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Trastornos de la motilidad esofagica ,[object Object],[object Object],[object Object],[object Object],[object Object],Gastroenterol Clin N Am 33 (2004) 107–124
Acalasia Es el trastorno motor mejor conocido del esófago
First described case of achalasia by Sir Thomas Willis in 1674.
 
Acalasia:Incidencia ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
Etiolog ía ,[object Object],[object Object],[object Object],[object Object],[object Object]
Etiolog ía ,[object Object],Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.
Acalasia: fisiopatología Ocurre degeneración de las neuronas en la pared del esófago, especialmente de las neuronas inhibitorias productoras de óxido nítrico, que causa la relajación del músculo liso esofágico necesaria para que se abra el EEI y para la contracción coordinada del esófago
Acalasia: fisiopatología Alteraciones neuroanatómicas ,[object Object],[object Object],[object Object],[object Object]
The American Journal of Gastroenterology Volume 100 Issue 6 Page 1404  - June 2005
The American Journal of Gastroenterology Volume 100 Issue 6 Page 1404  - June 2005
 
 
CLINICAL FEATURES  ,[object Object],Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.
Acalasia:Clínica ,[object Object],[object Object],[object Object]
Acalasia: Diagnostico ,[object Object],[object Object],[object Object],[object Object],[object Object]
Acalasia: Diagnostico Confirmar una relajación incompleta del EEI durante la deglución es mas importante para diagnosticarla que las características del esfínter en reposo
Acalasia: Dx. diferencial ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acalasia:Dx. Diferencial Trastornos con características manométricas y radiológicas que simulan acalasia idiopatica ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
 
Barium swallow in patient with achalasia of esophagus (a)
DIAGNOSTICO. ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
Barium swallow in patient with achalasia of esophagus (b)
Lateral radiograph of barium swallow in patient with achalasia of esophagus
Barium swallows of patient with secondary achalasia (a)
Barium swallows of patient with secondary achalasia (b)
 
 
 
 
 
 
 
 
 
 
 
 
Esophageal stricture
Acalasia Endoscopia
 
Endoscopic view of patient with achalasia of LES
Endoscopic appearance of benign strictures (E)
Endoscopic appearance of benign strictures (D)
Endoscopic appearance of benign strictures (G)
Acalasia: tratamiento ,[object Object],[object Object],[object Object],[object Object]
Correct positioning of a pneumatic balloon dilator for achalasia
 
Heller myotomy as therapy for achalasia (A)
Results of myotomy as therapy for achalasia Overall, 85% have consistently good to excellent outcomes, significantly higher than the results achieved with balloon dilation
Acalasia:tratamiento La toxina botulínica se une a los receptores colinérgicos presinápticos, e interfiere irreversiblemente con la liberación de acetilcolina
ESPASMO ESOFAGICO DIFUSO Alteración motora del músculo liso del esófago, caracterizada por múltiples contracciones repetidas de carácter espontáneo, comienzo simultáneo, gran amplitud, larga duración y presentación repetitiva que aparecen con la deglución
DIFFUSE ESOPHAGEAL SPASM ,[object Object],[object Object],[object Object],[object Object]
ESPASMO ESOFAGICO DIFUSO ,[object Object],[object Object],[object Object],[object Object],[object Object]
EED: Etiopatogenia ,[object Object],[object Object],[object Object],[object Object],[object Object]
EED: Cuadro clínico ,[object Object],[object Object],[object Object],[object Object],[object Object]
CLINICAL FEATURES ,[object Object],[object Object],[object Object],[object Object],[object Object]
CLINICAL FEATURES ,[object Object],[object Object],[object Object],[object Object]
EED:  Diagnóstico ,[object Object],[object Object],[object Object]
 
Barium swallow study in patient with diffuse esophageal spasm Few radiographic findings are present during fluoroscopy in patients with nutcracker esophagus or related nonspecific spastic disorders
 
Radiologic appearance of cricopharyngeal bar
Zenker's diverticulum
 
 
 
Diffuse esophageal spasm
 
 
Endoscopy No features are typical of these disorders, and the endoscopic appearance is normal. The test may detect alternative explanations for symptoms such as esophagitis or stricture.
Diagnostico diferencial ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object]

