Large Hiatal Hernia in a Patient With Bulimia Nervosa and Obesity: An Interdisciplinary Case Report

Introduction

Hiatal hernia (HH) is a condition affecting an increasing proportion of the adult population. Despite its prevalence, only 9% of those effected experience common clinical symptoms, such as heartburn, dysphagia, and vomiting [1]. This pathology is more frequently observed in females and in patients with an elevated body mass index (BMI) [2]. Established factors that precipitate HH include age-related alterations in the diaphragmatic muscle, elevated intra-abdominal pressure (eg, due to pregnancy or obesity), alcohol intake, smoking, and the presence of eating disorders, such as bulimia and anorexia [1,3–5]. Bulimia nervosa is defined as an eating disorder involving recurrent binge eating episodes followed by inappropriate compensatory behaviors to prevent weight gain, most commonly self-induced vomiting [6]. Moreover, the patient in this case presented with cardiogenic and pulmonary symptoms, which are considered atypical manifestations of HH [7–9]. The above factors can complicate establishing the correct diagnosis in cases of incomplete patient history-taking. In this context, we present a relatively rare clinical manifestation of HH observed in a patient concurrently affected by obesity and bulimia nervosa. Although endoscopic abnormalities have been documented in bulimia nervosa [4], HH remains exceptionally rare in eating disorders, with only isolated reports in anorexia nervosa [10], making our case of bulimia nervosa-associated HH particularly unique.

Case Report

A 39-year-old woman presented to the surgical department with a chief concern of postprandial vomiting, which had been ongoing for 2 years. The patient also reported concomitant symptoms of heartburn, postprandial discomfort, dyspnea, and excessive body weight.

During clinical history-taking, the patient revealed a long-standing struggle with obesity, which she attributed to her profession as a chef. In an attempt to manage her weight, she had undertaken numerous unsuccessful weight-loss attempts, including dietary restrictions, various diets, exercise, and dietary supplements. On March 2023, due to persistent weight management difficulties, she consulted a gastroenterologist and underwent esophagogastroduodenoscopy (EGD), which detected reflux esophagitis. Then, the patient admitted that in September 2023 she discovered a method that enabled her to lose 44 kg: self-induced vomiting after every meal. This practice continued for 1 year, leading to the development of bulimia nervosa. Consequently, in addition to significant weight loss, she began to experience involuntary postprandial vomiting. Other distressing symptoms emerged, including chest pain, heartburn, dyspnea, postprandial discomfort, and progressive general weakness. This deteriorating condition prompted the patient to seek medical attention.

The patient had consulted a gastroenterologist multiple times, receiving treatment with proton pump inhibitors (PPIs) and a prescribed diet. Additionally, due to chest pain and dyspnea, she saw a cardiologist, but no cardiac pathology was found. In June 2024, due to worsening symptoms, she consulted a local surgeon and was referred for endoscopic examination. The endoscopy revealed the presence of reflux esophagitis and a small HH. She was again prescribed PPIs; however, the medications provided minimal relief for her symptoms. Her postprandial vomiting and overall clinical deterioration subsequently progressed. In March 2025, the patient presented to our facility and was admitted for further diagnostic evaluation and management.

On physical examination, the patient’s skin and mucous membranes appeared pale. Her height was 163 cm, weight 93 kg (initially 137 kg), resulting in a BMI of 35.4 kg/m2. Complete blood count revealed anemia, with a hemoglobin level of 94 g/L and an erythrocyte count of 2.7×10/L. An ultrasound of the abdominal organs revealed a gallbladder polyp, indicating a need for cholecystectomy.

To further investigate her condition, EGD and multislice computed tomography (MSCT) of the abdominal organs with contrast enhancement were performed. The EGD findings confirmed grade 2 reflux esophagitis according to the Savary-Miller classification and identified a HH measuring 3.0×4.0 cm. MSCT of the abdominal organs with contrast enhancement demonstrated signs of an axial HH measuring 28×34×35 mm. Additionally, the MSCT revealed fatty infiltration of the liver.

