The prevalence of hiatal hernias found on upper gastrointestinal endoscopy range from 0.8–2.9%.2
In a retrospective cohort study including more than 3 million hospital admissions between 1981 and 1994, el-Serag and Sonnenberg3
found that 3% of all patients admitted to hospital were discharged with a primary or secondary diagnosis of a hiatal hernia. The relation between hiatal hernias and anaemia has been known at least since the 1930s.4
Yet, the actual source of blood loss was not known until Colin et al5
in 1967 suggested that the most common cause was haemorrhage from the area of the stomach, which rides over the crus at the neck of the hernial sac. In 1976, Alan J Cameron6
confirmed the relation between large hiatal hernias and anaemia. However, it was not until 10 years later, in 1986, Cameron and Higgins described linear gastric erosions on the crest of mucosal folds at or near the level of the diaphragm in patients with large hiatal hernias and anaemia.7
Though this was almost 20 years after Colin et al's
observations, the erosions have since been named after Cameron. These lesions are seen in about 5% of patients with a known hiatal hernia and are today a well-known (though often overlooked) cause of occult gastrointestinal bleeding and iron deficiency anaemia.7
The pathogenesis of the Cameron lesions is unknown, but a few causes have been investigated.5 7–10
Panzuto et al8
found Helicobacter pylori
infection in 61.9% (13 of 21) of patients with large hiatal hernias and iron deficiency anaemia, but anaemia was still present in all patients despite successful eradication. Cameron suggested mechanical trauma as the cause because the gastric folds at the level of constriction of the diaphragm rubbed against each other.7
Based on observations of the stomach in 450 patients undergoing open surgery for hernia repair, Colin et al5
suggested that the pressure difference between the abdomen and thorax caused a sliding movement of the hernia during respiration and, thereby, distress of the mucosa leading to oedema, pettechiae and actual ulceration. Acid may also be an important factor; Moskovitz et al9
observed healing of lesions in patients treated with H2-receptor blockers and iron supplement in contrast to those who only received iron.
First-line treatment of Cameron lesions are long-term high-dose PPI and iron supplement.
However, persistent anaemia and re-bleeding is seen in about 20% of patients.10
In such cases, surgical treatment with retraction of the hernia, closure of the weakness in the diaphragm and fundoplication may be necessary. In two series, with 59 and 49 patients with large hiatal hernias and associated anaemia, the majority had resolution of their anaemia after surgical repair.5 11
However, in a small study that randomised 21 patients to surgical correction and PPI treatment or PPI treatment alone, there was no difference in prevention of recurrent anaemia.8
- Cameron lesions are rare causes of chronic iron deficiency anaemia.
- They are found in 5% of patients with large hiatal hernias.
- Patients with hiatal hernias and unexplained anaemia should be carefully evaluated for presence of Cameron lesions.
- Standard treatment is high-dose PPI and iron supplement and, in refractory cases, surgical repair.