Severe Recurrent Abdominal Pain: An Anatomical Variant of Chilaiditi's Syndrome

Robert D. Glatter, MD; Robert S. April, MD; Paul Miskovitz, MD; L. Daniel Neistadt, MD

Disclosures

June 27, 2007

Abstract

A patient who presented to the emergency department with severe, recurrent abdominal pain demonstrated Chilaiditi's sign, a radiographic term for interposition of the hepatic flexure of the colon between the liver and right hemidiaphragm. Workup of this clinical case revealed anomalous colonic anatomy, which led to successful laparoscopic corrective surgery. We call attention to the potential importance of this sign when associated with clinically recurrent abdominal pain (Chilaiditi's syndrome).

Introduction

We report the case of a patient with severe recurrent abdominal pain who presented to our emergency department to bring the clinician's attention to the presence of a tell-tale diagnostic sign on computed tomography (CT) and/or abdominal plain x-ray (Chilaiditi's sign). The clinical presentation is instructive because of the little-known correlation of the sign to the syndrome -- recurrent abdominal pain associated with interposition of colon between the liver and the right hemidiaphragm and other colonic abnormalities. To our knowledge, this is the first known reported case of Chilaiditi's syndrome in which symptoms resulted from compression of the gastric outlet by the abnormally placed colon.

Case Report

A 23-year-old, previously healthy woman presented to the emergency department with acute, generalized abdominal pain. Similar episodes and visits to other emergency departments were documented over the past 6 years.

Physical examination revealed an alert young woman screaming loudly in pain. She was afebrile but in obvious distress. The episodes were associated with nausea and vomiting, and she preferred the lateral decubitus position during maximum pain. She reported other bouts in which emesis had relieved the crisis.

Examination of the abdomen did not reveal guarding, tenderness, or rebound. Bowel sounds were normal. No palpable abdominal masses were appreciated, and there was no costovertebral angle tenderness. The rest of the physical examination, including neurologic, cardiac, integumentary, and musculoskeletal aspects, was normal.

Laboratory studies revealed a white blood cell count of 13,500 cells/cu mm. Differential revealed 81% segmented neutrophils, 13% bands, and 4% lymphocytes; morphologic characteristics of the white blood cells included features of toxic granulation. Aspartate transaminase was 34 U/L; alanine transaminase was 22 U/L; alanine phosphatase was 68U/l; blood urea nitrogen was 20 mg/dL; and creatinine was 0.7 mg/dL. Urinalysis did not reveal hematuria or signs of infection.

The initial impression was functional abdominal pain. The patient was admitted for observation, hydration, and serial abdominal examinations. She was treated with odansetron for nausea and lorazepam for anxiety. Her condition subsided, and she was clinically normal and asymptomatic within 24 h. She was discharged from hospital.

Follow-up examinations revealed an important history of several similar attacks throughout her college years. During 1 attack, records showed that she had an abdominal x-ray that showed Chilaiditi's sign, which was not investigated further.

Her evaluation included a search for known causes of intermittent, nonsurgical abdominal pain; results of tests for porphyria, tabes dorsalis, urinary calculi, abdominal epilepsy, and familial Mediterranean fever were negative. The test for familial Mediterranean fever included genetic analysis of the codon for pyrin, taken from buccal smears. Ultrasonography of the abdomen showed a normal gallbladder and ducts. The patient underwent a complete gastroenterological workup. Markers for inflammatory bowel disease were absent. There was no history of an eating disorder and no psychiatric consultation or treatment. During a similar episode in college, abdominal x-ray showed Chilaiditi's sign. The patient reported recurrent bouts approximately 4-7 times annually over 7 years.

CT of the abdomen and pelvis was performed with and without IV contrast and with delayed views. These studies revealed that part of the transverse colon was interposed between the diaphragm and the liver. However, another prominent finding was the course of the transverse colon, which ran inferiorly and behind the liver to emerge in its subhepatic course in Winslow's canal. The colon passed in relation to the normal position of the first part of the duodenum in this narrowed subhepatic space. The point of fixation of the splenic flexure was displaced medially.

She was referred to a laparoscopic surgeon who removed 37 cm of colon, including the displaced segments noted in the description above. Pathology revealed nonspecific mucosal inflammatory changes, without ulcers or granulomas. She made an uneventful surgical recovery and has been symptom-free for 13 months since surgery.

Discussion

Hemidiaphragmatic interposition of the colon is rare[1] (0.25% to 0.28% of the general population). It was first described by Demetrious Chilaiditi in 1910.[2] This report, using early roentgenology, described the phenomenon of movement of the liver that allows the transverse colon to interpose between it and the hemidiaphragm.[2] His 3 cases contained within the original report involved intermittent abdominal pain that resolved without surgery. The sign is usually not associated with symptoms.

Chilaiditi's syndrome is a clinical abnormality consisting of episodic, recurrent, abdominal pain sometimes associated with colonic volvulus but occasionally with intermittent upper gastrointestinal obstruction by an ectopic segment of colon.[3,4] It is clearly always associated with Chilaiditi's sign.

The radiologic anatomy of the patient's colon was atypical and not seen in other case descriptions.[2,5] First, the colon had an anomalous fixation. The right colon followed its normal bed, but then coursed between the right kidney and the posterior aspect of the right lobe of liver. It then moved anteriorly above the right lobe and the medial segment of the left hepatic lobe and turned from the anterior location to a relatively posterior one, coursing lateral to and below the more proximal loop described above. At this point, the transition to transverse colon was seen. The interposed transverse colon appeared to move on a lax transverse mesocolon. The transverse colon then moved anteriorly and medially in the subhepatic space (Morison's pouch), crossing beneath the proximal duodenum and extending anterior to the pancreatic head to abut the anterior surface of the duodenal-jejunal flexure. The distal transverse colon lay posterior to the stomach and extended along the undersurface of the pancreas. The colon then extended to the vicinity of the splenic hilum and descended in its medial location anterior to the left kidney and along the lateral surface of the left psoas muscle to the pelvic level. The distal colon was normal.

In Figure 1, the unusual anatomy of the distal transverse colon is demonstrated, coursing below the body of the pancreas, then moving right and anterior to the descending duodenum in the area of Morison's pouch or subhepatic space. Figure 2 shows the upward course of the mid-transverse colon into Morison's pouch, next to the right kidney. This may be explained by the expansion of Morison's pouch, perhaps congenitally, allowing the passage. Finally, in Figure 3, the right colon may be seen moving superiorly into Morison's pouch, extending to the dome of the right hemidiaphragm.

Figure 1.

Late arterial phase after IV contrast shows distal transverse colon posterior to the gastric body and antrum plastered along the retroperitoneum just below the pancreatic body, extending right and anterior to the descending duodenum toward region of Morison's pouch or subhepatic space.

Figure 2.

The upward course of the mid transverse colon is clearly seen in Morison's pouch, adjacent to the right kidney. Morison's pouch is expanded, probably congenitally, allowing this passage.

Figure 3.

The right colon is seen extending superiorly into Morison's pouch (an expanded space at the expense of the right lobe of the liver) to extend to the dome of the right hemidiaphragm.

In summary, this unusual anatomy of a Chilaiditi's syndrome consisted of one-half the length of the transverse colon interposed in the space between the hemidiaphragm and the right lobe of liver and moving abnormally into the subhepatic space and Winslow's canal.

Since laparoscopic treatment has been successful with colonic malformations,[6,7] it is worthwhile to reemphasize the potential relationship of this simply diagnosed radiologic sign with possible serious colonic etiologies for patients who present with episodic recurrent abdominal pain.

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