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Laryngopharyngeal Reflux
         (LPR)



         Frederick Mars Untalan MD
 LPR is the abnormal reflux of gastric contents
  into the esophagus
 The acidic properties of the chyme causes
  damage to the esophageal mucosa
Pediatric Reflux

 Functional
  Gastroesophageal
  Reflux
 GERD
 Secondary
  Gastroesophageal
  Reflux
Typical presentation of LPR
 Crying/Irritability
 Poor feeding
 Regurgitation
 Epigastric pain
 FTT/weight loss
 Sore throat
 Waterbrash
 Hematemesis
 Anemia
Atypical presentation of LPR
 Apnea/Bradycardia      Sandifer’s syndrome
 ALTEs                  Hoarseness/
 Wheezing/Asthma         Laryngitis
 Stridor                Otalgia
 Recurrent pneumonia    Sinusitis
 Chronic cough
LPR Untreated
 Resolves by 2 years
  of age in 60% of
  GERD
 Persists until age 4
  in 30%
 ½ stricture, ½
  malnutrition
LPR in Otolaryngology

 Chronic Sinusitis – avoid FESS
 Chronic Cough
 Globus Pharyngeus- osteophytes, FB,
  cricopharyngeus, tonsils, goiter, web, cervical lad,
  mass
 Dysphagia
Diagnosing LPR

                 Tetra-probe
Gastroesophageal Reflux
Disease
Reflux Contents

  Stomach produces caustic substances that aid in
   digestion
  Parietal cells-HCl
  Chief Cells-
       Pepsinogen
  Mucous Neck Cells-
              Lipase
Reflux Contents cont.
  In addition to the stomach, other organs involved
   in digestion also secrete damaging substances.
  Pancreas- Trypsinogen, amylase, lipase
  Liver - Bile salts
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
Medical Treatment of GERD
 Acid Suppressants
   Antacids – Al toxicity & osteomalacia
   H-2 Blockers – Usually sufficient

  Proton Pump Inhibitors –
    Omeprazole; Rapebprazole
Surgical Treatment of GERD
Under Pressure
 Each sphincter is maintained at a high resting
  pressure.
 This prevents movement of ingesta and chyme
  into the esophageal body when fasting.
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
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
Causes of LPR

 Decreased resting tone of the LES
 Transient LES relaxations
 Delayed gastric emptying
 Impaired esophageal
  clearance
 Reduced salivation
 Anesthesia
Prevalence and impact
The LPR / ENTARDS iceberg

        Persistent symptoms &complications

              Frequent symptoms
              (seen by MD)


                  Occasional symptoms
                  (not seen by MD)
LPR ETIOLOGY
 Common Cavity Phenomenon
 LES Pressure
 Motility vs Clearance
 Saliva acid neutralization
LPR MANIFESTATIONS
 Heartburn/Regurgitation
 Dysphagia/Odynophagia
 Barrett’s Esophagus….. Cancer
 Pulmonary complications
 Throat complications
LPR TREATMENT
 Acid suppression

   H2 /   PPI / Antacids
 Improve Motility
   Metoclopramide/Cisapride
 Antireflux surgery
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
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
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
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
Complications
        Early                  Late
   Pain                  multiple treatments
   perforation           benign strictures
   pneumoperitoneum       (20%)
   pneumomediastinum     swallowing problems
   gastric distension      motility disturbance

   bleeding ( 1%)
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
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
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
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
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
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
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
Traumatic perforation
 Penetrating injury:
   stab injuries, gunshot wounds
 blunt injury
   MVA, cervical spine injury
Penetrating injury

 Approximately 19% of all oesophageal injury
 Stabbing usually involves cervical oesophagus
 Gunshot wounds thoracic oesophagus
   Often associated injuries
Oesophageal perforation from blunt
 trauma

 Exceedingly rare
   Blast injury, MCA, fracture dislocation of Cx spine
 Diagnosis usually delayed due to associated injuries
Laryngopharyngeal reflux / ENTARDS

