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Achalasia cardia
- 1. Achalasia cardia Target audience – Residents Date- 10.9.2021 Moderator – Dr A. K.Srivastava Professor Speaker – Dr Pooja Pandey PGJR2 Department of general surgery MIMS, Barabanki 10/9/2021 1
- 2. Achalasia cardia Learning objectives • Surgical anatomy of esophagus • Physiology of esophagus –Swallowing • Physiologic reflux • Test for the esophageal motility • Classification of esophageal motility disorder • Introduction on Achalasia cardia • Clinical presentation • How to diagnose • Treatment 10/9/2021 2
- 3. Achalasia cardia • Surgical anatomy • 25-30 cm long . • Posterior mediastinum. • Pharynx to the cardia of the stomach . • Musculature :- striated transitional zone smooth muscle 10/9/2021 3
- 4. Achalasia cardia Course of esophagus 10/9/2021 4
- 5. Achalasia cardia Constrictions •Importance – Foreign body Endoscopy 10/9/2021 5
- 6. Achalasia cardia •Blood supply •Importance – Mobilisation of esophagus 10/9/2021 6
- 7. Achalasia cardia •Venous drainage •Importance- Collateral pathway 10/9/2021 7
- 8. Achalasia cardia •Nervous supply •Importance Vocal cord Aspiration 10/9/2021 8
- 9. Achalasia cardia •Lymphatic •Importance Regional spread Wide spread 10/9/2021 9
- 10. Achalasia cardia •Function • Primary function – transport material from pharynx to the stomach . • Secondary function – constrain the amount of air that is swallowed and the amount of material that is refluxed . • N.B- Transport of food bolus from mouth through esophagus into the stomach begins with swallowing -postrelaxation contraction of LES (In transit- co-ordinated peristaltic contraction ) 10/9/2021 10
- 11. Achalasia cardia Physiology •Swallowing •3phases • Oral • Pharyngeal • Esophageal 10/9/2021 11
- 12. Achalasia cardia Physiology •Swallowing •6 Events of oropharyngeal swallowing 10/9/2021 12
- 13. Achalasia cardia Physiology •Swallowing •Esophageal phase •Upper esophageal sphincter – Normal manometric values •Total length – 4-5cm •Resting pressure -60 mmHg •Relaxation time -0.58 sec •Residual pressure- 0.7-3.7mm Hg 10/9/2021 13
- 14. Achalasia cardia •Physiology •Swallowing •Esophageal phase •Peristalsis 3 types Primary Secondary Tertiary 10/9/2021 14
- 15. Achalasia cardia Physiology •Swallowing •Esophageal phase •Peristalsis 3 types 10/9/2021 15
- 16. Achalasia cardia Physiology •Swallowing •Esophageal phase Primary Secondary Tertiary *Progressive *2-4cm/sec *Generate intraluminal pressure-40- 80mmHg *Reach LES-9sec **Progressive **Abdominal distension or Irritation of the esophagus rather than voluntary swallowing . ***Non progressive ***Non peristaltic ***Monophasic or multiphasic ***Occur after voluntary swallowing or spontaneous between swallows throughout the esophagus . ***Uncordinated contraction of the smooth muscle – esophageal spasm 10/9/2021 16
- 17. Achalasia cardia Physiology •Swallowing Esophageal phase •Lower esophageal sphincter – Normal manometric values •Total length – 3-5cm •Abdominal length- 2-4cm •Resting pressure- 6-26 mmHg •Relaxation time- 8.4sec •Residual pressure- 3mmHg 10/9/2021 17
- 18. Achalasia cardia Physiology •Physiologic reflux •More common when awake and in the upright position than during sleep in the supine position. •The LES has intrinsic myogenic tone, which is modulated by neural and hormonal mechanisms. • Α-adrenergic neurotransmitters or β-blockers stimulate the les, and α-blockers and β-stimulants decrease its pressure 10/9/2021 18
- 19. Achalasia cardia Physiology • Physiologic reflux • The hormones gastrin and motilin have been shown to increase LES pressure; and cholecystokinin, estrogen, glucagon, progesterone, somatostatin, and secretin decrease LES pressure. • The peptides bombesin, l-enkephalin, and substance P increase LES pressure; and calcitonin generated peptide, gastric inhibitory peptide, neuropeptide Y, and vasoactive intestinal polypeptide decrease LES pressure 10/9/2021 19
- 20. Achalasia cardia Physiology • Physiologic reflux • Pharmacologic agents such as antacids, cholinergics, agonists, domperidone, metoclopramide, and prostaglandin F2 are known to increase LES pressure; and anticholinergics, barbiturates, calcium channel blockers, caffeine, diazepam, dopamine, meperidine, prostaglandin E1 and E2, and theophylline decrease LES pressure. • Peppermint, chocolate, coffee, ethanol, and fat are all associated with decreased les pressure and may be responsible for esophageal symptoms after a sumptuous meal. 10/9/2021 20
