What is LPR?

LPR stands for laryngopharyngeal reflux. The term reflux describes the backward or return flow of stomach acid. Reflux is often associated with heartburn, the result of stomach acid irritating the throat.

In LPR, stomach acid flows not only back up to the esophagus (food pipe) but also further up to the throat. The problem is that LPR causes unspecific symptoms besides those normally associated with reflux. People often don’t realize that their symptoms are caused by LPR, and it can take many years before the condition gets diagnosed. For this reason, LPR is also known as silent reflux.

Symptoms: How to Recognize LPR

Because LPR reaches not only the food pipe but also the throat, it causes unspecific symptoms rather than heartburn. These symptoms are caused by inflammation of the mucous membranes in the throat.

The most common symptoms include[1]

  • hoarseness and trouble with speaking[2];
  • sore throat;
  • the feeling of a lump in the throat;
  • difficulty with swallowing;
  • excessive mucus in the throat and respiratory tract;
  • chronic cough;
  • frequent throat-clearing;
  • asthma and breathing difficulties;
  • frequent eructation (burping);
  • general irritation of the mucous membranes;
  • nausea;
  • enamel erosion and caries;
  • ear infections;
  • recurrent flu-like infections;
  • worsening of other respiratory conditions.

You can find a detailed description of symptoms in this article on LPR symptoms.

How LPR Develops

In LPR, the reflux acid rises to the throat and respiratory tract. It was thought for a long time that the damage is only caused by the acid; but while acid does irritate the mucous membranes, this is not the whole story.

The stomach acid contains pepsin that is carried along with the reflux as it rises through the food pipe. Pepsin is an enzyme that digests proteins in an essential process of food digestion that typically occurs inside the stomach.

Pepsin is usually inactive outside the stomach because it only works in an acidic environment, which makes sense because the stomach is very acidic. You would not expect pepsin to be active in the throat, because the pH is too high (too basic/alkaline). However, the acid reflux lowers the pH so that pepsin can be active outside the stomach. Similarly, acidic food passing down the throat can have the same effect.

Because of this abnormal acidic environment, pepsin can also do its job, namely digesting proteins, outside the stomach. It digests proteins in the mucous tissue, thereby irritating the cells and causing inflammation.[3]

The irritation of the mucosa occurs in two phases:

  1. During the first phase, pepsin-containing reflux acid travels up to the throat and respiratory airways. It penetrates the mucous membranes and stays there.
  2. In the second phase, pepsin is activated by the acid. The acid may come either from further reflux or from foods or drinks.

This article about the mechanism of LPR explains in detail how reflux causes damage.

Causes of LPR

Reflux is usually held back by sphincters at the lower and upper ends of the esophagus.[4] Sphincters are valves that can open or close to respectively let things through or block them.

The valve at the lower end of the esophagus is called the lower esophageal sphincter (LES). It sits directly above the stomach and is the first anti-reflux barrier. The LES is supposed to prevent the backflow of reflux from the stomach into the esophagus.

The valve sitting at the upper end of the esophagus is the upper esophageal sphincter (UES). It prevents reflux from passing from the esophagus into the throat and airways.

Together, these two valves provide twofold protection against reflux. If one or both valves do not function properly, the likelihood of reflux increases.

Certain factors can strain the sphincters and weaken them over time:[5],[6],[7],[8]

  • Too much stomach pressure caused by
    • large meals;
    • weightlifting
  • Hiatal hernia, which weakens the valves and promotes reflux. A small hiatal hernia frequently goes unnoticed.[9]
  • Foods and drinks that encourage reflux, such as chocolate and coffee
  • Specific medications.

Problems with esophageal peristalsis

The esophagus moves the food via wavelike movements into the stomach. This type of movement is called peristalsis, and it can also transport reflux back into the stomach.[10]

Problems with the functioning of this natural peristalsis enable the rise of reflux into the throat and airways. In turn, reflux can also damage the esophagus, thereby further interfering with peristalsis. This is a vicious cycle that aggravates reflux symptoms over time.

Diagnosis of LPR

The diagnosis of LRP is a challenge. One problem is that it is not possible to measure reflux directly. The presence of reflux is instead assessed indirectly, for example, by measuring the pH in the throat.

