Laryngopharyngeal reflux / ENTARDS


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ENT Acid Related Disorders

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Laryngopharyngeal reflux / ENTARDS

  1. 1. Laryngopharyngeal Reflux (LPR) Frederick Mars Untalan MD
  2. 2.  LPR is the abnormal reflux of gastric contents into the esophagus The acidic properties of the chyme causes damage to the esophageal mucosa
  3. 3. Pediatric Reflux Functional Gastroesophageal Reflux GERD Secondary Gastroesophageal Reflux
  4. 4. Typical presentation of LPR Crying/Irritability Poor feeding Regurgitation Epigastric pain FTT/weight loss Sore throat Waterbrash Hematemesis Anemia
  5. 5. Atypical presentation of LPR Apnea/Bradycardia  Sandifer’s syndrome ALTEs  Hoarseness/ Wheezing/Asthma Laryngitis Stridor  Otalgia Recurrent pneumonia  Sinusitis Chronic cough
  6. 6. LPR Untreated Resolves by 2 years of age in 60% of GERD Persists until age 4 in 30% ½ stricture, ½ malnutrition
  7. 7. LPR in Otolaryngology Chronic Sinusitis – avoid FESS Chronic Cough Globus Pharyngeus- osteophytes, FB, cricopharyngeus, tonsils, goiter, web, cervical lad, mass Dysphagia
  8. 8. Diagnosing LPR Tetra-probe
  9. 9. Gastroesophageal RefluxDisease
  10. 10. Reflux Contents  Stomach produces caustic substances that aid in digestion  Parietal cells-HCl  Chief Cells- Pepsinogen  Mucous Neck Cells- Lipase
  11. 11. Reflux Contents cont.  In addition to the stomach, other organs involved in digestion also secrete damaging substances.  Pancreas- Trypsinogen, amylase, lipase  Liver - Bile salts
  12. 12. Esophageal damage Largely depends on contents of reflux Gastric acid only: mild damage Combination of gastric acid, pancreatic enzymes, bile salts, pepsin: severe mucosal damage
  13. 13. Medical Treatment of GERD Acid Suppressants  Antacids – Al toxicity & osteomalacia  H-2 Blockers – Usually sufficient Proton Pump Inhibitors – Omeprazole; Rapebprazole
  14. 14. Surgical Treatment of GERD
  15. 15. Under Pressure Each sphincter is maintained at a high resting pressure. This prevents movement of ingesta and chyme into the esophageal body when fasting.
  16. 16. Control of reflux Main control is the mechanical and intrinsic tone of the LES Other mechanisms: -Interdigitating rugal folds -Right diaphragmatic crus -Oblique entrance into stomach -Gastric distention -Abdominal portion of esophagus
  17. 17. LES The gastroesophageal junction Ring of increased thickness A high pressure zone, not a true sphincter. Resting tone from myogenic and neurogenic forces THE MAJOR DEFENSE AGAINST REFLUX
  18. 18. Causes of LPR Decreased resting tone of the LES Transient LES relaxations Delayed gastric emptying Impaired esophageal clearance Reduced salivation Anesthesia
  19. 19. Prevalence and impact
  20. 20. The LPR / ENTARDS iceberg Persistent symptoms &complications Frequent symptoms (seen by MD) Occasional symptoms (not seen by MD)
  21. 21. LPR ETIOLOGY Common Cavity Phenomenon LES Pressure Motility vs Clearance Saliva acid neutralization
  22. 22. LPR MANIFESTATIONS Heartburn/Regurgitation Dysphagia/Odynophagia Barrett’s Esophagus….. Cancer Pulmonary complications Throat complications
  23. 23. LPR TREATMENT Acid suppression  H2 / PPI / Antacids Improve Motility  Metoclopramide/Cisapride Antireflux surgery
  24. 24. Reflux Strictures 2-10% of LPR Decreasing incidence due to PPI Chronic inflammation and fibrosis Most are less than 1cm in length Common in scleroderma
  25. 25. Surgery for reflux strictures Indications:  Frequent dilatations while on maximal PPI  Oesophageal perforation complicating dilatation  Non-dilatable stricture, eg longitudinal strictures  More than one previous failed anti-reflux surgery  Severely disordered oesophageal body motility
  26. 26. Malignant Oesophageal Obstruction Early curable oesophageal cancers uncommonly cause oesophageal obstruction  Radical resection is required Most oesophagectomies will prove to be palliative because occult metastatic disease Represents locally advanced oesophageal cancer requiring palliative treatment Palliated patients usually survive 4-6 months
  27. 27. Laser treatment Nd:YAG is most widely used Alleviates obstruction ( 90%) Controls haemorrhage Complications ( 1-5% )  No procedural mortality  Hurley JF et al Aust N Z J Surg 1997
  28. 28. Complications Early Late Pain  multiple treatments perforation  benign strictures pneumoperitoneum (20%) pneumomediastinum  swallowing problems gastric distension  motility disturbance bleeding ( 1%)
  29. 29. Combination of laser treatment External or internal XT Internal after-loading iridium-192 improves first dysphagia-free interval in SCC group  Sander R et al Gastrointest Endosc 1991
  30. 30. Chemically induced tumour necrosis Ethanol or polidocanol Tumour oedema/ swelling may temporary worsen dysphagia Inexpensive and readily available As effective as laser but more pain  Carazzone A et al Eur J Surgery 1999
  31. 31. Radiotherapy External beam XT  Poor palliation of dysphagia ( 40%)  Serious complications  Pulmonary fibrosis, fistula, strictures Brachytherapy  Selectron remote control after-loading machine  Relief of dysphagia : 70 % SCC, 60 % adenoCa
  32. 32. Investigations Gastrografin and/or barium oesophagram  22% positive barium on negative gastrogafin  Buecker A et al.Radiology 1997  11%25% false negative results  Jones WG et al. Ann Thorac Surg 1992
  33. 33. Primary repair Usually recommended in early injuries Recent series extended to late injuries with acceptable results ( 1/9 mortality)  Lawrence DR et al. Ann Thorac Surg 1999 Leak rate: 23% in early injury, 50 % late injury Reinforced primary repair: leak rate 7%  Wright CD et al. Ann Thorac Surg 1995
  34. 34. Iatrogenic perforation Intraluminal injury  endoscopy, bougienage, pneumatic dilatation, variceal sclerotherapy or ligation, endoprosthesis insertion Operative injury  antirflux surgery, cardiomyotomy, anterior cervical spine surgey, thoracic aneurysm repair, tube thoracostomy
  35. 35. etiology Iatrogenic injury accounts 70% of perforations In normal oesophagus ( injury in cervical part)  Piriform fossa is most common location  Kyphosis, hyper-extension of the neck, cervical osteophytes, oesophageal diverticulum Obstructed oesophagus  injury in thoracic part  75-90% endoscopic injuries are in lower oesophagus
  36. 36. Traumatic perforation Penetrating injury:  stab injuries, gunshot wounds blunt injury  MVA, cervical spine injury
  37. 37. Penetrating injury Approximately 19% of all oesophageal injury Stabbing usually involves cervical oesophagus Gunshot wounds thoracic oesophagus  Often associated injuries
  38. 38. Oesophageal perforation from blunt trauma Exceedingly rare  Blast injury, MCA, fracture dislocation of Cx spine Diagnosis usually delayed due to associated injuries