is due to late complications of gastroesophageal reflux.Ellis reported his lifetime experience with transthoracic short esophageal myotomy without an antireflux procedure. One hundred seventy-nine patients were analyzed at a mean follow-up of 9 years, ranging from 6 months to 20 years. Overall, 89% of patients were improved at the 9-year mark. He also observed that the level of improvement deteriorated with time, with excel-lent results (patients continuing to be symptom free) decreasing from 54% at 10 years to 32% at 20 years. He concluded that a short transthoracic myotomy without an antireflux procedure provides excellent long-term relief of dysphagia, and, contrary to Malthaner and Pearson’s experience, does not result in com-plications of gastroesophageal reflux. Both studies document nearly identical | Surgery_Schwartz. an esophagectomy for progressive disease. They concluded that there was a deterioration of the initially good results after surgical myotomy and hiatal repair for achalasia, which is due to late complications of gastroesophageal reflux.Ellis reported his lifetime experience with transthoracic short esophageal myotomy without an antireflux procedure. One hundred seventy-nine patients were analyzed at a mean follow-up of 9 years, ranging from 6 months to 20 years. Overall, 89% of patients were improved at the 9-year mark. He also observed that the level of improvement deteriorated with time, with excel-lent results (patients continuing to be symptom free) decreasing from 54% at 10 years to 32% at 20 years. He concluded that a short transthoracic myotomy without an antireflux procedure provides excellent long-term relief of dysphagia, and, contrary to Malthaner and Pearson’s experience, does not result in com-plications of gastroesophageal reflux. Both studies document nearly identical |
Surgery_Schwartz_7101 | Surgery_Schwartz | excellent long-term relief of dysphagia, and, contrary to Malthaner and Pearson’s experience, does not result in com-plications of gastroesophageal reflux. Both studies document nearly identical results 10 to 15 years following the procedure, and both report deterioration over time, probably due to progres-sion of the underlying disease. The addition of an antireflux procedure if the operation is performed transthoracically has no significant effect on the outcome.Brunicardi_Ch25_p1009-p1098.indd 106601/03/19 6:05 PM 1067ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-65. (Continued )Table 25-10Reasons for failure of esophageal myotomyREASONAUTHOR, PROCEDURE (N)ELLIS, MYOTOMY ONLY (N = 81)GOULBOURNE, MYOTOMY ONLY (N = 65)MALTHANER, MYOTOMY + ANTIREFLUX (N = 22)Reflux4%5%18%Inadequate myotomy2%—9%Megaesophagus2%——Poor emptying4%3%—Persistent chest pain1%——Data from Malthaner RA, et al. Long-term results in surgically managed esophageal achalasia. Ann Thorac Surg. | Surgery_Schwartz. excellent long-term relief of dysphagia, and, contrary to Malthaner and Pearson’s experience, does not result in com-plications of gastroesophageal reflux. Both studies document nearly identical results 10 to 15 years following the procedure, and both report deterioration over time, probably due to progres-sion of the underlying disease. The addition of an antireflux procedure if the operation is performed transthoracically has no significant effect on the outcome.Brunicardi_Ch25_p1009-p1098.indd 106601/03/19 6:05 PM 1067ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-65. (Continued )Table 25-10Reasons for failure of esophageal myotomyREASONAUTHOR, PROCEDURE (N)ELLIS, MYOTOMY ONLY (N = 81)GOULBOURNE, MYOTOMY ONLY (N = 65)MALTHANER, MYOTOMY + ANTIREFLUX (N = 22)Reflux4%5%18%Inadequate myotomy2%—9%Megaesophagus2%——Poor emptying4%3%—Persistent chest pain1%——Data from Malthaner RA, et al. Long-term results in surgically managed esophageal achalasia. Ann Thorac Surg. |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.