- 21. Achalasia cardia Assessment of esophageal function •(a) Tests to detect structural abnormalities of the esophagus; •(b) Tests to detect functional abnormalities of the esophagus; •(c) Tests to detect increased esophageal exposure to gastric juice; and •(d) Tests of duodenogastric function as they relate to esophageal disease. 10/9/2021 21
- 22. Achalasia cardia Esophageal motility study (EMS) • Indication • Motor abnormality of the esophagus –on the basis of complaints of dysphagia, odynophagia, or noncardiac chest pain. • Barium swallow or endoscopy unclear about structural abnormality. • To confirm the diagnosis of specific primary esophageal motility disorders (i.e. Achalasia, diffuse esophageal spasm [DES], nutcracker esophagus, and hypertensive LES). 10/9/2021 22
- 23. Achalasia cardia Esophageal motility study (EMS) • Indication • Identifies nonspecific esophageal motility abnormalities and motility disorders secondary to systemic disease such as scleroderma, dermatomyositis, polymyositis, or mixed connective tissue disease. • Symptomatic GERD , manometry of the esophageal body can identify a mechanically defective les and evaluate the adequacy of esophageal peristalsis and contraction amplitude. • Preoperative evaluation of patients before antireflux surgery, 10/9/2021 23
- 24. Achalasia cardia •Esophageal motility A. Grade I flap valve appearance. Note the ridge of tissue that is closely approximated to the shaft of the retroflexed endoscope. It extends 3 to 4 cm along the lesser curve. 10/9/2021 24
- 25. Achalasia cardia •Esophageal motility B. Grade II flap valve appearance. The ridge is slightly less well defined than in grade I and it opens rarely with respiration and closes promptly. 10/9/2021 25
- 26. Achalasia cardia •Esophageal motility C. Grade III flap valve appearance. The ridge is barely present, and there is often failure to close around the endoscope. It is nearly always accompanied by a hiatal hernia 10/9/2021 26
- 27. Achalasia cardia •Esophageal motility D. Grade IV flap valve appearance. There is no muscular ridge at all. The gastroesophageal valve stays open all the time, and squamous epithelium can often be seen from the retroflexed position. A hiatal hernia is always present. 10/9/2021 27
- 29. Achalasia cardia EMS •The pressure profile is repeated with Each of the five radially oriented Transducers- •The average values for sphincter pressure •Above gastric baseline, •Overall sphincter length, •And abdominal length of the sphincter are calculated. 10/9/2021 29
- 30. Achalasia cardia •A mechanically defective sphincter is identified by having one or more of the following characteristics: • An average LES pressure of <6 mmHg •An average length exposed to the positive-pressure environment in the abdomen of 1 cm or less, and/or •An average overall sphincter length of 2 cm or less. 10/9/2021 30
- 31. Achalasia cardia • High-Resolution Manometry- normal study 10/9/2021 31
- 32. Achalasia cardia • High-Resolution Manometry- defective LES 10/9/2021 32
- 33. Achalasia cardia • High-Resolution Manometry- Achalasia cardia 10/9/2021 33
- 34. Achalasia cardia • High-Resolution Manometry- DES 10/9/2021 34
- 35. Achalasia cardia • Esophageal Impedance 10/9/2021 35
- 36. Achalasia cardia •Esophageal Transit Scintigraphy. •The esophageal transit of a 10-mL water bolus containing technetium-99m (99mTc) sulfur colloid can be recorded with a gamma camera. • Using this technique, delayed bolus transit has been shown in patients with a variety of esophageal motor disorders, including achalasia, scleroderma, DES, and nutcracker esophagus. 10/9/2021 36
- 37. Achalasia cardia •Video- and Cineradiography •Computerized capture of videofluoroscopic images and manometric tracings is now available and is referred to as manofluorography. • Manofluorographic studies allow precise correlation of the anatomic events, such as opening of the upper esophageal sphincter, with manometric observations, such as sphincter relaxation 10/9/2021 37
- 39. Achalasia cardia Chicago classification of esophageal motility 10/9/2021 39 Type I (classic) achalasia: Impaired LES relaxation, absent peristalsis, and normal esophageal pressure. • Type II achalasia: Impaired LES relaxation, absent peristalsis, and increased panesophageal pressure. • Type III (spastic) achalasia: Impaired LES relaxation, absent peristalsis, and distal esophageal spastic contractions.
