A 75 year old woman presented with recurrent episodes of shortness of breath and chest pain in the previous three months requiring multiple admissions. The diagnosis of acute pulmonary oedema was made but no cause could be found on previous admissions. Her cardiothoracic ratio was normal on chest radiography, her left ventricular function, both systolic and diastolic, were normal by transthoracic echocardiogram. Her symptoms occurred typically at bedtime, especially after a heavy dinner, and were associated with orthopnea, paroxysmal nocturnal dyspnea, and ankle oedema. Physical examination showed regular pulses with a normal blood pressure finding of 124/61 mm Hg. The jugular venous pressure was raised, the heard sounds were normal, and no murmur could be heard. There was bilateral ankle oedema as well as basal crackles heard over both lungs. An electrocardiogram showed normal sinus rhythm without any ischaemic or hypertensive changes. Careful examination of the chest radiograph showed congested lung field with mild bilateral pleural effusion compatible with acute pulmonary oedema. There was also a round shadow behind the heart with an air-fluid level within it. Blood tests including complete blood counts, renal and liver function test, and creatinine kinase activity were within normal limits. Transthoracic echocardiography was repeated when the patient was in the supine position for an hour and had a full stomach. It showed normal left ventricular function but the left atrium was severely compressed by an extrinsic structure confirmed by multiple views (fig 1). Spiral computed tomography of the thorax showed a large hiatus hernia with intrathoracic extension. The hernia was located behind the left atrium causing anterior shift of the heart (fig 2). Subsequently coronary angiography showed normal coronary anatomy. Right heart catheterisation showed that baseline right atrial pressure and pulmonary capillary wedge pressure during prolonged supine positioning were 8 mm Hg and 18 mm Hg respectively. However, after sitting upright for 30 minutes, the right atrial pressure and pulmonary capillary wedge pressure decreased to 5 mm Hg and 6 mm Hg respectively, confirming the diagnosis of significant left atrial compression by the sliding hiatus hernia. She was successfully treated with conservative measures including frequent small meals, avoidance of a late dinner, and sleeping in slanting position using several pillows. She had no further recurrence of acute pulmonary oedema in the subsequent 12 months.

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Figure 1

 Echocardiogram in apical four chamber view showing extrinsic compression of the posterior wall (arrows) of the left atrium by a large mass. LV, left ventricle; LA, left atrium.

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Figure 2

 Computed tomogram of the thorax showing a large, mixed type hiatus hernia compressing the left atrium from posterior aspect (arrow). LV, left ventricle; LA, left atrium; HH, hiatus hernia; Ao, descending aorta.

DISCUSSION

Hiatus hernia is a common condition and its incidence increases with age.¹ It does not produce symptoms itself in most patients, but may contribute to the pathogenesis of reflux oesophagitis. Infrequently, sliding hiatus hernia may become incarcerated and strangulated, which may subsequently lead to acute chest pain, dysphagia, and a mediastinal mass.² Furthermore, cardiac compression with haemodynamic collapse has been reported in patients with complicated or large hiatus hernia.^3,4 To our knowledge, this is the first reported case of recurrent acute heart failure caused by sliding hiatus hernia. As reported previously,^5,6 hiatus hernia may mimic a left atrial mass on transthoracic echocardiography, and is usually shown by spiral computed tomography as shown in this case. However, the clinical significance of these findings remains unclear. In this case, we performed detail cardiac haemodynamic measurements during supine and upright posture, and clearly showed the direct compressive effect of the hiatus hernia on the left atrium. This resulted in an increase in pulmonary capillary wedge pressure and subsequently contributed to the development of acute pulmonary oedema in this patient. This case shows that hiatus hernia is a potentially reversible cause of recurrent acute heart failure; accurate diagnosis and successful treatment of hiatus hernia can prevent further recurrence of acute heart failure.