By Elias Darido, M.D. Board-Certified Surgeon | Bariatric Surgeon | Houston Heartburn Surgery Center Published: May 17, 2026 | Last Reviewed: May 17, 2026
Every week, patients come to my office carrying the same frustration. They have been told, sometimes for years, that their hiatal hernia is “small” – and that a small hernia is not something to operate on. Meanwhile, they can barely sleep. They are afraid to eat. They have been on acid-suppressing medication for so long they cannot remember life without it. Some of them have developed trouble swallowing and still been reassured there is nothing seriously wrong.
I want to address this directly, because it is one of the most consequential misconceptions in gastroesophageal medicine: GERD severity is not determined by hiatal hernia size alone. Lower esophageal sphincter pressure, esophageal motility, gastric motility, and a range of other physiological factors, including many we do not yet fully understand, all play a role. Some patients with a large hiatal hernia have no reflux whatsoever. Others with a small hernia experience severe, refractory, life-altering disease. What matters is not the size of the hernia on imaging. It is what the reflux is doing to the esophagus lining and motility, and what years of undertreated acid exposure ultimately does to a patient’s wellbeing and quality of life.
GERD Severity Is Not Determined by Hiatal Hernia Size Alone
When a radiologist or gastroenterologist measures a hiatal hernia on imaging, they are measuring the diameter of the opening in the diaphragm through which the stomach has partially migrated into the chest. A hernia smaller than two or three centimeters is commonly labeled “small” and, under traditional management guidelines, treated conservatively, meaning medication and observation.
The problem with this approach is that it treats the hiatal hernia and not the patient. Indeed, hiatal hernia size is not the primary determinant of reflux severity. GERD is a multifactorial disease, and hernia size is only one variable among many. Lower esophageal sphincter pressure, esophageal motility, gastric motility, the efficiency of gastric emptying, and a range of other physiological factors, many of which we do not yet fully understand, all contribute to how much reflux occurs and how damaging it is to the esophagus.
This explains a clinical reality that any experienced foregut surgeon has observed: some patients with a large hiatal hernia have little or no reflux symptoms, while others with a small hiatal hernia suffer severe, refractory, debilitating GERD. The hernia is part of the picture. It is rarely the whole picture.
What this means in practice is that managing a patient’s reflux disease based primarily on the centimeter measurement of their hernia, without a thorough evaluation of their esophageal and gastric function, is an incomplete approach. A small defect in the diaphragm can still fundamentally be associated with a compromised anti-reflux barrier.
When Medications Stop Working – And Why That Matters
Proton pump inhibitors, or PPIs, are among the most prescribed medications in the United States. Drugs like omeprazole, pantoprazole, and esomeprazole reduce the stomach’s acid production, which can reduce the burning sensation associated with reflux. Newer potassium-competitive acid blockers like vonoprazan (Voquezna) work through a slightly different mechanism but serve the same purpose: suppress acid.
What these medications cannot do is stop reflux from happening. They can make the fluid that enters the esophagus less acidic, but they cannot prevent the fluid or bile, from refluxing in the first place.
When a patient tells me they are still having debilitating reflux despite being on a PPI, an H2 blocker, and even a PCAB, I do not hear “the reflux isn’t that bad.” I hear an alarm. Refractory symptoms in the setting of maximum medical therapy mean the disease has reached stage 3. These patients need a surgical evaluation, not a higher dose.
The Long-Term Cost of Staying on PPIs
There is also a conversation we must have about what long-term PPI use means for a patient’s health. These medications are extraordinarily effective for short-term acid suppression and are generally well tolerated. But the data on prolonged use, years to decades, tells a more complicated story.
Chronic PPI use has been associated with reduced absorption of key nutrients, particularly magnesium, calcium, vitamin B12, and iron. Over time, magnesium deficiency can contribute to muscle cramps, fatigue, and cardiac arrhythmias. Calcium and B12 deficiency have implications for bone density and neurological function. There is also a well-documented association between long-term PPI use and increased risk of certain enteric infections, as stomach acid serves as one of the body’s primary defenses against pathogens.
None of this means PPIs are dangerous medications when used appropriately. But “appropriately” means short-to-medium-term acid suppression while an underlying problem is diagnosed and treated, not indefinite suppression because a hernia was deemed too small to fix. A patient who has been on PPIs for five or ten years for refractory reflux from a structural cause has been managed, not treated.
GERD Is a Progressive Disease – And the Esophagus Pays the Price
This is the part of the conversation that I find most urgently undertreated in gastroenterology practice: GERD is not a static condition. Left undertreated, it progresses. And the esophagus, unlike the stomach, is not designed to handle acid exposure. It has no protective mucosal lining. Every episode of reflux is a chemical insult to esophageal tissue.