- 40. Achalasia cardia Chicago classification of esophageal motility 10/9/2021 40
- 41. Achalasia cardia •Introduction •Failure to relax. •Primary motility disorder of the esophagus is achalasia. •*Incidence of 1 per 100,000 population per year worldwide. •*Prevalence – 9-10 per 100,000 people . 10/9/2021 41 *Maingot’s abdominal operation 13th edition pg no 972
- 42. Achalasia cardia • Aetiopathogenesis • Idiopathic- it occurs due to absence/degeneration of auerbach’s plexus throughout the body of oesophagus, causing improper integration of parasympathetic impulse . • Acquired variety- in america, caused by trypanosoma cruzi which destroys ganglion cells of auerbach’s plexus.(Chagas disease). • Stress • Emotional factors • vitamin B1 deficiencies 10/9/2021 42
- 43. Achalasia cardia Pathogenesis • Neurogenic degeneration, which is either idiopathic or due to infection. • This degeneration results in hypertension of the LES a failure of the sphincter to relax on swallowing elevation of intraluminal esophageal pressure 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 esophagus, and elevation of intraluminal pressure from repetitive pharyngeal air swallowing . 10/9/2021 43
- 44. Achalasia cardia Clinical features •Women around 20-40 yrs. of age are commonly affected • Female: male::3:2 • Progressive Dysphagia-which is more for liquids than solid food. •Regurgitation and recurrent pneumonia are common •Malnutrition and ill health •Retrosternal discomfort - pain also radiates to interscapular region •Odynophagia and weight loss 10/9/2021 44
- 46. Achalasia cardia Triad of Achalasia • Staging I - Proximal dilatation <4cm • Staging II- Dilatation b/w 4-7 cm • Staging III- Dilatation >7cm Dysphagia Weight loss Regurgitation 10/9/2021 46
- 47. Achalasia cardia Investigations Oesophagoscopy dilated sac containing stagnant food and fluid due to stasis LES is closed with air insufflation, rosette apperance Oesophageal manometry- Aperistalsis in body of oesophagus Ultrasound- detects subepithelial tumor infiltration in 2ndy achalasia due to distal carcinoma 10/9/2021 47
- 48. Achalasia cardia Oesophagoscopy • FIGURE 22-1 Example of retained food and saliva at the time of upper endoscopy in a patient with an esophageal motility disorder. 10/9/2021 48
- 49. Achalasia cardia •Investigations •Barium swallow- • bird beak appearance of lower oesophagus, • Dilatation of proximal oesophagus • Absence of fundic gas bubble • Sigmoid oesophagus • X-ray chest- retrocardiac air fluid level lateral view • Plain X-ray abdomen erect-fundic air bubble is absent due to stasis of fluid in oesophagus 10/9/2021 49
- 50. Achalasia cardia Bird’s beak appearance 10/9/2021 50
- 51. Achalasia cardia •High Resolution Manometry 10/9/2021 51
- 52. Achalasia cardia Conservative Treatment •Forceful dilatation- using pneumatic balloon under fluoroscopic control within LOS(300mmHg pressure applied for 15 sec) .(S/E- eso.perf) • Injection treatment- inj botulinum toxin is injected in LES endoscopically ,blocks Ach release (Recurr-6months) •Drugs- sublingual nifedipine gives short term relief 10/9/2021 52
- 53. Achalasia cardia Conservative Treatment •Nifedipine (10-30 mg administered 30-45 minutes before meals). • Isosorbide dinitrate (5-10 mg administered 10-15 minutes before meals). •Phosphodiesterase-5 inhibitors, such as sildenafil used to treat patients with achalasia. 10/9/2021 53
- 54. Achalasia cardia Surgical Treatment •Open myotomy •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) Prevention of postoperative reflux. 10/9/2021 54
