Perforated Duodenal Ulcer Presenting With Subphrenic Abscess
Perforated Duodenal Ulcer Presenting With Subphrenic Abscess
Despite recent improvements in both diagnostic and therapeutic strategies for peptic ulcer disease, perforated peptic ulcer still represents the major cause of gastrointestinal perforation and the second most common complication of peptic ulcer disease.
When a perforated peptic ulcer is clinically suspected it represents an emergent condition prompting immediate surgery. However, the clinical onset of a perforated gastric or duodenal ulcer may be atypical or the perforation may be clinically overlooked in the presence of comorbidities or it can be masqueraded by concurrent therapies. In our patient's case, it can be argued that an anti-inflammatory effect was somehow induced by the multi-kinase inhibitor drug imatinib, which our patient had been taking daily for seven years. However, a direct gastrointestinal toxicity of tyrosine kinase inhibitors in patients with chronic myeloid leukemia has also been described. As far as the misdiagnosis of acute bronchopneumonia is concerned, it was largely based on an erroneous interpretation of the abnormal chest X-ray findings (not shown). While the presence of basal pulmonary infiltrates and/or pleural effusion should be well recognized as an indirect evidence of a subdiaphragmatic infection, this was not appreciated in our patient's case. As far as the missed diagnosis of the right subphrenic abscess is concerned, we can only argue that its air component had likely been mistaken for the hepatic flexure as in Chilaiditi's syndrome, despite the absence of austral folds.
Regardless, whenever a perforated peptic ulcer is not clinically suspected the contribution of imaging studies may be substantial and the diagnostic role of CT is undisputed. This is particularly true since the advent of multi-detector technology that allows isotropic data set acquisition resulting in high-resolution images on both the axial as well as the coronal and sagittal planes.
Using CT, diagnosis of alimentary tract perforation can be based on both direct and indirect findings. Aside from free intraperitoneal air, direct findings of gastrointestinal tract perforation include the evidence of discontinuation of the bowel wall and/or the leakage of water-soluble contrast material. The former is now facilitated by the use of thin slice collimations with coronal and sagittal reformations as in multi-detector CT. As far as the leakage of water-soluble contrast material is concerned, it simply relies on oral administration of iodinated contrast media; however, this is considered a controversial practice in patients with a clinical suspicion of gastrointestinal tract perforation.
In our patient's case, the diagnosis of perforated peptic ulcer was indeed based on the leakage of the iodinated contrast material at the level of the duodenal bulb (Figure 3B) although the evidence of extraluminal air close to the duodenal bulb (Figure 3A) could also have been considered highly suggestive of a perforated duodenal ulcer. In the present case, however, oral administration of iodinated contrast material was deemed necessary to precisely identify the perforation site in view of a laparoscopic approach that nowadays represents the therapeutic option of choice even in the presence of an abscess. Our patient, however, underwent an open laparotomy because of his poor clinical condition and despite the anatomic details provided by MDCT it was necessary to administer methylene blue through his nasogastric tube to identify the perforated ulcer. This was masked by an inflammatory block involving the duodenal bulb along with the lesser omentum, the hepatic flexure of the colon and the inferior margin of the left hepatic lobe.
(Enlarge Image)
Figure 3.
Multi-detector contrast-enhanced computed tomography. Coronal reformatted images obtained before (A) and after (B) oral administration of 500cmof 3 percent diluted diatrizoate meglumine are shown. In (A) extraluminal air can be seen in the perihepatic space (asterisk) as well as in the hepatoduodenal ligament (arrow). The fluid component of the abscess (circle) can also be detected beside the gallbladder. In (B) the extraluminal leakage of the water-soluble iodinated contrast media can be well appreciated at the level of the hepatoduodenal ligament (arrowhead) in place of the extraluminal air.
While most gastroduodenal perforations will manifest on CT with either direct or indirect findings, there may be cases in which they cannot be detected. In such cases, a self-sealed perforation site or a perforation contained by adjacent organs can be postulated.
More commonly, the perforation may be clinically silent and lead to the formation of abscesses in the peritoneal cavity. Indeed, abscesses were found in 12 out of 73 patients (16 percent) with gastrointestinal perforation.
In our patient's case, the diagnosis of a subphrenic abscess was prompted by abnormal abdominal X-ray film findings (Figure 1) and then confirmed by contrast-enhanced MDCT (Figure 2). As far as the former are concerned, while the huge air-fluid level depicted in the right subphrenic space (Figure 1A) could be considered consistent with a subphrenic abscess, the supine film pointed to the correct diagnosis of a perforated duodenal ulcer since the extraluminal air could be traced back to the hepatoduodenal ligament through the subhepatic space (Figure 1B). However, since the diagnosis of duodenal ulcer was not even clinically suspected, a contrast-enhanced MDCT had to be performed.