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Acalasia

Notas del editor

  1. Although the aetiology of primary achalasia is not known, certain recognised diseases can cause oesophageal motor abnormalities similar or identical to those of primary achalasia. In Chagas disease seen in Central and South America, for example, oesophageal infection with the protozoan parasite Trypanosoma cruzi can result in loss of intramural ganglion cells that causes aperistalsis and incomplete LOS relaxation. 21 Malignancies can also cause an achalasia-like disorder (pseudoachalasia) either by invading the oesophageal neural plexuses directly (for example, adenocarcinoma of the oesophagogastric junction) or through release of uncharacterised humoral factors that disrupt oesophageal function as part of a paraneoplastic syndrome. 22 Primary and secondary achalasia cannot be distinguished reliably on the basis of manometric criteria alone
  2. Esophageal motor innervation. The striated muscle of the proximal esophagus is innervated directly by the somatic efferent cholinergic fibers of the vagus nerve originating from the nucleus ambiguus. On the other hand, smooth muscle of the distal esophagus is innervated by the pre-ganglionic vagus nerve fibers from the dorsal motor nucleus. They release acetylcholine as the neurotransmitter affecting two types of postganglionic neurons in the myenteric plexus: excitatory cholinergic neurons and inhibitory nitrinergic neurons. Park, Woosuk & Vaezi, Michael F. Etiology and Pathogenesis of Achalasia: The Current Understanding. The American Journal of Gastroenterology   100  (6), 1404-1414. doi: 10.1111/j.1572-0241.2005.41775.x
  3. Figure 2.  Both LES smooth muscle and inhibitory neurons of the myenteric plexus have cholecystokinin receptors. In normal esophagus, administration of cholecystokinin-octapeptide (CCK-OP) results in LES relaxation because the inhibitory neurons override the direct excitation of the LES smooth muscle. However, in achalasia, the LES smooth muscle excitation is unopposed due to the loss of the inhibitory neurons in the myenteric plexus. As a result, CCK-OP causes LES contraction
  4. Figure 3.  In early stage of achalasia, the esophageal myenteric inflammation, caused by an unknown etiologic factor or factors, may cause neuritis and ganglionitis with no ganglion cell loss or fibrosis. Functional esophageal dysmotility such as vigorous achalasia may be the predominant manifestation. Progressive destruction of the myenteric ganglion cells and neural fibrosis occurs resulting in classic achalasia.
  5. Figure 4.  Possible pathophysiologic mechanism in achalasia. An initial insult, possibly a viral infection or an unknown environmental factor, may start a cascade of inflammatory events leading to myenteric plexus inflammation. Those with genetic susceptibility may mount an autoimmune response and develop antimyenteric autoantibodies with associated HLA class II antigens. Development of antimyenteric autoantibodies results in chronic inflammation and further destruction of the inhibitory myenteric neurons. Classic achalasia develops as the end result of progressive destruction of the inhibitory myenteric neurons.
  6. CLINICAL FEATURES The annual incidence of achalasia is approximately 0.5 to 1 per 100,000 population. [ 403 ] The disease affects both sexes equally and can occur at any age. Onset is usually in the third to fifth decades, and less than 5% of patients have symptoms before adolescence. Symptoms rather than physical findings are the hallmarks of this disease. The duration of symptoms at presentation averages several years, and the manifestations vary widely. [ 404 ] [ 405 ] Dysphagia is almost uniformly the predominant symptom. [ 404 ] Dysphagia for solid foods is eventually present in nearly all patients but in only 40% at symptom onset; dysphagia for liquids is reported by at least two thirds.
  7. Figure 9-4. Barium swallow in a patient with achalasia of the esophagus. This study shows a dilated esophagus in a patient with achalasia of the lower esophageal sphincter (A). The gastroesophageal junction does not open, resulting in a classical bird's beak appearance at the distal end of the esophagus (B). The serrated margin (arrow) in the midesophagus is referred to by radiologists as tertiary contractions.
  8. Figure 9-4. Barium swallow in a patient with achalasia of the esophagus. This study shows a dilated esophagus in a patient with achalasia of the lower esophageal sphincter (A). The gastroesophageal junction does not open, resulting in a classical bird's beak appearance at the distal end of the esophagus (B). The serrated margin (arrow) in the midesophagus is referred to by radiologists as tertiary contractions.