- 55. Achalasia cardia Treatment • Heller’s cardiomyotomy (laparoscopic cardiomyotomy ) • surgical 7-10cm long incision made through lower oesophageal end and carried over to stomach ,muscles are cut till mucosa bulges out. •Myotomy should be extended upto aortic arch and distally up to stomach to 1-2cm below the junction. 10/9/2021 55
- 56. Achalasia cardia • Heller’s cardiomyotomy • 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 provide reflux protection in the area of the divided sphincter. • If an extensive dissection of the cardia has been done, a more formal Belsey repair is performed. 10/9/2021 56
- 57. Achalasia cardia • Heller’s cardiomyotomy • 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. 10/9/2021 57
- 58. Achalasia cardia •Modified Heller’s cardiomyotomy •Left thoracotomy incision in the sixth intercostal space along the upper border of the seventh rib. 10/9/2021 58
- 59. Achalasia cardia Fundoplication- Dor and Toupet 10/9/2021 59
- 60. Achalasia cardia Recent Advances Peroral endoscopic myotomy (POEM) •First described in 2010 by Inoue et al •Allows a long myotomy to be performed from the lumen of the esophagus with an endoscope. •Type 3 achalasia (vigorous achalasia) 10/9/2021 60
- 61. Achalasia cardia • Peroral endoscopic myotomy (POEM) • 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 10/9/2021 61
- 62. Achalasia cardia • Peroral endoscopic myotomy (POEM) 10/9/2021 62 A. After performing a submucosal injection, a mucosotomy is performed to gain access to the submucosal space. B. The submucosal tunnel is continued down the length of the esophagus and onto the stomach using intermittent injections of methylene blue solution and electrocautery.
- 63. Achalasia cardia • Peroral endoscopic myotomy (POEM) 10/9/2021 63 C. Following creation of the submucosal tunnel, the myotomy is performed. There are numerous variations on this approach; however, the ultimate goal is to divide at minimum the circular fibers on the esophagus and onto the stomach. D. Following completed myotomy, the mucosotomy created at the beginning is then closed with either clips or endoscopic sutures
- 64. Achalasia cardia Complications •The rate of esophageal squamous cell carcinoma is increased in patients with achalasia compared to the general population. •There is also some concern for increased risk of adenocarcinoma; however, this risk is significantly lower than that for squamous cell carcinoma. 10/9/2021 64
- 65. References • Schwartz’s principle of surgery vol-2 11th edition pg no 1080-1086 • Sabiston text book of surgery vol-2 1st south asia edition pg no 1010-1020 • Bailey & Love’s short practice of surgery 27th edition pg no 1095-1099 • Maingot’s abdominal operation 13th edition (980-987) 10/9/2021 65
- 66. Questions • Q1)What is achalasia ? Explain it’s pathophysiology? • Q2) What is the prognosis of achalasia?When should a diagnosis of achalasia be considered? • Q3)What are the findings on the barium swallow that indicates achalasia ? • Q4)What are the findings on the esophageal manometry that indicates achalasia ? • Q5)What is the goal of therapy for achalasia? • Q6)What are the treatment options for achalasia? • Q7)Expand the POEM and how it helps in treatment of achalasia ? 10/9/2021 66
Editor's Notes
- Achalasia cardia – failure of relaxation of LES and aperistalsis of esophageal body with functional obstruction at esophagogastric junction and gradual dilation of esophagus. It occurs due to destruction of the nerves to LES as primary pathology and degeneration of neuromuscular function of esophagus is secondary pathology.
