DYSPHAGIA ANATOMY OF THE OESOPHAGUS Hollow muscular tube which begins at level of C6 and end at the OG junction T12 25cm in length from upper border of the cricopharyngeus 40cm from the upper incisors ID: 1039265
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1. ByDr Olayiwola AdeyemiDYSPHAGIA
2. ANATOMY OF THE OESOPHAGUSHollow muscular tube which begins at level of C6 and end at the OG junction (T12)25cm in length from upper border of the cricopharyngeus/ 40cm from the upper incisorsLack serosa layerContains 2 different types of muscleUpper 1/3- striated muscleLower 2/3- smooth muscleLined by squamous epithelium except for lower 2-3cm which correspond to the squamo-columnar junction(OG junction)Has segmental blood supply
3. Divided into 3 partCervicalThoracicAbdominalAreas of anatomic narrowingCricopharyngeusBronchoaortic constrictionDiaphragmaticArterial supply: inf. Thyroid, inf. Phrenic esophageal branches of aorta, gastric arteryVenous drainage: inf. Thyroid, bronchiocephalic, left hemiazygous, azygous vein, splenic vein and inferior phrenic vein
4. Lymphatic drainage: lymphatic drainage are arranged longitudinally and it drains into paraoesophageal, perieosphageal and lateral esophageal groupNerve supply: vagus and intrinsic supply (mainly Auberch plexus)Types of peristalsisPrimary: progressive and triggered by swallowingSecondary: progressive and generated by distention or irritationTertiary: non progressive initiated by left over food in the esophagusLES is a physiologic with resting pressure of 10-25
5. DefinitionA subjective awareness of difficulty in swallowing caused by impaired progression of matter from pharynx to stomach.TYPESpreoesophageal dysphagiaesophageal dysphagia
6. PREOESOPHAGEAL DYSPHAGIADifficulty emptying bolus material from the oropharynx into the esophagus.Abnormal function proximal to the esophagusCausesMyaesthenia gravisMuscular dysthrophyBulbar poliomyelitisPseudobulbar palsyParkinson’s disease
7. OESOPHAGEAL DYSPHAGIADifficulty passing food down the esophagus.CausesCongenitalAcquired
8. Oesophageal DysphagiaCausesCongenitalAssociated with esophageal atresia/ tracheooesophageal fistulaWebsDysphagia lusoria AcquiredDiseases of the wall of the esophagusIntraluminal lesionsExtrinsic pressure on the esophagusDiseases of the stomach
9. Disease of the wall of the esophagusCarcinoma of the esophagusBenign tumoursOesophagitis/ strictureCorrosive burns ( acids, alkalis, various chemicals)Reflux oesophagitisPerforationOesophageal diverticulaeNeuromuscular dysfunctionAchalasia cardiaDiffuse spasmConnective tissue diseasesSclerodermaSLEPolyarteritis nodosa
10. OESOPHAGEAL DYSPHAGIAAcquiredDiseases of the wall of the esophagusIntraluminal lesionsExtrinsic pressure on the esophagusDiseases of the stomach
11. Intraluminal LesionsImpacted foreign bodiesBolus obstruction e.g welle!Oesophageal web→ Plummer-Vinson SyndromeSchatzki’s ring
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13. OESOPHAGEAL DYSPHAGIAAcquiredDiseases of the wall of the esophagusIntraluminal lesionsExtrinsic pressure on the esophagusDiseases of the stomach
14. Extrinsic pressure on the esophagusGoitre – neck or mediastinumEnlarged mediastinal lymph nodesMediastinal tumoursAneurysm of ascending or arch of the aorta
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18. OESOPHAGEAL DYSPHAGIAAcquiredDiseases of the wall of the esophagusIntraluminal lesionsExtrinsic pressure on the esophagusDiseases of the stomach : Carcinoma of the cardia.
19. MANAGEMENT OF DYSPHAGIAHistoryPhysical examinationInvestigationsTreatment
20. HistoryAGENeonate -CongenitalChild: -Foreign bodyThird or fourth decade: -AchalasiaElderly: -Carcinoma
21. HistoryHistory of accidental or suicidal ingestion of corrosive, or swallowing of a foreign bodyHistory of dyspepsiaHistory of alcoholism/smokingDuration of Symptoms
22. Duration of symptomsVery short history suggests inflammatory or traumatic lesionLong and intermittent – AchalasiaLong and progressive – Stricture Short and progressive – Carcinoma
23. MANAGEMENT OF DYSPHAGIAHistoryPhysical examinationInvestigationsTreatment
24. Physical examinationUsually unhelpfulWeight lossAnaemiaDehydrationPeripheral lymph nodesEpigastric mass
25. MANAGEMENT OF DYSPHAGIAHistoryPhysical examinationInvestigationsTreatment
26. InvestigationsChest X-ray FB, Widened mediastinum, retrosternal or mediastinal massesBarium swallow. Precedes oesophagoscopy- very importantOesophagoscopy identifies lesion and allows biopsyManometry achalasiaCT scan, MRI, USSFull Blood Count, BUE, LFTs, etc.