  9. Figure 9-5. Lateral radiograph from a barium swallow in a patient with achalasia of the esophagus. There is lack of an opening of the gastroesophageal junction; however, unlike the esophagus in Figure 9-4B, the esophagus is not dilated. Irregular margins of the distal esophagus are the result of tertiary contractions. An air-fluid level is seen in the proximal esophagus. This case demonstrates that not all patients with achalasia of the esophagus have dilated, tortuous, and sigmoid esophagus.
  10. Figure 9-6. A­B, Barium swallows of a patient with secondary achalasia. The barium swallows in this figure represent the appearance of the esophagus in a patient with adenocarcinoma of the gastroesophageal junction, which can produce a motility disorder identical to primary or idiopathic achalasia. The gastroesophageal junction shows a bird's beak appearance, and on multiple spot films there was no evidence of an opening of the esophagogastric region. Case reports of metastatic tumor from prostate, breast, lymphoma, lung carcinoma, hepatocellular carcinoma, colon carcinoma, esophageal lymphangioma, and pleural mesothelioma causing secondary achalasia have been described.
  11. Figure 9-6. A­B, Barium swallows of a patient with secondary achalasia. The barium swallows in this figure represent the appearance of the esophagus in a patient with adenocarcinoma of the gastroesophageal junction, which can produce a motility disorder identical to primary or idiopathic achalasia. The gastroesophageal junction shows a bird's beak appearance, and on multiple spot films there was no evidence of an opening of the esophagogastric region. Case reports of metastatic tumor from prostate, breast, lymphoma, lung carcinoma, hepatocellular carcinoma, colon carcinoma, esophageal lymphangioma, and pleural mesothelioma causing secondary achalasia have been described.
  12. Figure 6-28. Esophageal stricture. A barium esophagogram demonstrates the presence of a high-grade, smooth-walled distal esophageal stricture that resulted from reflux esophagitis [1]. Patients with this complication of reflux disease usually note amelioration of heartburn as they develop the symptom of dysphagia. The dysphagia is for solids and not liquids (unless their is solid food impaction first), indicating the presence of a lumen-narrowing lesion. The absence of anorexia and weight loss and slow rate of progression of dysphagia are good indications that the lesion is a benign peptic process. The presence of anorexia and weight loss and rapid progression of dysphagia raises the likelihood that the lesion is malignant and most likely an adenocarcinoma arising in a Barrett's esophagus (see Fig. 6-29). (From Stewart et al. [27]; with permission.) References: [1]. Orlando RC, Reflux esophagitis. In Textbook of Gastroenterology. Edited by Yamada T, Alpers DH, Laine L. et al. Philadelphia: Lippincott Williams and Wilkins; 1999 1235-1263 [27]. Stewart ET, Dodds WJ, Radiology of the esophagus. In Alimentary Tract Radiology. Edited by Freeny PC, Stevenson GW. Philadelphia: Mosby; 1994 192-263
  13. Figure 9-3. Endoscopic view from a patient with achalasia of the lower esophageal sphincter (LES). Note that the region of the LES is tightly closed. Usually a small amount of pressure is needed before the endoscope pops into the stomach. Above the LES there is a wide-mouth diverticulum known as the epiphrenic diverticulum.
  14. Figure 11-18. Endoscopic appearance of benign strictures. Acid-septic strictures and Schatzki's rings are the most common strictures requiring dilation. Although in most instances endoscopic examination allows obvious distinction between the two, variation in air insufflation and the differences in magnification over short distances between the lower esophageal sphincter and the endoscope can make the assessment of the lower esophagus difficult in some patients. A subtle peptic stricture may be missed endoscopically, or, more precisely, may be confused with a Schatzki's ring. Contrast radiology can be a more sensitive technique for demonstrating subtle rings and strictures and for calibrating the lumen more precisely. A–C, Endoscopic photographs of several Schatzki's rings. D–G, peptic strictures. Note the esophageal pseudodiverticula proximal to the peptic stricture in panels F and G. Their presence increases the risk of unguided dilatation of the esophagus and mandates the use of a guidewire technique. H, Tight anastomotic stricture (suture at 10 o'clock) and “watermelon esophagus” viewed endoscopically. The watermelon seeds and kernel of corn provide a reference for the pinhole quality of this stricture.