- the transition from pharynx to esophagus occurs at the lower border of the sixth cervical vertebra. Topographically this corresponds to the cricoid cartilage anteriorly and the palpable transverse process of the sixth cervical vertebra laterally (Fig. 25-1). The esophagus is firmly attached at its upper end to the cricoid cartilage and at its lower end to the diaphragm; during swallowing, the proximal points of fixation move craniad the distance of one cervical vertebral body The musculature of the esophagus can be divided into an outer longitudinal and an inner circular layer. The upper 2 to 6 cm of the esophagus contains only striated muscle fibers. From then on, smooth muscle fibers gradually become more abundant. Most clinically significant esophageal motility disorders involve only the smooth muscle in the lower two-thirds of the esophagus. When a long surgical esophageal myotomy is indicated, the incision needs to extend only this distance. The longitudinal muscle fibers originate from a cricoesophageal tendon arising from the dorsal upper edge of the anteriorly located cricoid cartilage. The two bundles of muscle diverge and meet in the midline on the posterior wall of the esophagus about 3 cm below the cricoid (see Fig. 25-4). From this point on, the entire circumference of the esophagus iscovered by a layer of longitudinal muscle fibers. This configuration of the longitudinal muscle fibers around the most proximal part of the esophagus leaves a V-shaped area in the posterior wall covered only with circular muscle fibers. Contraction of the longitudinal muscle fibers shortens the esophagus. The circular muscle layer of the esophagus is thicker than the outer longitudinal layer. In situ, the geometry of the circular muscle is helical and makes the peristalsis of the esophagus assume a wormlike drive, as opposed to segmental and sequential squeezing. As a consequence, severe motor abnormalities of the esophagus assume a corkscrew-like pattern on the barium swallow radiogram.
- The esophagus lies in the midline, with a deviation to the left in the lower portion of the neck and upper portion of the thorax, and returns to the midline in the midportion of the thorax near the bifurcation of the trachea (Fig. 25-2). In the lower portion of the thorax, the esophagus again deviates to the left and anteriorly to pass through the diaphragmatic hiatus.
- Three normal areas of esophageal narrowing are evident on the barium esophagogram or during esophagoscopy. The uppermost narrowing is located at the entrance into the esophagus and is caused by the cricopharyngeal muscle. Its luminal diameter is 1.5 cm, and it is the narrowest point of the esophagus. The middle narrowing is due to an indentation of the anterior and left lateral esophageal wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm. The lowermost narrowing is at the hiatus of the diaphragm and is caused by the gastroesophageal sphincter mechanism. The luminal diameter at this point varies somewhat, depending on the distention of the esophagus by the passage of food, but has been measured at 1.6 to 1.9 cm. These normal constrictions tend to hold up swallowed foreign objects, and the overlying mucosa is subject to injury by swallowed corrosive liquids due to their slow passage through these areas.
- Cervical portion – Inferior thyroid artery from thyrocervical trunk. Thoracic portion – Bronchial artery one from right side and two from left side(75%) , oesophageal artery from aorta Abdominal portion – ascending branch of left gastric artery from celiac artery and inferior phrenic artery from abdominal aorta On entering the wall it forms T shaped longitudinal network in the submucosal and muscular plexus hence mobilization from stomach to the aortic arch is possible without devascularisation -less chance for the ischaemia and necrosis. Caution, however, should be exercised as to the extent of esophageal mobilization in patients who have had a previous thyroidectomy with ligation of the inferior thyroid arteries proximal to the origin of the esophageal branches
- Blood from the capillaries of the esophagus flows into a submucosal venous plexus, and then into a periesophageal venous plexus from which the esophageal veins originate. In the cervical region, the esophageal veins empty into the inferior thyroid vein; in the thoracic region, they empty into the bronchial, azygos, or hemiazygos veins; and in the abdominal region, they empty into the coronary vein (Fig. 25-9). The submucosal venous networks of the esophagus and stomach are in continuity with each other, and, in patients with portal venous obstruction, this communication functions as a collateral pathway for portal blood to enter the superior vena cava via the azygos vein.
