A 76-year-old man presents to the emergency department (ED) complaining of a sudden onset of abdominal pain. The pain started about 4 hours before presentation to the ED and has been persistent; it is present in the upper abdomen and is centered in the epigastrium. He describes the pain as deep and burning. There is no associated nausea or vomiting. He does not report any changes in his bowel habits and has not experienced any recent fevers. The review of systems is also negative for any recent unintended weight loss or trauma. The patient also reports having had "indigestion" in the past that caused pain similar to what he is currently experiencing, though much less in intensity. His past medical history is significant for coronary artery disease and hypertension. He takes two medications, both for his high blood pressure, but does not drink excessively and does not smoke.
On physical examination, the patient is pale and in obvious severe discomfort. His heart rate is 122 bpm and his blood pressure is 110/65 mm Hg. He is breathing with rapid shallow breaths at a rate greater than 30 breaths/min. His temperature is normal at 99.2ºF (37.3ºC), and his pulse oximetry reading while breathing room air shows a saturation rate of 100%. The cardiovascular and respiratory findings are unremarkable. The patient has significant tenderness in the epigastric region, with a rigid abdomen. There is little to no tenderness to palpation in the lower quadrants; a reliable assessment of the upper quadrants is not possible because of the tenderness in the epigastric region. Hyperactive bowel sounds are heard on auscultation. The patient's stool is brown and guaiac positive.
An electrocardiogram is performed and is noted to be unremarkable except for sinus tachycardia. A complete blood count (CBC) and a chemistry panel are sent. The CBC reveals mild anemia, with a hemoglobin concentration of 127 g/L (12.7 g/dL). On the chemistry panel, there is evidence of a slight azotemia, with a blood urea nitrogen level of 17.1 mmol/L (48 mg/dL) and a creatinine value of 106 µmol/L (1.2 mg/dL). The remainder of the laboratory investigations is unremarkable. Plain radiographs of the abdomen are performed (see Figures 1A and 1B).
What is the diagnosis? Pneumoperitoneum from duodenal ulcer perforation
Clear definition of both the inner wall and outer wall of the bowel on Figure 2A (the Rigler sign; see below for explanation) and the presence of free air under the right hemidiaphragm on Figure 2B demonstrate pneumoperitoneum. The term "pneumoperitoneum" refers to air in the peritoneal cavity. The differential diagnosis of pneumoperitoneum includes iatrogenic causes (eg, peritoneal dialysis; abdominal surgery, including laparoscopy and laparotomy, after which pneumoperitoneum can persist for up to 28 days), blunt or penetrating trauma, perforation of the hollow viscera (eg, gastric ulcer, duodenal ulcer), pneumatosis intestinalis or pneumatosis coli, vaginal insufflation, and gas from the mediastinum (eg, from barotrauma).
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Figure 2.
Although many patients with perforated peptic ulcers initially present with severe abdominal pain as well as epigastric tenderness and classic signs of peritonitis, patients who are elderly, are immunocompromised, or have altered mental status may have only minimal signs and symptoms. In one study of patients older than 60 years of age with perforated ulcers, only 70% had abdominal pain. Other patients reported symptoms that included dyspepsia, anorexia, nausea, and vomiting. Severe abdominal pain was present in only 16% of patients.[2] About 6% of patients with perforated ulcers have no abdominal findings. In most cases of perforation from ulcer disease, gastric and duodenal contents (ie, bile, ingested food, swallowed bacteria) leak into the peritoneum, resulting in peritonitis and increased risk of infection and abscess formation. In addition to sepsis, subsequent third-spacing of fluid into the peritoneal cavity caused by the peritonitis can lead to hypotension and shock.[1]
The underlying pathophysiology of a duodenal ulcer is a common condition that is characterized by the presence of a well-demarcated mucosal defect in the duodenum. Approximately 95% of duodenal ulcers are found in the first part of the duodenum; most are smaller than 1 cm in diameter. A prompt and accurate diagnosis combined with treatment can prevent potentially serious complications, such as perforation (which occurred in this case). The duodenal mucosa resists damage from the effects of gastric acid and the proteolytic enzyme pepsin because of the protective qualities of the mucous/gel layer produced by the mucus-secreting epithelial cells, bicarbonate secretions from other gastric and duodenal cellular components, and protective prostaglandins. If gastric acid and pepsin penetrate the mucous layer and reach the epithelial cells, ion pumps in the basolateral cell membrane regulate intracellular pH by removing excess hydrogen ions; healthy epithelial cells migrate to the site of the injury; and mucosal blood flow serves to remove any excess acid diffused through the injured mucosa. Despite these barriers and mechanisms to prevent permanent injury, ulcerations can occur. Any pathophysiologic or iatrogenic process that increases gastric acidity (eg, disease states with increased maximal and basal acid output), decreases prostaglandin production (eg, nonsteroidal anti-inflammatory drug [NSAID] use, which inhibits the cyclooxygenase-1 [COX-1] pathway), or interferes with the mucous layer (eg, Helicobacter pylori infection leading to stimulation of gastric acid production) can result in the formation of peptic ulcer disease.[1,3]