  15. Figure 11-18. Endoscopic appearance of benign strictures. Acid-septic strictures and Schatzki's rings are the most common strictures requiring dilation. Although in most instances endoscopic examination allows obvious distinction between the two, variation in air insufflation and the differences in magnification over short distances between the lower esophageal sphincter and the endoscope can make the assessment of the lower esophagus difficult in some patients. A subtle peptic stricture may be missed endoscopically, or, more precisely, may be confused with a Schatzki's ring. Contrast radiology can be a more sensitive technique for demonstrating subtle rings and strictures and for calibrating the lumen more precisely. A–C, Endoscopic photographs of several Schatzki's rings. D–G, peptic strictures. Note the esophageal pseudodiverticula proximal to the peptic stricture in panels F and G. Their presence increases the risk of unguided dilatation of the esophagus and mandates the use of a guidewire technique. H, Tight anastomotic stricture (suture at 10 o'clock) and “watermelon esophagus” viewed endoscopically. The watermelon seeds and kernel of corn provide a reference for the pinhole quality of this stricture.
  16. Figure 11-18. Endoscopic appearance of benign strictures. Acid-septic strictures and Schatzki's rings are the most common strictures requiring dilation. Although in most instances endoscopic examination allows obvious distinction between the two, variation in air insufflation and the differences in magnification over short distances between the lower esophageal sphincter and the endoscope can make the assessment of the lower esophagus difficult in some patients. A subtle peptic stricture may be missed endoscopically, or, more precisely, may be confused with a Schatzki's ring. Contrast radiology can be a more sensitive technique for demonstrating subtle rings and strictures and for calibrating the lumen more precisely. A–C, Endoscopic photographs of several Schatzki's rings. D–G, peptic strictures. Note the esophageal pseudodiverticula proximal to the peptic stricture in panels F and G. Their presence increases the risk of unguided dilatation of the esophagus and mandates the use of a guidewire technique. H, Tight anastomotic stricture (suture at 10 o'clock) and “watermelon esophagus” viewed endoscopically. The watermelon seeds and kernel of corn provide a reference for the pinhole quality of this stricture.
  17. Figure 9-34. Correct positioning of a pneumatic balloon dilator for treatment of achalasia. The waist seen at the middle of the balloon (white arrows) is created by resistance of the lower esophageal sphincter to dilation. Using fluoroscopy and the tip of the endoscope for guidance, a safety pin was placed on the patient’s chest at the level of the lower esophageal sphincter to assist with positioning. Black arrowheads outline the air-filled balloon.
  18. Figure 12-14. Heller myotomy as therapy for achalasia. A, It is vital that both circular and longitudinal muscles are completely divided and that the mucosa bulges freely. The myotomy must be carried either to the aortic arch or high enough on the esophagus to include all thickened smooth muscle. The distal extent of the gastric component is controversial. There is no question that extending the myotomy for 1 to 2 cm into the stomach lowers the rate of recurrent achalasia. This incision also greatly increases the risk of reflux, however. B, Some surgeons advocate long myotomy and the routine addition of the Belsey Mark IV antireflux operation. I am not a proponent of this combined procedure. If properly performed, a myotomy carried just onto the gastric side of the gastroesophageal junction relieves the characteristic obstructive symptoms without rendering the lower esophageal sphincter incompetent and inducing reflux as a new problem. In performing the Heller myotomy the surgeon must avoid two pitfalls: injury to the vagus nerves and incision through the mucosa into the esophageal lumen. (Adapted from Skinner [16].) References: [16]. Skinner DB, In Atlas of Esophageal Surgery New York: Churchill Livingstone; 1991 157-159
  19. Figure 12-15. Results of myotomy as therapy for achalasia. Overall, 85% of patients have consistently good to excellent outcomes [2], significantly higher than the results achieved with balloon dilation. More importantly, less than 2% of patients have poor postoperative results [2]. References: [2]. Okike N, Payne WS, Neufeld DM, et al. Esophagomyotomy versus forceful dilation for achalasia of the esophagus: Results in 899 patients. Ann Thorac Surg 1979 28 119
