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Cameron lesions are a rare cause of upper gastrointestinal bleeding that is localized to the gastric body mucosa of patients with large hiatal hernias. It causes occult bleeding and chronic iron-deficiency anemia. These lesions are often missed on initial endoscopy and can cause fatal complications. To avoid the high morbidity and mortality associated with this condition, it must be promptly diagnosed and treated. This activity reviews the evaluation and treatment of Cameron lesion and highlights the role of the interprofessional team in evaluating and treating patients with this condition. Objectives: Summarize the pathophysiology of Cameron lesions. Outline the typical presentation of a patient with Cameron lesions. Describe the laboratory and imaging findings associated with Cameron lesions. Review some interprofessional team strategies that can contribute to improved outcomes for patients with Cameron lesions. Access free multiple choice questions on this topic.

Gastrointestinal (GI) bleeding is the most common diagnosis among GI-related hospital admissions. Of all the GI hemorrhages, nearly 50% are due to upper GI bleeding. The most common causes of upper GI bleed include peptic ulcer disease, gastroesophageal varices, esophagitis, angioectasia, and vascular lesions. The etiology is unknown in about 8% of the cases.[1]  Cameron lesion is a rare cause of occult upper GI bleed (see Image. Cameron Lesion). Cameron lesions are linear gastric ulcers or erosions on the mucosal folds at the diaphragmatic impression in patients with a large hiatal hernia. Cameron lesions were first described in 1986 by Cameron and Higgins. The lesions were seen in people who had the chest x-ray showing one-third or more of the stomach above the diaphragm. Of the total cases, 50% were found to be anemic.[2][3]

Various theories have been proposed for the possible pathogenesis of Cameron lesions, with mechanical trauma caused by constant rubbing of mucosal folds at the constriction level of the diaphragm being the most likely cause. It has been postulated that different forces act at the neck of the gastric sac during breathing, including the upward sliding movement of the stomach, negative intrathoracic pressure causing outward and upward force, and impinging force by the crura during gastric sliding through the diaphragm.[4] Other mechanisms include gastric acid injury, focal ischemia due to diaphragmatic pressure on the herniated sac, and gut wall edema due to venous obstruction leading to vascular stasis.[5] Cameron lesions have not been shown to have a positive correlation with nonsteroidal anti-inflammatory drug use, Helicobacter pylori infection, or the absence of protein pup inhibitor usage. However, binge drinking in some studies has been related to the Cameron lesions.[6]

The prevalence rates of hiatal hernia range from 0.8 to 2.9 in all patients undergoing upper gastrointestinal endoscopy. Cameron lesions are seen in 5% of patients with known hiatal hernia discovered in upper endoscopic studies.[7][8] Cameron lesions may heal spontaneously within a couple of days, contributing to the underreporting of these lesions. The size of the hiatal hernia correlates directly with the prevalence of these lesions. Since the frequency of hiatal hernia increases with age, most cases are reported in the elderly population.[9] It is rare in the pediatric subgroup of patients, with the youngest patient being 3. The prevalence is higher in women as compared to men.[10] Most of the cases have been reported from developed countries, including North America and Western Europe. There are few cases reported from Africa, but this could be attributed to underreporting. There has been no correlation with any environmental factors or genetics. Studies have shown that inadequate fiber intake and high sitting position during defecation could be possible risk factors for developing Cameron lesions.[11]

Macroscopically, the lesions appear as white, linear, superficial erosions on the crests of inflamed mucosal folds at the site of diaphragmatic indentation. A biopsy is not recommended to make the diagnosis of Cameron lesions. Histopathological examination in the past has revealed gastric atrophy, fibrosis, necrosis, and infiltration by immune-related cells. Microscopic characteristics have shown changes in vascular obstruction indicative of ischemic gastropathy. These changes include inflammatory markers, hemorrhagic infiltrates, fibrin deposition, sloughing of the epithelium, cryptic atrophy, and coagulative necrosis.[12]

Cameron lesions can present with a broad range of clinical features. The patients can be completely asymptomatic in the beginning. Cameron lesions have been identified as an etiology for occult upper gastrointestinal blood loss, at times leading to iron deficiency anemia.[13] The usual presentation in these cases includes anemia symptoms like fatigue, pallor, melena, palpitations, or dyspnea on exertion.[14] The larger hernias (>3 cm) are associated more frequently with iron deficiency anemia than the small hernias (<3 cm).[9] This is because the size of the lesions increases with an increase in the hiatal hernia size. The patients may also present with gastroesophageal reflux disease-like symptoms with epigastric discomfort. Rarely, patients may experience life-threatening overt GI bleed.[5]