In the United States, the prevalence of duodenal ulcer is estimated to be 6%-15% in the general population. The majority of individuals with duodenal ulcers do not have clinically significant disease. The prevalence is closely linked to the presence of H pylori infection. Among individuals infected with H pylori , the lifetime prevalence is approximately 20%. Internationally, the prevalence of the disease varies among countries and, as in the US, is linked to rates of H pylori infection. [3,4]
Duodenal ulcers can result in significant morbidity and mortality. Their main complication is pain; however, serious complications can include ulcer hemorrhage, perforation, penetration, and obstruction. Complications and mortality are generally greater in elderly patients than in other patient populations, possibly because of a higher incidence of comorbid disease and an increased use of NSAIDs in this group.[3,4]
When a perforation is suspected, as in this case, an upright chest or left lateral decubitus radiograph can detect as little as 1-2 mL of gas under the diaphragm or lateral margin of the liver, especially if strict positioning techniques are used. Therefore, these studies should be the first diagnostic modalities used. Supine abdominal radiographs are generally of limited value in diagnosing pneumoperitoneum. Computed tomography (CT) scanning is highly sensitive for depicting pneumoperitoneum, and it has the added benefit of assisting the clinician in identifying the underlying etiology in many patients.[1,5,6]
Numerous signs are described for diagnosing pneumoperitoneum on plain radiographs. One of the best known, the Rigler sign (also known as the double-wall or bas-relief sign), is a visualization of the outer surface of a bowel loop wall resulting from free air in the peritoneal cavity. The intraluminal gas provides negative contrast and outlines the internal wall. The cupola sign, typically seen on supine radiographs, is an inverted cup-shaped arcuate lucency overlying the lower thoracic spine and projecting caudally to the heart. This sign is formed as air accumulates anteriorly in the median subphrenic space under the central leaf of the diaphragm. The umbilical ligaments, the urachus, and particularly the falciform ligament are sometimes identified as linear radiopaque structures in the presence of free air.[1,3,5,7]
Another common sign is a collection of gas in the right upper quadrant adjacent to the liver, lying mainly in the subhepatic space and in the hepatorenal fossa, that is visible as an oval or triangular gas shadow not in obvious continuity with the rest of the bowel. This collection is usually present in the medial aspect of the right upper quadrant, with a superomedial to inferolateral orientation.[1,3,5,7]
The football sign is visualization of the entire peritoneal cavity as an oval gas shadow, with the vertically oriented falciform ligament representing the seam of an American football. This sign is most often seen in the pediatric patient but not in the adult patient, because in the adult patient, there is usually not enough air relative to the size of the peritoneal cavity.[1,7]
Nonsurgical management of a perforated ulcer is associated with prohibitive morbidity and mortality rates, especially in high-risk groups, such as immunocompromised patients and the elderly. Surgical management is generally indicated. Initial management includes gastric decompression with a nasogastric tube, pain control, intravenous hydration, and administration of broad-spectrum antibiotics. Closure with a piece of omentum (Graham patch) and truncal vagotomy with pyloroplasty (by incorporating the perforation) are two common approaches to the surgical management of a perforated duodenal ulcer. The patient in this case underwent an omental patch repair for the duodenal perforation.
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You are examining a patient with a history of peptic ulcer disease who presents with acute abdominal pain, rigidity, and tenderness. You suspect that the patient may have pneumoperitoneum resulting from a perforated ulcer. Which of the following choices should be the initial imaging modality when evaluating this patient? Upright chest x-ray. Abdominal CT scan with contrast 8%
When a perforation is suspected, an upright chest or left lateral decubitus x-ray can detect as little as 1-2 mL of gas under the diaphragm or lateral margin of the liver, especially if strict positioning techniques are used. Therefore, these studies should be the first diagnostic modalities used. Supine abdominal radiographs are generally of limited value in diagnosing pneumoperitoneum. Computed tomography (CT) scanning is highly sensitive for depicting pneumoperitoneum, and this modality has the added benefit of assisting the clinician in identifying the underlying etiology in many patients. Contrast is not necessary to identify free air on the CT scan. In addition, as x-ray is generally much more readily available than CT, an x-ray should be obtained initially to avoid a delay in diagnosis.
Assuming the above patient has a perforated peptic ulcer, which of the following management strategies is most appropriate?Surgical management, broad-spectrum antibiotics, pain control, IV hydration.Nonsurgical management of a perforated ulcer is associated with prohibitive morbidity and mortality rates, especially in high-risk groups, such as immunocompromised patients and the elderly. Surgical management is generally indicated. Initial management includes gastric decompression with a nasogastric tube, pain control, intravenous hydration, and administration of broad-spectrum antibiotics.