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Laryngopharyngeal reflux / ENTARDS

  • 1. Laryngopharyngeal Reflux (LPR) Frederick Mars Untalan MD
  • 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. Pediatric Reflux  Functional Gastroesophageal Reflux  GERD  Secondary Gastroesophageal Reflux
  • 4. Typical presentation of LPR  Crying/Irritability  Poor feeding  Regurgitation  Epigastric pain  FTT/weight loss  Sore throat  Waterbrash  Hematemesis  Anemia
  • 5. Atypical presentation of LPR  Apnea/Bradycardia  Sandifer’s syndrome  ALTEs  Hoarseness/  Wheezing/Asthma Laryngitis  Stridor  Otalgia  Recurrent pneumonia  Sinusitis  Chronic cough
  • 6. LPR Untreated  Resolves by 2 years of age in 60% of GERD  Persists until age 4 in 30%  ½ stricture, ½ malnutrition
  • 7. LPR in Otolaryngology  Chronic Sinusitis – avoid FESS  Chronic Cough  Globus Pharyngeus- osteophytes, FB, cricopharyngeus, tonsils, goiter, web, cervical lad, mass  Dysphagia
  • 8. Diagnosing LPR Tetra-probe
  • 10. Reflux Contents  Stomach produces caustic substances that aid in digestion  Parietal cells-HCl  Chief Cells- Pepsinogen  Mucous Neck Cells- Lipase
  • 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. 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. Medical Treatment of GERD  Acid Suppressants  Antacids – Al toxicity & osteomalacia  H-2 Blockers – Usually sufficient Proton Pump Inhibitors – Omeprazole; Rapebprazole
  • 15.
  • 16. Under Pressure  Each sphincter is maintained at a high resting pressure.  This prevents movement of ingesta and chyme into the esophageal body when fasting.
  • 17. 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
  • 18. 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
  • 19. Causes of LPR  Decreased resting tone of the LES  Transient LES relaxations  Delayed gastric emptying  Impaired esophageal clearance  Reduced salivation  Anesthesia
  • 21. The LPR / ENTARDS iceberg Persistent symptoms &complications Frequent symptoms (seen by MD) Occasional symptoms (not seen by MD)
  • 22. LPR ETIOLOGY  Common Cavity Phenomenon  LES Pressure  Motility vs Clearance  Saliva acid neutralization
  • 23. LPR MANIFESTATIONS  Heartburn/Regurgitation  Dysphagia/Odynophagia  Barrett’s Esophagus….. Cancer  Pulmonary complications  Throat complications
  • 24.
  • 25.
  • 26. LPR TREATMENT  Acid suppression  H2 / PPI / Antacids  Improve Motility  Metoclopramide/Cisapride  Antireflux surgery
  • 27. 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
  • 28.
  • 29.
  • 30. 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
  • 31.
  • 32. 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
  • 33.
  • 34.
  • 35.
  • 36.
  • 37.
  • 38. 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
  • 39.
  • 40. Complications Early Late  Pain  multiple treatments  perforation  benign strictures  pneumoperitoneum (20%)  pneumomediastinum  swallowing problems  gastric distension  motility disturbance  bleeding ( 1%)
  • 41. 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
  • 42. 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
  • 43. 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
  • 44. 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
  • 45.
  • 46. 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
  • 47.
  • 48. 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
  • 49. 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
  • 50. Traumatic perforation  Penetrating injury:  stab injuries, gunshot wounds  blunt injury  MVA, cervical spine injury
  • 51. Penetrating injury  Approximately 19% of all oesophageal injury  Stabbing usually involves cervical oesophagus  Gunshot wounds thoracic oesophagus  Often associated injuries
  • 52. Oesophageal perforation from blunt trauma  Exceedingly rare  Blast injury, MCA, fracture dislocation of Cx spine  Diagnosis usually delayed due to associated injuries