- Parasympathetic – vagus nerve Few contribution from CN 9and 11 Damage to these nerves interferes not only with the function of the vocal cords but also with the function of the cricopharyngeal sphincter and the motility of the cervical esophagus, predisposing the individual to pulmonary aspiration on swallowing Afferent visceral sensory pain fibers from the esophagus end without synapse in the first four segments of the thoracic spinal cord, using a combination of sympathetic and vagal pathways. These pathways are also occupied by afferent visceral sensory fibers from the heart; hence, both organs have similar symptomatology.
- In the submucosa So dense than blood Run in longitudinal than transverse cervical – cephalad In abdominal – caudad In thoracic portion -the submucosal lymph plexus extends over a long distance in a longitudinal direction before penetrating the muscle layer to enter lymph vessels in the adventitia. As a consequence of this nonsegmental lymph drainage, a primary tumor can extend for a considerable length superiorly or inferiorly in the submucosal plexus. Consequently, free tumor cells can follow the submucosal lymphatic plexus in either direction for a long distance before they pass through the muscularis and on into the regional LNs. The cervical esophagus has more direct segmental lymph drainage into the regional nodes, and, as a result, lesions in this portion of the esophagus have less submucosal extension and a more regionalized lymphatic spread. The cervical esophagus has more direct segmental lymph drainage into the regional nodes, and, as a result, lesions in this portion of the esophagus have less submucosal extension and a more regionalized lymphatic spread. The efferent lymphatics from the cervical esophagus drain into the paratracheal and deep cervical LNs, and those from the upper thoracic esophagus empty mainly into the paratracheal LNs. Efferent lymphatics from the lower thoracic esophagus drain into the subcarinal nodes and nodes in the inferior pulmonary ligaments. The superior gastric nodes receive lymph not only from the abdominal portion of the esophagus, but also from the adjacent lower thoracic segment.
- UES- 4-5cm in length , tone -60mmHg, preventing a steady flow of air into the esophagus LES-24mmHg remains elevated just enough to prevent reflux
- Cricopharyngeal sphincter- 60mmhg Intrathoracic pressure :- -6mm hg Intra abdominal -6mmhg The peristaltic wave generates an occlusive pressure varying from 30 to 120 mmHg (see Fig. 25-14). The wave rises to a peak in 1 second, lasts at the peak for about 0.5 seconds, and then subsides in about 1.5 seconds. The whole course of the rise and fall of occlusive pressure may occupy one point in the esophagus for 3 to 5 seconds.
- Body of esophagus- 40-80mmHg Duration -2.3-3.6 sec LES not a true sphincter it’s a high pressure zone
- First, reflux episodes occur in healthy volunteers primarily during transient losses of the gastroesophageal barrier, which may be due to a relaxation of the LES or intragastric pressure overcoming sphincter pressure The average frequency of these “unguarded moments” or of transient losses of the gastroesophageal barrier is far less while asleep and in the supine position than while awake and in the upright position. Second, in the upright position, there is a 12-mmHg pressure gradient between the resting, positive intra-abdominal pressure measured in the stomach and the most negative intrathoracic pressure measured in the esophagus at midthoracic level. This gradient favors the flow of gastric juice up into the thoracic esophagus when upright This is due to the apposition of the hydrostatic pressure of the abdomen to the abdominal portion of the sphincter when supine. In the upright position, the abdominal pressure surrounding the sphincter is negative compared with atmospheric pressure, and, as expected, the abdominal pressure gradually increases the more caudally it is measured. This pressure gradient tends to move the gastric contents toward the cardia and encourages the occurrence of reflux into the esophagus when the individual is upright. In contrast, in the supine position, the gastroesophageal pressure gradient diminishes, and the abdominal hydrostatic pressure under the diaphragm increases, causing an increase in sphincter pressure and a more competent cardia.
- ophageal junction (GEJ), a rise in pressure above the gastric baseline signals the beginning of the LES. The respiratory inversion point is identified when the positive excursions that occur in the abdominal cavity with breathing change to negative deflections in the thorax. The respiratory inversion point serves as a reference point at which the amplitude of LES pressure and the length of the sphincter exposed to abdominal pressure are measured. As the pressure-sensitive station is withdrawn into the body of the esophagus, the upper border of the LES is identified by the drop in pressure to the esophageal baseline. From these measurements, the pressure, abdominal length, and overall length of the sphincter are determined (Fig. 25-19).