  20. DIFFUSE OESOPHAGEAL SPASM Diffuse oesophageal spasm is a condition of unknown aetiology that is manifested clinically by episodes of dysphagia and chest pain, radiographically by tertiary contractions of the oesophagus, and manometrically by uncoordinated (“spastic”) activity in the smooth muscle portion of the oesophagus.32 The pathophysiology and natural history of the disorder are poorly understood. Furthermore, authorities disagree on precisely how spastic activity manifests itself manometrically. Comparisons between studies on diffuse oesophageal spasm have been compromised by the lack of universally accepted diagnostic criteria for the condition. Different investigators have used different diagnostic criteria and, consequently, it is likely that patients with a number of different disorders have been included in studies on diffuse oesophageal spasm. In the absence of a diagnostic gold standard for a disorder, conclusions regarding the validity of any diagnostic test are suspect.
  21. ESPASMO ESOFAGICO DIFUSO El Espasmo Esofágico Difuso (EED), típico, es un trastorno raro, al menos 5 veces menos frecuente que la Acalasia. Puede aparecer en ambos sexos y a cualquier edad, pero es más frecuente después de los 50 años; tradicionalmente se ha definido como una alteración motora del músculo liso del esófago, caracterizada por múltiples contracciones repetidas de carácter espontaneo, y por contracciones de comienzo simultáneo, gran amplitud, larga duración y presentación repetitiva que aparecen con la deglución; las variantes de esta entidad muestran algunas de estas anomalías motoras pero no todas; los síndromes variantes son mas frecuentes en la practica clínica que el cuadro clásico.
  22. Cuadro clínico. Es muy variable y puede producir desde síntomas graves e incapacitantes hasta pasar completamente inadvertido (en este último caso el espasmo difuso suele descubrirse en forma casual al practicar, por otro motivo, un examen radiológico con papilla baritada). El dolor retrosternal es una de sus consecuencias clínicas; a veces se irradia a la espalda o hacia los brazos, con una distribución semejante a la de la angina de pecho. El dolor puede aparecer espontáneamente o desencadenarse tras la ingestión de bebidas frías o durante períodos de tensión emocional. El carácter constrictivo del dolor y su localización retrosternal determinan que pueda confundirse a veces con el dolor anginoso. El dolor del espasmo, como el de la angina, puede desaparecer con la administración de nitroglicerina, por lo que este dato es de poco valor para el diagnóstico diferencial. El otro síntoma característico del espasmo es la disfagia, que puede notarse junto con el dolor o ser independiente. Algunos pacientes nunca aquejan disfagia, y otros padecen disfagia sin dolor. La disfagia suele ser episódica e igual para sólidos y líquidos.
  23. CLINICAL FEATURES (see also Chapter 6 ) Although these spastic motility disorders have been detected in all age groups, the mean age at presentation approximates 40 years. A female predominance exists among patients with hypermotility contraction wave abnormalities as the sole findings. [ 559 ] Of patients presenting for manometric evaluation and subsequently diagnosed with a spastic disorder, chest pain is reported by 80% to 90%. The pain generally is retrosternal, may radiate directly into the back, and often is more severe than the recurrent pain characteristic of coronary artery disease. A dull residual discomfort persisting after the severe episode abates can help differentiate the pain from angina pectoris. Pain episodes may last from minutes to hours, and swallowing is generally not impaired during the episodes. Dysphagia is reported by 30% to 60% of patients with spastic findings. [ 559 ] [ 560 ] This symptom is intermittent, varying on a daily basis from mild to very severe. It does not usually have a direct relationship to chest pain, but it is often more severe during periods when pain is more frequent or severe. Regurgitation of a food or liquid bolus into the mouth may accompany dysphagia but is infrequent in comparison with achalasia. In addition, in contrast to achalasia, dysphagia is generally neither progressive nor severe enough to cause weight loss. Heartburn is a component of the syndrome in up to 20% of patients. [ 559 ] The disparity between symptoms and manometric findings is pronounced. Mechanisms other than motor dysfunction contribute to the clinical presentation and complicate attempts at a concise clinical description. In fact, the chest pain reported by patients with spastic disorders may not only be unrelated to motor dysfunction, it may originate from nonesophageal sites—further adding to the vague clinical picture. Other gastrointestinal symptoms typical of functional bowel disorders are reported with relatively high prevalence. Symptoms of psychological dysfunction, particularly those of anxiety, depression, and somatization, are also common. [ 550 ] [ 557 ] Studies continue to accumulate, pointing to the following hypothesis: Symptoms in the spastic disorders are frequently unrelated to dysmotility but reflect sensory disturbances and psychological characteristics linked to these motor disorders. A