On admission, a psychiatrist diagnosed bulimia nervosa. Her treatment included cognitive-behavioral therapy and fluoxetine 20 mg 3 times daily for 6 weeks. Based on the comprehensive history, physical examination, and diagnostic findings, the patient was diagnosed with HH; concomitant diagnoses included bulimia nervosa, a gallbladder polyp, class II obesity, and mild anemia due to chronic disease. Following consultations with multidisciplinary specialists, including a psychiatrist, surgical intervention for the HH was recommended. The patient underwent a combined laparoscopic cruroplasty, Toupet fundoplication, and cholecystectomy. Intraoperatively, HH type III was identified, with the hernial orifice measuring 5.0 cm (Figure 1). The postoperative diagnosis was hiatal hernia, type III.

The postoperative period was without complications, with no observed episodes of postprandial vomiting. In the postoperative period, in addition to infusion therapy, the patient received ondansetron 4 mg intramuscularly and esomeprazole 40 mg intravenously once daily. The patient was discharged on postoperative day 3 with recommendations for oral PPI therapy and antidepressant medication, which was prescribed by the psychiatrist. At 3-month postoperative follow-up, the patient reported complete resolution of vomiting, heartburn, dyspnea, and chest pain.

Discussion

The strengths of our approach included multidisciplinary evaluation that succeeded where single-specialty care had failed, thorough history-taking that revealed concealed purging behaviors, and integrated surgical and psychiatric treatment. Limitations included delayed diagnosis resulting in disease progression, an insufficient 3-month follow-up that was too short to assess long-term outcomes, and a single-case design preventing causal conclusions or generalization to all patients with eating disorders.

The presented clinical case of HH, combined with bulimia nervosa and obesity, is indeed rare in clinical practice. This case is clinically significant because the patient had sought medical attention multiple times before presenting to our facility but did not achieve a satisfactory outcome, leading to worsening of her condition, likely due to the progression of HH. Many specialists assert that surgical intervention should be recommended to patients when symptoms are present and progressive [11,12].

HH is a condition frequently associated with various comorbidities that can complicate its presentation and management. These commonly include obesity, gastroesophageal reflux disease, cholelithiasis and other diseases of the biliary tract, and, in some instances, respiratory or cardiovascular symptoms stemming from mechanical compression [13,14]. Recognizing these prevalent associations is vital for a thorough patient assessment.

The pathophysiology of bulimia nervosa–induced HH likely involves multiple mechanisms. While the literature documents endoscopic abnormalities in patients with bulimia nervosa and recognizes eating disorders as HH risk factors [1,3], the specific mechanical and metabolic pathways remain understudied. The repetitive vomiting characteristic of bulimia nervosa [15] would theoretically generate increased intra-abdominal pressure, and the patient’s 44-kg weight loss may have contributed to anatomical changes. The accelerated development of a large type III hernia in our patient, compared with the gradual progression typically seen in obesity-associated HH [2], suggests that the combination of purging behaviors and rapid weight loss created conditions conducive to hernia formation.

The development of HH in this instance could have been directly provoked by the self-induced vomiting characteristic of bulimia nervosa, which consistently led to elevated intra-abdominal and intragastric pressures. Furthermore, some literature suggests that rapid weight loss can weaken the diaphragmatic muscle, subsequently contributing to hernia formation [10]. As previously mentioned, the patient also struggled with excess weight, a well-established risk factor for HH development [1,2].

The patient’s primary and most distressing symptom was postprandial vomiting. Only because of thorough history-taking, it was revealed that the patient had a habit of self-induced vomiting to purge recently consumed food. This crucial clarification played a key role in guiding subsequent management. According to the literature, nausea and vomiting are symptoms that necessitate careful differential diagnosis, as their etiologies can range from gastrointestinal disorders and infections to metabolic and psychiatric conditions [16,17].