27. MANAGEMENT OF DYSPHAGIAHistoryPhysical examinationInvestigationTreatment
28. TREATMENTDepends on the diagnosis
29. ACHALASIA OF THE CARDIA
30. DEFINITIONMotility disorder of esophagus of unknown aetiology characterized by:Absence of peristalsis in the body of the esophagusHigh resting pressure in the lower esophageal sphincterInadequate or incomplete relaxation of the LES in response to swallowingHypertrophy and dilatation of the esophagus
31. AETIOLOGYCause is unknownNeurological basisGenerally acceptedSupported by absence/ or diminished ganglion cells of Auerbach’s plexus.Vagus nerve dysfunctionIndicated by abnormalities of gastric secretion, also supports neurologic aetiologySimilar clinical condition created in cats by destruction of the vagal nucleiChagas’ disease(Trypanosoma cruzi infection)In south AmericaShow changes in Auerbach’s plexus indistinguishable from those of Achalasia
32. AETIOLOGYChagas Disease (Trypanosoma cruzi infecton) In South America Produces lesions indistinguishable from achalasia
33. PathologyOesophageal obstruction at the gastro-oesophageal junction with thickening and tonic contraction of the sphincterProximal esophageal dilatation with hypertrophy of the muscle layerAdvanced cases show marked proximal dilatation with food stasis and tortuosity of the esophagus
34. Clinical FeaturesHigh incidence in patients btw 30- 60yrsM:F is 1:1Dysphagia with sticking sensation in the substernal areaPrecipitated by an emotional disorderOdynophagia in 30% of patents, especially with cold fluidsWeight loss – long standing achalasiaMalignant change ( middle of esophagus)
35. Clinical FeaturesRetrosternal PainRegurgitation of food after meals and in late stages during sleepTracheobronchopulmonary soilage results in recurrent bouts of bronchitis, pneumonia and lung abscess.Weight loss-long standing achalasiaMalignant change
36. InvestigationsCXR: widened mediastinum with or without an air fluid level Absent gastric air bubbleBarium swallow with fluoroscopy: shows dilated esophagus, lack of peristalsis, retained food in the esophagus
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39. InvestigationsOesophagoscopy Stasis, dilated esophagus with retained food oesophagitis r/o carcinoma or other causes of strictureManometric evaluation -failure of relaxaton of the LES -absent peristalsis in the body of the esophagus -elevated LES pressure
40. TREATMENTAim is to relieve obstruction caused by the hypertensive LESMedicalSurgical
41. TREATMENTMedical – 50- 60 % satisfactoryDilatation of lower sphincterMechanicalPneumatic- Stark dilatorHydrostatic- Negus hydrostatic bagComplications: Perforation, gastro-oesophageal refluxNitrates and calcium channel blockers. Results limited by side effectsBotulinum toxin
42. TREATMENTPer oral endoscopic myotomyHELLER MYOTOMY
43. CORROSIVE OESOPHAGEAL STRICTURES
44. INTRODUCTION44 Occurs in both developed and developing countriesBimodal age distributionChildren under the age of 5 years AdultsThe bimodal age distribution also reflects the aetiology in the different age groups
45. AETIOLOGY45Ingestion of strong acid or alkaliChildren under 5 years of age- accidental ingestion The result of an inquisitive toddler ingesting improperly stored corrosive substanceUsually the first swallow of the noxious substance stops further ingestion
46. AETIOLOGY46In adults the ingestion of large amounts of caustic agents is a suicide attemptRecently forceful ingestion of caustic substances as instant justice for suspected robbers Other causes: long term indwelling nasogastric tube, chronic reflux oesophagitis
47. PATHOLOGY47Ingestion of strong acid produces coagulation necrosis which limits the depth of injuryIngestion of strong alkali produces liquefaction necrosis and an increased depth of injury
48. PATHOLOGY48Considerable damage to the mouth, buccal cavity, pharynx, esophagus, stomach down to the jejunumThe laryngotracheal inlet may be affectedToxic fumes may damage the lung parenchyma
49. PATHOLOGY49Oesophagus mostly damaged at physiological points of narrowing-cricopharyngeus, level of tracheal bifurcation, distal thoracic esophagusSeverity of injury depends on the concentration of the agent, duration of contact with the mucosa and the nature of the agent- alkalis cause severe damage to the esophagus