  24. CLINICAL FEATURES (see also Chapter 6 ) Although these spastic motility disorders have been detected in all age groups, the mean age at presentation approximates 40 years. A female predominance exists among patients with hypermotility contraction wave abnormalities as the sole findings. [ 559 ] Of patients presenting for manometric evaluation and subsequently diagnosed with a spastic disorder, chest pain is reported by 80% to 90%. The pain generally is retrosternal, may radiate directly into the back, and often is more severe than the recurrent pain characteristic of coronary artery disease. A dull residual discomfort persisting after the severe episode abates can help differentiate the pain from angina pectoris. Pain episodes may last from minutes to hours, and swallowing is generally not impaired during the episodes. Dysphagia is reported by 30% to 60% of patients with spastic findings. [ 559 ] [ 560 ] This symptom is intermittent, varying on a daily basis from mild to very severe. It does not usually have a direct relationship to chest pain, but it is often more severe during periods when pain is more frequent or severe. Regurgitation of a food or liquid bolus into the mouth may accompany dysphagia but is infrequent in comparison with achalasia. In addition, in contrast to achalasia, dysphagia is generally neither progressive nor severe enough to cause weight loss. Heartburn is a component of the syndrome in up to 20% of patients. [ 559 ] The disparity between symptoms and manometric findings is pronounced. Mechanisms other than motor dysfunction contribute to the clinical presentation and complicate attempts at a concise clinical description. In fact, the chest pain reported by patients with spastic disorders may not only be unrelated to motor dysfunction, it may originate from nonesophageal sites—further adding to the vague clinical picture. Other gastrointestinal symptoms typical of functional bowel disorders are reported with relatively high prevalence. Symptoms of psychological dysfunction, particularly those of anxiety, depression, and somatization, are also common. [ 550 ] [ 557 ] Studies continue to accumulate, pointing to the following hypothesis: Symptoms in the spastic disorders are frequently unrelated to dysmotility but reflect sensory disturbances and psychological characteristics linked to these motor disorders. A
  25. Diagnóstico. Radiología. La imagen radiológica "en sacacorchos", debida a las contracciones enérgicas y simultáneas en el cuerpo esofágico, es muy característica. Sin embargo, se observa sólo en una minoría de los casos (fig. 20.8 ). Endoscopia. Al igual que en la acalasia, la utilidad de la fibroendoscopia consiste en descartar procesos orgánicos (neoplasias, esofagitis, anillos) que produzcan secundariamente alteraciones motoras del esófago. Manometría esofágica. El diagnóstico definitivo del espasmo esofágico difuso se establece mediante el estudio manométrico. Los criterios diagnósticos varían según los distintos autores. El criterio fundamental es la presencia de ondas simultáneas alternando con ondas peristálticas. A estos hallazgos pueden asociarse un aumento de la amplitud y duración de las contracciones del cuerpo esofágico. Algunos pacientes con síntomas sugestivos de espasmo difuso no reúnen todos los criterios manométricos para establecer el diagnóstico. Estos casos deben evaluarse con reserva, ya que las anomalías manométricas leves se observan con cierta frecuencia en individuos normales. A menudo la repetición de la manometría después de un cierto tiempo demuestra una progresión de las alteraciones que ayuda a establecer el diagnóstico definitivo.
  26. Figure 9-12. Barium swallow study in a patient with diffuse esophageal spasm. Note the corkscrew or rosary-bead appearance along the length of the distal esophagus.
  27. Figure 9-1. Radiologic appearance of cricopharyngeal bar. The indentations (arrow) seen in the barium swallow, usually occurring at the level of cervical vertebra 4 or 5, represent either a nonrelaxing or a noncompliant upper esophageal sphincter. The patient usually has oropharyngeal dysphagia; however, asymptomatic individuals can have this radiologic finding.