Discussion
Despite recent improvements in both diagnostic and therapeutic strategies for peptic ulcer disease, perforated peptic ulcer still represents the major cause of gastrointestinal perforation and the second most common complication of peptic ulcer disease.
When a perforated peptic ulcer is clinically suspected it represents an emergent condition prompting immediate surgery. However, the clinical onset of a perforated gastric or duodenal ulcer may be atypical or the perforation may be clinically overlooked in the presence of comorbidities or it can be masqueraded by concurrent therapies. In our patient's case, it can be argued that an anti-inflammatory effect was somehow induced by the multi-kinase inhibitor drug imatinib, which our patient had been taking daily for seven years. However, a direct gastrointestinal toxicity of tyrosine kinase inhibitors in patients with chronic myeloid leukemia has also been described. As far as the misdiagnosis of acute bronchopneumonia is concerned, it was largely based on an erroneous interpretation of the abnormal chest X-ray findings (not shown). While the presence of basal pulmonary infiltrates and/or pleural effusion should be well recognized as an indirect evidence of a subdiaphragmatic infection, this was not appreciated in our patient's case. As far as the missed diagnosis of the right subphrenic abscess is concerned, we can only argue that its air component had likely been mistaken for the hepatic flexure as in Chilaiditi's syndrome, despite the absence of austral folds.
Regardless, whenever a perforated peptic ulcer is not clinically suspected the contribution of imaging studies may be substantial and the diagnostic role of CT is undisputed. This is particularly true since the advent of multi-detector technology that allows isotropic data set acquisition resulting in high-resolution images on both the axial as well as the coronal and sagittal planes.
Using CT, diagnosis of alimentary tract perforation can be based on both direct and indirect findings. Aside from free intraperitoneal air, direct findings of gastrointestinal tract perforation include the evidence of discontinuation of the bowel wall and/or the leakage of water-soluble contrast material. The former is now facilitated by the use of thin slice collimations with coronal and sagittal reformations as in multi-detector CT. As far as the leakage of water-soluble contrast material is concerned, it simply relies on oral administration of iodinated contrast media; however, this is considered a controversial practice in patients with a clinical suspicion of gastrointestinal tract perforation.
In our patient's case, the diagnosis of perforated peptic ulcer was indeed based on the leakage of the iodinated contrast material at the level of the duodenal bulb (Figure 3B) although the evidence of extraluminal air close to the duodenal bulb (Figure 3A) could also have been considered highly suggestive of a perforated duodenal ulcer. In the present case, however, oral administration of iodinated contrast material was deemed necessary to precisely identify the perforation site in view of a laparoscopic approach that nowadays represents the therapeutic option of choice even in the presence of an abscess. Our patient, however, underwent an open laparotomy because of his poor clinical condition and despite the anatomic details provided by MDCT it was necessary to administer methylene blue through his nasogastric tube to identify the perforated ulcer. This was masked by an inflammatory block involving the duodenal bulb along with the lesser omentum, the hepatic flexure of the colon and the inferior margin of the left hepatic lobe.
(Enlarge Image)
Figure 3.
Multi-detector contrast-enhanced computed tomography. Coronal reformatted images obtained before (A) and after (B) oral administration of 500cmof 3 percent diluted diatrizoate meglumine are shown. In (A) extraluminal air can be seen in the perihepatic space (asterisk) as well as in the hepatoduodenal ligament (arrow). The fluid component of the abscess (circle) can also be detected beside the gallbladder. In (B) the extraluminal leakage of the water-soluble iodinated contrast media can be well appreciated at the level of the hepatoduodenal ligament (arrowhead) in place of the extraluminal air.
While most gastroduodenal perforations will manifest on CT with either direct or indirect findings, there may be cases in which they cannot be detected. In such cases, a self-sealed perforation site or a perforation contained by adjacent organs can be postulated.
More commonly, the perforation may be clinically silent and lead to the formation of abscesses in the peritoneal cavity. Indeed, abscesses were found in 12 out of 73 patients (16 percent) with gastrointestinal perforation.
In our patient's case, the diagnosis of a subphrenic abscess was prompted by abnormal abdominal X-ray film findings (Figure 1) and then confirmed by contrast-enhanced MDCT (Figure 2). As far as the former are concerned, while the huge air-fluid level depicted in the right subphrenic space (Figure 1A) could be considered consistent with a subphrenic abscess, the supine film pointed to the correct diagnosis of a perforated duodenal ulcer since the extraluminal air could be traced back to the hepatoduodenal ligament through the subhepatic space (Figure 1B). However, since the diagnosis of duodenal ulcer was not even clinically suspected, a contrast-enhanced MDCT had to be performed.
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