- This “high-resolution manometry” is a variant of the conventional manometry in which multiple, circumferential recording sites are used, in essence creating a “map” of the esophagus and its sphincters. High-resolution catheters contain 36 miniaturized pressure sensors positioned every centimeter along the length of the catheter. The vast amount of data generated by these sensors is then processed and presented in traditional linear plots or as a visually enhanced spatiotemporal video tracing that is readily interpreted. The function of the esophageal body is assessed with 10 to 15 wet swallows. Amplitude, duration, and morphology of contractions following each swallow are visually displayed (Fig. 25-21).
- The position, length, and function of the lower esophageal sphincter (LES) are demonstrated by a high-pressure zone that should relax at the inception of swallowing and contract after the water or solid bolus passes through the LES. Simultaneous acquisition of data for the upper esophageal sphincter, esophageal body, LES, and gastric pressure minimizes the movement artifacts and study time associated with conventional esophageal manometry. This technology significantly enhances esophageal diagnostics, bringing it into the realm of “image”-based studies. High-resolution manometry may allow the identification of focal motor abnormalities previously overlooked. It has enhanced the ability to predict bolus propagation and increased sensitivity in the measurement of pressure gradients.
- In normal individuals, there is complete relaxation of the LES during a swallow (to a measured level <8 mm Hg above gastric pressure). However, in patients with achalasia, the LES relaxation during swallow may be incomplete or absent all together. Additional manometric findings consistent with achalasia include an elevated resting LES pressure of >45 mm Hg and aperistalsis in the distal two-thirds of the esophagus
- Total bolus transit time- time elapsed between bolus entry at 20cm above LES and bolus exit at 5cm above LES . Normal liquid- 0.35-1.54sec Pasty food -0.39-1.05sec Solid-1sec – 12.8sec.
- INTEGRATED RELAXATION PRESSURE- is the esophageal pressure topography metric used to know adequacy of esophagogastric junction , DISTAL CONTRACTILE INTEGRAL- vigor of contraction .product of amplitude,duration and length of the contraction between proximal and distal
- India – incidence- 0.4-1.1 in 1lakh Prevalence- 7.9-12.6 per 1lakh (research gate epidemiology and demographics )
- There is no cure for achalasia; rather, treatment is aimed at palliating the symptoms that patients experience. Therapies are directed at reducing the contractility in the LES, thus allowing for adequate esophageal emptying. Overall, the goal is early diagnosis and therapy to prevent late complications while preserving esophageal function. When evaluating the different subtypes, it has been found that type II patients were significantly more likely to respond to any therapy (Botox, 71%; pneumatic dilation, 91%; or Heller myotomy, 100%) than type I (56% overall) or type III patients (29% overall).
- Although initial response to medical therapy is approximately 50%, long-term success is limited by side effects, which include headache, orthostatic hypotension, and edema. Sidenafil They have been found to inhibit the contractile activity of the esophageal musculature in patients with achalasia,resulting in decreased LES tone
- There is no cure for achalasia; rather, treatment is aimed at palliating the symptoms that patients experience. Therapies are directed at reducing the contractility in the LES, thus allowing for adequate esophageal emptying. Overall, the goal is early diagnosis and therapy to prevent late complications while preserving esophageal function.
- Belsey mark IV Fundoplication is performed via left posterolateral thoracotomy .goal is to return the high pressure zone of the cardia otherwise known as the LES to its normal anatomical position below the diaphragm.
- The antireflux mechanism in human beings is composed of three components: a mechanically effective LES, efficient esophageal clearance, and an adequately functioning gastric reservoir. A defect of any one of these three components can lead to increased esophageal exposure to gastric juice and the development of mucosal injury.
- Gastroesophageal reflux disease after surgical myotomy continues to be a frequent problem, with rates approaching 30%.33 The addition of a surgical fundoplication has been found in a blinded, randomized controlled trial to reduce the rate of abnormal acid exposure in the esophagus from 47% to 9%.
- 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 antireflux valve cannot be created, exposing the patient to a 40% to 50% risk of GERD post procedure.
- Similar to surgical myotomy, gastroesophageal reflux disease remains a common complication following POEM and is reported in 10% to 46% of patients success rates of over 90% at 1 year follow-up.