Another problem is that a reflux test is only a snapshot, whereas reflux is a dynamic and ongoing process. For this reason, one single test to diagnose or rule out LPR does not exist.

A crucial initial part of the diagnostic process is a detailed assessment of the symptoms. The Reflux Symptom Index (RSI) is a useful test to find out whether the symptoms point towards LPR.

One test that is commonly used for the diagnosis is manometry. Manometry measures esophageal peristalsis and the pressure of the lower and upper esophageal sphincters.[11] Similarly, electrogastrography or electrogastrograms (EGG) measure the movements of the stomach.[12]

There are two tests that measure reflux more directly: a 24-hour pH monitoring, e.g., with the Restech device, and a test that detects pepsin in saliva.[13]

There are also imaging methods such as laryngoscopy and gastroscopy, which can detect abnormalities in the larynx (voice box) or stomach respectively by the use of viewing scopes.[14],[15]

An esophageal barium swallow exam visualizes the swallowing process, while a gastric emptying scan detects problems with stomach emptying.[16],[17]

You find more details about diagnosis of LPR in this article about tests for LPR.

Treatment of LPR

There are three recognized treatment approaches for LPR: medication, surgery, and diet adaptation.

Medication (does not address the cause of LPR)

Medications are commonly used to treat LPR because they are easy to administer. Unfortunately, their benefit is minimal. Some are well tolerated but ineffective, while others are more effective but cause more side effects.

Nevertheless, the following medications are used to treat LPR:

  • Proton-pump inhibitors (PPIs) are beneficial for the treatment of classic reflux; however, for LPR, they are no more effective than a placebo. Despite that their benefit for the treatment of LPR is a controversial subject of discussion, they are frequently prescribed for LPR.[18]
  • Prokinetic agents act on the contractions of the stomach and esophageal muscle, thereby promoting the transport of food through the digestive system. These kinds of medications are useful if LPR is caused by gastric emptying problems (gastroparesis). Because prokinetic agents affect the nervous system, however, they can cause a lot of side effects, and rarely, they can cause permanent adverse events that persist even after stopping the medication.[19] That is why that type of medication is used less commonly and is rarely used long-term.
  • H2 receptor blockers inhibit acid production. They work similarly to PPIs, but because they are less efficient than PPIs, they are rarely used.[20] They have the advantage though that they cause fewer side-effects than PPIs.
  • Gaviscon forms a layer of foam above the stomach contents, thereby preventing the stomach contents from rising towards the esophagus. Different versions of Gaviscon exist. The version that is sold also varies between countries. Gaviscon Advance (only available in the UK, or online) helps best with LPR. Gaviscon advance can reduce LPR symptoms but does not eliminate them. Other Gaviscon formulations contain less alginate and are not as effective.[21]

Surgery

Surgery always involves the risk of complications and is only recommended in extreme cases. Moreover, surgery is much less promising for LPR than it is for classic reflux.

The most established surgery for LPR is the Nissen fundoplication.[22],[23] During the fundoplication, the upper part of the stomach is wrapped around the esophagus, so tightening the valve. This stops the reflux, or at least significantly reduces it.

There is also the Stretta procedure, which stimulates the growth of the lower esophageal sphincter by using electrostimulation. It is not technically a surgery as no incisions are performed. However, it involves sedation and some level of invasiveness.

For the surgery to be successful, it is essential that it is done by an experienced surgeon. This article about surgical procedures for LPR explains different surgical approaches in detail.

Nutrition

Dietary changes represent another possibility for treating LPR. The advantage is that nutritional changes reduce the reflux itself rather than just its symptoms. You find more information about this in this article about diet and LPR.[24]


References

[1] Vaezi MF, Hicks DM, Abelson TI, Richter JE. Laryngeal signs and symptoms and gastroesophageal reflux disease (GERD): a critical assessment of cause and effect association. Clin Gastroenterol Hepatol. 2003;1(5):333-44.

[2] Lechien JR, Huet K, Khalife M, et al. Impact of laryngopharyngeal reflux on subjective and objective voice assessments: a prospective study. J Otolaryngol Head Neck Surg. 2016;45(1):59.