The presence of a psychogenic factor immediately raised suspicion of bulimia nervosa, which was subsequently confirmed by a psychiatrist according to the diagnostic criteria of DSM-5 for bulimia nervosa [6]. This condition is characterized by self-induced vomiting, use of weight-loss medications, consumption of large amounts of food in a short period, and escalating feelings of guilt after eating, among other symptoms [15]. The diagnosis of bulimia nervosa and the recommendation for cognitive-behavioral therapy combined with antidepressants played a significant role in the patient’s overall treatment.

In our presented case, intraoperatively, a type III HH was identified based on its anatomical classification. It is worth noting that, according to Fuchs et al, type I and type III hernias are associated with pathological reflux due to circumferential weakening of the phreno-esophageal membrane, often resulting from overeating and distension of the gastric fundus. In contrast, type II and type IV hernias are not directly linked to gastroesophageal reflux disease [18].

Regarding the HH itself, the surgical intervention for the paraesophageal hernia proved successful in the short term. Postoperatively, the patient was free of heartburn, postprandial discomfort, chest pain, and dyspnea, the latter being an atypical manifestation of HH often associated with larger hernias [7,19]. Importantly, paraesophageal hernias, due to their anatomical configuration, are particularly known to cause cardiac and pulmonary symptoms such as chest pain and dyspnea through direct compression or mediastinal shift [18,20,21]. Numerous cases in the literature describe chest pain and cardiac symptoms as primary symptoms, often mimicking acute coronary syndrome, particularly in elderly patients [9,21]. For instance, Khan et al reported an 81-year-old woman with multiple comorbidities who presented to the emergency department with chest pain. Despite stable hemodynamics, a normal ECG, and normal troponin levels, a CT scan revealed a retrocardiac HH. She was successfully treated with PPIs [9]. Similarly, Gimenez et al reported a case of a patient who presented with ECG changes mimicking ST-elevation myocardial infarction, which was ultimately attributed to a giant hiatal hernia causing cardiac compression [22]. Furthermore, Ono et al described a patient with pseudo-hyperacute T waves on ECG, initially concerning for acute coronary syndrome, and further investigation revealed these changes were caused by a giant HH. The ECG abnormalities resolved following appropriate management of the HH [23]. Although our patient demonstrated no ECG abnormalities, clinicians must consider the potential for such cardiac manifestations in HH.

Our comprehensive literature search across PubMed and Google Scholar databases revealed no previous reports of HH in patients with bulimia nervosa, despite documented endoscopic abnormalities in this population [4]. While HH has been reported in anorexia nervosa [10], the present case appears to be the first documented case involving bulimia nervosa, particularly with concurrent obesity. The absence of similar cases suggests either substantial underreporting or the genuine rarity of this association.

This case highlights 3 essential lessons. First, clinicians must specifically inquire about stigmatized behaviors such as purging when evaluating unexplained gastrointestinal symptoms. Second, psychiatric conditions can cause organic pathology requiring dual treatment approaches. Third, and most critically, complex surgical-psychiatric presentations demand true multidisciplinary collaboration – treating only one component ensures failure and continued morbidity.

Conclusions

This case report documents a large type III paraesophageal hernia in a patient with bulimia nervosa and obesity, demonstrating the critical importance of the multidisciplinary approach in both diagnosis and treatment. The successful outcome was achieved only through the coordinated efforts of surgeons, gastroenterologists, and psychiatrists, with surgical repair combined with cognitive-behavioral therapy and pharmacological management of the eating disorder. We hypothesize that repetitive increases in intra-abdominal pressure from self-induced vomiting, combined with rapid weight loss–induced diaphragmatic weakness, can accelerate HH formation beyond what obesity alone would cause. We recommend that clinicians specifically inquire about eating disorder behaviors in patients presenting with unexplained upper gastrointestinal symptoms, particularly when standard treatments fail. For patients with confirmed HH and eating disorders, concurrent surgical and psychiatric treatment appears crucial, as addressing only the anatomical defect without treating the underlying behavioral pathology may result in treatment failure.