  28. Figure 9-2. Zenker's diverticulum. Radiograph of a 70-year-old patient with oropharyngeal dysphagia, coughing, choking spells, and recurrent pneumonia. Note the outpouching of the pharynx above the level of the cricopharyngeus (arrow). This outpouching is located in the posterior wall of the pharynx. Zenker's diverticulum is a true pulsion diverticulum and is the result of increased intrapharyngeal pressures during swallowing as a result of a noncompliant or nonrelaxing upper esophageal sphincter. There may be penetration of the barium into the laryngeal inlet and spilling into the tracheobronchial tree. The treatment of this condition in the setting of severe symptoms is usually cricopharyngeal myotomy.
  29. Figure 9-35. A barium esophagram from a patient with diffuse esophageal spasm. Transit of barium through the esophageal body is impaired, and the barium column has a very distorted appearance resembling a cluster of diverticula.
  30. An issue that arises in defining diffuse oesophageal spasm primarily by the presence of simultaneous contractions is that such contractions can be found in patients with a variety of recognised disorders, including diabetes mellitus, alcoholism, amyloidosis, and scleroderma, as well as in patients who have gastro-oesophageal reflux disease that is not associated with other diseases. 34 This situation is similar to that described above for achalasia in which motility abnormalities identical to those of primary achalasia can be seen in other disorders, such as Chagas disease and gastric cancer. Unlike the situation for achalasia however it is not common practice to categorise diffuse oesophageal spasm as primary or secondary in nature. Furthermore, the physiological and clinical consequences of the low amplitude simultaneous contractions seen in scleroderma may differ substantially from those of the normal or high amplitude simultaneous contractions seen in patients with idiopathic diffuse oesophageal spasm. Consequently, it may be inappropriate to include patients with low amplitude simultaneous contractions under the rubric of “diffuse oesophageal spasm
  31. Another problem in identifying diffuse oesophageal spasm primarily by the presence of simultaneous oesophageal contractions is that, in some cases, it may be difficult to distinguish diffuse oesophageal spasm from the atypical disorders of LOS relaxation. In addition to inadequate LOS relaxation, simultaneous oesophageal contractions are a hallmark of primary achalasia. Inadequate LOS relaxation has been described in diffuse oesophageal spasm, and the only feature used to distinguish these two disorders manometrically is the arbitrary requirement that some normal peristalsis be preserved in diffuse oesophageal spasm. 33 For a patient who has the clinical and radiographic features of classic achalasia, whose manometric examination shows inadequate LOS relaxation and simultaneous oesophageal contractions, and whose dysphagia resolves with pneumatic dilation, it seems inappropriate to call the disorder diffuse oesophageal spasm simply because there are occasional normal peristaltic sequences. This constellation of findings is better characterised as an atypical disorder of LOS relaxation. The manometric features proposed for a diagnosis of diffuse oesophageal spasm are: (1) simultaneous contractions associated with >10% of wet swallows and (2) mean simultaneous contraction amplitude >30 mm Hg (fig 2). Features that can be found commonly but are not required for manometric diagnosis include: (1) spontaneous contractions, (2) repetitive contractions, (3) multiple peaked contractions, and (4) intermittent normal peristalsis. If there is incomplete relaxation of the LOS (defined as a mean swallow induced fall in resting LOS pressure to a nadir value >8 mm above gastric pressure), the condition is better classified as an atypical disorder of LOS relaxation.
  32. Tratamiento. Varía según la gravedad de los síntomas. En casos leves a menudo es suficiente explicar al paciente el origen de sus molestias y asegurarle que la enfermedad no es peligrosa. Al mismo tiempo se le debe aconsejar que mastique cuidadosamente y evite tragar deprisa. En casos más graves se han utilizado diversos agentes farmacológicos, en particular anticolinérgicos, nitritos y antagonistas del calcio. En los pacientes que continúan presentando síntomas puede realizarse una dilatación forzada, con la que se consigue su alivio, aunque éste suele ser temporal y, en todo caso, inferior al que se obtiene en la acalasia. Por último, en los casos incapacitantes se ha realizado una miotomía larga, que es básicamente una miotomía de Heller extendida desde el EEI hasta el punto donde se observa manométricamente signos de espasmo; este procedimiento se completa con una técnica antirreflujo. Los resultados del tratamiento quirúrgico son muy variables, y éste debe restringirse a pacientes con buen estado general y síntomas verdaderamente incapacitantes