An 82-year-old was admitted to our geriatrics service for undernutrition with sarcopenia and failure to thrive. He required intensive rehabilitation to enable safe return home. On admission to hospital, he was hemodynamically stable with an oxygen saturation of 97 % on room air, and was in no apparent distress. His weight was 46.5 kg, which corresponded to a body mass index (BMI) of 16.8 kg/m2. Our patient’s medical history was significant only for remote bilateral femoral herniorrhaphy, developmental dysplasia of the right acetabulum, and benign prostatic hypertrophy. There were no constitutional symptoms or features concerning for a malignancy to account for his weight loss, but he had a poor oral intake in the prior 6 months. He had a resolving cough secondary to an upper respiratory tract infection as well as mild, intermittent epigastric discomfort and constipation, but did not have obstructive symptoms such as nausea, emesis or obstipation.

Physical examination revealed no lymphadenopathy. There was clear bilateral air entry into the lung bases with no appreciable adventitial sounds. His abdomen was soft with no peritoneal findings. Of note, bowel sounds were particularly prominent even on chest auscultation, and a non-enlarged liver was readily palpable below the costal margin, which we initially attributed to his sarcopenic habitus. Laboratory investigations revealed no anemia, leukocytosis, hypercalcemia, and normal liver enzymes and thyroid stimulating hormone. Fecal occult blood testing and serum protein electrophoresis were also negative. Chest radiographs were obtained to rule out an occult pneumonia (Fig. 1), but instead, elevation of the right hemidiaphragm with bowel below was found, which is consistent with Chilaiditi’s sign.

Fig. 1
figure 1

a Posteroanterior view of a chest radiograph showing bowel loops under the right hemidiaphragm. b Lateral view of the same chest radiograph showing interposed bowel between the diaphragm and liver

Full size image

Bowel interposed between the liver and diaphragm was described as early as 1865, and the eponym is attributed to Demetrius Chilaiditi, who in 1910 first proposed a pathophysiological explanation for this radiographic observation [1]. While the precise mechanisms are unknown, the potential space needed for bowel intrusion likely involves a combination of hypermobile bowel mesentery with laxity or absence of the suspensory ligaments of the transverse colon or hepatic falciform ligament [2]. The term Chilaiditi’s sign refers to the presence of this asymptomatic anatomical variant on imaging, whereas Chilaiditi’s syndrome describes the heterogenous symptoms caused by the interposition and associated diaphragmatic elevation including bowel obstruction, constipation, abdominal or chest pain, and dyspnea [2].

Radiographic detection of Chilaiditi’s sign is rare with an estimated prevalence of 0.028–0.25 %; it is four times more likely to be observed in men, and increases with age [3]. Small bowel involvement such as in our patient is even less common, accounting for 3–5 % of cases [3]. Despite the rarity of small bowel interposition, Fig. 1 does illustrate all three classical radiographic features necessary for diagnosis. Specifically, there is a substantial degree of bowel interposition causing right hemidiaphagmatic elevation; the interposed bowel is sufficiently distended with air to produce separation of the diaphragm and liver; and the interposition displaces the liver inferiorly such that the upper margin is below the left hemidiaphragm [1].

Awareness of Chilaiditi’s sign is relevant to emergency and general medicine for several reasons. Although the bowel haustra and plicae circulares are clearly evident in our radiographs, in instances where there is less bowel insufflation, the crescentic radiolucency overlying the liver can give the impression of free air under the diaphragm or a subphrenic abscess, potentially resulting in unnecessary surgical intervention [3–5]. Computed tomography is the imaging of choice for the hemodynamically stable patient in this situation [4, 5]. Among trauma patients, diaphragmatic herniation and hemidiaphragmatic eventration with paralysis secondary to phrenic nerve damage should be considered [2]. Congenital and acquired medical conditions can further predispose patients, and the presence of Chilaiditi’s sign warrants clinical correlation with possible underlying causes such as hepatic lobe agenesis, cirrhosis and ascites, morbid obesity, cachexia, and obstructive pulmonary diseases, which widen the lower thoracic diameter [2–4].

Management of Chilaiditi’s syndrome is typically conservative, and may include bed rest, fluid supplementation, and nasogastric decompression if there is an associated bowel obstruction [2]. Our patient did have constipation, but no other obstructive symptoms, and we did not feel his presentation was in keeping with Chilaiditi’s syndrome based on clinical assessment. With an aggressive exercise program alongside a high-calorie, high-protein diet, the biometrics improved to 51.4 kg and a BMI of 18.7 kg/m2 without complications such as refeeding syndrome. Of note, we did obtain repeat radiographs prior to discharge home when his abdominal pain and constipation had resolved, and a persistent Chilaiditi’s sign remained.