Cameron lesions pose a diagnostic challenge to physicians. The laboratory tests show iron deficiency with low hemoglobin levels and microcytic hypochromic anemia. Iron studies reveal low iron and ferritin levels with high total iron-binding capacity.[15] The chest x-ray may help visualize the hiatal hernia, showing a large posterior mediastinum structure. A barium swallow is also a non-invasive modality to diagnose hiatal hernia. The hernias are usually seen on radiographic films but not the Cameron lesions.[8] Endoscopy is the gold standard for diagnosis, although it is not uncommon to overlook these lesions due to their unique location. They are often missed on the initial endoscopy and are usually discovered on subsequent endoscopies.[16] The endoscopic evaluation involves careful antegrade and retrograde visualization of the region of the hernia sac and adjacent mucosa. Endoscopic findings include mucosal erythema, edema, and ecchymotic bleeding, along with the Cameron lesions in the gastric mucosal folds. Cameron lesions usually present as linear erosions of the gastric mucosa, frequently with erythematous borders.[17] Newer diagnostic studies like magnification chromoendoscopy may be useful to demonstrate the mucosal defects. They have also been shown to be useful in situations where there are no well-defined lesions. The usefulness of capsule endoscopy has not been fully documented. Given the short transit time and the cost involved, it is unlikely to be a diagnostic modality of choice.[18]

The treatment options include medical management, surgery, and endoscopic intervention.[2] The medical management consists of acid suppression with a proton pump inhibitor to help hasten mucosal healing and iron supplementation for concurrent iron deficiency anemia. Most patients have some acid-related problems (reflux disease, esophagitis) and are usually on acid inhibitors. This combination therapy has shown good results, with a noticeable improvement in the ulcer’s healing and the correction of the hemoglobin levels.[6] Endoscopic band ligation of actively bleeding Cameron lesions has shown good results in a limited number of cases. Endoscopic hemostasis is difficult in such scenarios due to technical and anatomical reasons. Cauterization and Epinephrine injection have been tried in some cases with temporary improvement.[19] The surgical options include fundoplication. It is recommended in patients with uncontrolled bleeding from these lesions, medically refractory disease, and complicated hernia with incarceration, volvulus, or perforation. Considering the close relation of hiatal hernia and Cameron lesions, fundoplication has been considered to be a reasonable treatment.[20][21]

Cameron lesion has several differential diagnoses based on the patient’s age, comorbidities, and overall health. Some conditions have similar clinical features and need to be differentiated from Cameron lesions based on the presenting signs and symptoms and endoscopy. These include telangiectasias, ulcers, esophagitis, Mallory-Weiss tear, diverticulosis, Dieulafoy lesion, and neoplasms (see Image. Cameron Lesion and Ulcer).[22]

The outcomes of medical therapy are excellent. There has been good healing with acid inhibitors and iron supplementation at 6 weeks. Some studies have shown complications in the form of persistent anemia and rebleeding. The majority of patients who have been unresponsive to medical therapy continue to lose blood and require multiple transfusions.[23] Surgical treatment with fundoplication remains the mainstay of treatment in non-responsive cases. The surgical treatment has shown good results, with no recurrent ulcer or hemorrhage seen in the follow-up period.[24]

The diagnosis is usually missed due to the non-specific findings. It may result in delayed treatment, eventually resulting in adverse complications. The fatal complication is spontaneous hemorrhage if left untreated. The other complication includes worsening iron deficiency anemia, which in severe cases may cause hemodynamic instability and worsening of pre-existing comorbidities.[13]

Patients should minimize the risk factors by lifestyle modifications including, avoiding alcohol use, avoiding fried and fatty foods, and avoiding the exercises that increase the intraabdominal pressure. Regular follow-up with the primary physician for monitoring the labs and with the gastroenterologist for monitoring the progression is necessary.

The majority of Cameron lesion cases go undiagnosed due to the absence of acute signs and symptoms, an occult bleeding pattern, and difficulty in visualization on endoscopy. The lesions are difficult to diagnose due to their location and small size. They often require multiple endoscopies before the diagnosis is made. Clinicians, including gastroenterologists, should consider this condition in the differentials for intermittent or massive GI bleed. Once diagnosed, the patient should be started on appropriate medical therapy and have regular follow-ups to ensure resolution. If the lesions and the symptoms persist, the physician should refer the patient for endoscopic and surgical management.[1][23] An interprofessional healthcare team consisting of clinicians, nursing staff, and pharmacists operating as a collaborative unit is the best means to achieve optimal results in cases of Cameron lesions.