[3] Johnston N, Dettmar PW, Bishwokarma B, Lively MO, Koufman JA. Activity/stability of human pepsin: implications for reflux attributed laryngeal disease. Laryngoscope. 2007;117(6):1036-9.

[4] Brown J, Shermetaro C. Laryngopharyngeal Reflux. [Updated 2019 Jun 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519548/

[5] Wright LE, Castell DO. The adverse effect of chocolate on lower esophageal sphincter pressure. Am J Dig Dis. 1975;20(8):703-7.

[6] Lohsiriwat S, Puengna N, Leelakusolvong S. Effect of caffeine on lower esophageal sphincter pressure in Thai healthy volunteers. Dis Esophagus. 2006;19(3):183-8.

[7] Nebel OT, Castell DO. Fat Inhibition of the Lower Esophageal Sphincter: A Mechanism for Fatty Food Intolerance. Ann Intern Med. 1972;76:860.

[8] Brahm NC, Kelly-Rehm MC. Antidepressant-mediated gastroesophageal reflux disease. Consult Pharm. 2011;26(4):274-8.

[9] Kahrilas PJ. The role of hiatus hernia in GERD. Yale J Biol Med. 1999;72(2-3):101–111.

[10] Diener U, Patti MG, Molena D, Fisichella PM, Way LW. Esophageal dysmotility and gastroesophageal reflux disease. J Gastrointest Surg. 2001;5(3):260-5.

[11] Holloway RH. Esophageal manometry. GI Motility online. 2006.

[12] McCallum RW, Soykan I. What is the value of electrogastrography in reflux disease? OESO foundation. Mai 1998. Abgerufen am 14.08.2019.

[13] Sifrim D. The Role of Salivary Pepsin in the Diagnosis of Reflux. Gastroenterol Hepatol (N Y). 2015;11(6):417–419.

[14] Campagnolo AM, Priston J, Thoen RH, Medeiros T, Assunção AR. Laryngopharyngeal reflux: diagnosis, treatment, and latest research. Int Arch Otorhinolaryngol. 2014;18(2):184–191.

[15] Vaezi MF. New tests for the evaluation of laryngopharyngeal reflux. Gastroenterol Hepatol (N Y). 2013;9(2):115–117.

[16] Chen A, Tuma F. Barium Swallow. [Updated 2019 Apr 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493176/

[17] Banks KP, McWhorter N. Gastric Emptying Scan. [Updated 2019 May 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK531503/

[18] Reimer C, Bytzer P. Management of laryngopharyngeal reflux with proton pump inhibitors. Ther Clin Risk Manag. 2008;4(1):225–233.

[19] Rao AS, Camilleri M. Review article: metoclopramide and tardive dyskinesia. Aliment Pharmacol Ther. 2010;31(1):11-9.

[20] Tougas G, Armstrong D. Efficacy of H2 receptor antagonists in the treatment of gastroesophageal reflux disease and its symptoms. Can J Gastroenterol. 1997;11 Suppl B:51B-54B.

[21] McGlashan JA, Johnstone LM, Sykes J, Strugala V, Dettmar PW. The value of a liquid alginate suspension (Gaviscon Advance) in the management of laryngopharyngeal reflux. Eur Arch Otorhinolaryngol. 2009;266(2):243-51.

[22] van der Westhuizen L, Von SJ, Wilkerson BJ, Johnson BL, Jones Y, Cobb WS, Smith DE. Impact of Nissen fundoplication on laryngopharyngeal reflux symptoms. Am Surg. 2011;77(7):878-82.

[23] Carroll TL, Nahikian K, Asban A, Wiener D. Nissen Fundoplication for Laryngopharyngeal Reflux After Patient Selection Using Dual pH, Full Column Impedance Testing: A Pilot Study. Ann Otol Rhinol Laryngol. 2016;125(9):722-8.

[24] Koufman JA. Low-acid diet for recalcitrant laryngopharyngeal reflux: therapeutic benefits and their implications. Ann Otol Rhinol Laryngol. 2011;120(5):281-7.

Gerrit Sonnabend
 

Gerrit is a German data scientist & medical publisher. His formal education is in qualitative research. He had severe reflux himself. Read more about him here.