50. PATHOLOGY50Necrosis and sloughing of tissuesUlceration of variable depthIn severe cases perforation into the mediastinum, pericardium, pleural or peritoneal cavityUlceration results in secondary infectionCompounded by acid refluxIntense fibrotic reactionHealing results in stricture in 3 weeks to three months
51. PATHOLOGY51 Bremner classified corrosive stricture into 3 degreesFirst degree: Hyperaemia and oedema of the mucosa onlySecond degree: Damage extends to the submucosa, blisters with vesicles and pseudomembrane formationThird degree: Necrosis extends to perioesophageal tissues with mediastinal, pleural or peritoneal perforation. There is eschar formation
52. CLINICAL FEATURES52There is a history of ingestion of a caustic fluidObtain a history of estimated amount and nature of ingested agentDysphagiaBurning pain in the mouth, throat, retrosternum and epigastrium especially on swallowing
53. CLINICAL FEATURES53Nausea, vomiting and diarrhoea. Vomitus may be bloodstainedDifficulty in breathing, stridor, hoarsenessShock-hypotension, rapid thready pulse, pallor, sweating- in severe casesDiscoloured and oedematous skin around the mouth and the mucosa of the mouthTemperature from secondary infection, mediastinitis, pneumonia from aspiration
54. CLINICAL FEATURES54 COMPLICATIONSShockPerforation of the esophagus or stomachBleedingMediastinitisPneumoniaSepticaemiaStrictureGastric outlet obstructionMalignant change
55. CLINICAL FEATURES55 CAUSTIC STRICTUREHistory of caustic ingestionIncreasing dysphagiaMalnutritionDehydrationAnaemiaElectrolyte imbalanceVitamin deficiencies
56. MANAGEMENT56 INVESTIGATIONSX-Rays- Chest and abdomen to detect evidence of perforation or respiratory complicationsWhen general status is stable- flexible fibreoptic oesophagogastroduodenoscopyBarium swallow at 3 to 4 weeks
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59. ACUTE MANAGEMENT59Admit patient and place on NPODo not induce vomiting to avoid repeat exposure of injured area to the agentFluid resuscitationBroad spectrum antibiotic therapyProphylactic acid suppression medication
60. MANAGEMENT60Pain reliefSteroids?????Intubation or tracheostomy and ventilation if there is significant laryngotracheal injuryParenteral nutrition
61. MANAGEMENT61First degree injury- no specific treatment- graded oral intakeFor more severe injury- careful dilatation from three weeksFeeding gastrostomy or jejunostomyResection of esophagus with cervical oesophagostomy and a feeding gastrostomy for transmural necrosis with mediastinitis- delayed reconstruction
62. MANAGEMENT62 ESTABLISHED STRICTUREIntermittent dilatation- antegrade or retrogradeOesophageal reconstruction with colon, stomach or jejunum
63. CARCINOMA OF THE OESOPHAGUS
64. AETIOLOGYNot definitely knownEndemic/ high prevalence areasChina, Japan, Iran, Chile, Puerto Rico etc.Associated factorsAge- 5th – 6th decadeDietary factors – alcohol, tobacco, malnutrition & NitrosaminePremalignant – Plummer-Vinson Syndrome, Barret’s esophagus, Lye burns of esophagusFamilial lesions – tylosis
65. PATHOLOGYSquamous cell Ca commonest ( >95%)Primary adenocarcinomaAdenocarcinoma in a Barret’s esophagusAdenoid cystic CaMucoepidermoid Ca
66. Pathology Early lesionErosive lesionsPlaquesPapillaryAdvanced lesionFungating lesionUlcerative lesionInfilterative lesion ( tend to produce malignant strictures)
67. Clincal featuresProgressive dysphagiaFrom solid → semisolid → liquid and salivaWeight loss and weaknessRegurgitation/ Aspiration/ Haematemesis/ MelaenaAdjacent structure involvementPersistent back pain : paravertebral fasciaHoarseness & Dysphonia : Recurrent Laryngeal NerveHiccups : Phrenic nerve & diaphragmRespiratory difficulty: tracheal, bronchi
68. InvestigationsDiagnosticBarium swallowOesophagoscopy + biopsy/ smear for cytologyChest x-rayCT scan of chestUSS abdomenSupportiveFBCBUE, CrLFT’s
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71. TREATMENTDepends on stageEarly lesionsLimited to esophagus, no lymph node or metastasisSuitable for curative resectionAdvanced lesionsBenefit from palliative treatment
72. TREATMENTSurgerycurativepalliativeChemotherapyRadiotherapyOesophageal intubationPhotodynamic therapy
73. TREATMENTPalliative surgeryBypass; stomachGastric tubesWhole stomachColonResection + replacement/ bypassEndoprosthesis
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75. THANK YOU