Over time, repeated acid exposure triggers an inflammatory cascade in the esophageal wall. The body attempts to protect itself through a process called fibrosis, the deposition of scar tissue. The esophagus retracts into the chest and shortens making surgical repair more difficult. Furthermore, chronic inflammation destroys the delicate nerve fibers that control esophagus motility that is needed to coordinating swallowing. This is the mechanism by which years of GERD eventually leads to dysphagia, or difficulty swallowing.
Initially, patients notice that certain foods, dense proteins, bread, and rice, seem to “stick.” They adjust their diet without mentioning it to their doctor. They start taking smaller and smaller bites. They avoid steak and bread. They drink water after each bite of food. Over time, the difficulty progresses. The esophagus becomes less compliant, less able to generate the peristaltic force needed to propel a food bolus into the stomach. On high-resolution esophageal manometry, this shows up as impaired peristaltic amplitude, hypotensive peristalsis, or in more advanced cases, patterns consistent with ineffective esophageal motility, a condition where the esophageal muscle simply cannot produce coordinated, forceful contractions.
This is not a separate disease from GERD. It is a consequence of GERD. It is what happens when acid injury accumulates in the esophageal wall over years.
Erosive Esophagitis on Endoscopy: A More Important Indicator Than Hernia Size
If a patient’s upper endoscopy shows erosive esophagitis, even at a low grade such as LA Grade A, in the setting of ongoing PPI therapy, that finding should be treated with great seriousness. Erosive esophagitis while on acid suppression means the reflux burden is outpacing the medication’s ability to protect the mucosa. It is objective endoscopic evidence of inadequate disease control.
Similarly, an irregular Z-line, the transition zone between the squamous esophageal lining and the columnar gastric lining, signals that acid has been reaching the distal esophagus repeatedly over time, causing a shift in the mucosal architecture. These are early warning signs of a disease trajectory that, if left uncorrected, can progress to more serious complications.
In my practice, I place considerably more weight on these endoscopic and manometric findings than on the centimeter measurement of a hiatal hernia. A patient with erosive esophagitis on PPI therapy and early signs of esophageal motility impairment on manometry has advanced, poorly controlled GERD, regardless of what their hernia looks like on endoscopy or CT scan.
What a Proper Evaluation Should Include
If you have been told your reflux is “not bad enough” to address surgically based on hernia size alone, I would encourage you to seek a second opinion from a specialist who evaluates GERD with a complete diagnostic picture. That picture should include:
A 24-hour pH impedance study or pH probe to quantify the actual acid and non-acid reflux burden. A high-resolution esophageal manometry study to assess lower esophageal sphincter pressure and esophageal peristaltic function. An upper endoscopy with careful evaluation of the distal esophagus, Z-line, and gastric cardia. A thorough review of how long the patient has been symptomatic, how many medications have failed, and what their quality of life actually looks like.
The goal is not to find a reason to operate. The goal is to understand the true severity of the disease, and then have an honest, evidence-based conversation about whether continued medical management is in the patient’s best interest, or whether a definitive structural repair is the more appropriate path.
A Note to Patients Who Feel Dismissed
If you have been living with debilitating reflux, struggling to eat, losing sleep, and wondering whether your symptoms are being taken seriously, I want you to know that you are not imagining it. GERD is not just heartburn. At its worst, it is a progressive disease that erodes quality of life and, if undertreated long enough, can cause lasting damage to the esophagus.
The size of your hiatal hernia on imaging is one data point. It is not the diagnosis. It is not the verdict on whether you deserve better treatment.
If you are dealing with refractory GERD and feel you have not gotten the answers you need, I welcome you to reach out for a consultation. My approach is to evaluate the complete clinical picture, not just the size of a hernia, and give you a clear, honest assessment of your options.
Key Clinical Points
- GERD severity is not determined by hiatal hernia size alone. Lower esophageal sphincter pressure, esophageal motility, gastric motility, and many other factors, including ones we do not yet fully understand, all contribute to reflux severity. Some patients with a large hiatal hernia have no reflux; others with a small hernia suffer severe, debilitating disease.
- Refractory symptoms despite PPI, H2 blocker, and PCAB therapy indicate a structural problem that medication cannot resolve. These patients need surgical evaluation.
- Long-term PPI use carries real nutritional and systemic risks. Indefinite suppression of a structural problem is not the same as treatment.
- GERD is a progressive disease. Chronic acid exposure causes esophageal inflammation, fibrosis, and eventual motility impairment, the mechanism behind GERD-related dysphagia.
- Erosive esophagitis on endoscopy while on acid suppression, and impaired peristalsis on manometry, are more meaningful indicators of severe, poorly controlled GERD than hernia size.
- Patients with these findings deserve a thorough surgical evaluation, regardless of what their imaging shows.
Elias Darido, M.D. | Houston Heartburn Surgery Center | 2100 W. Loop South, Suite 1115A
Houston, TX 77027
(832) 945-8717 Schedule a Consultation