A rapid response event was activated for a patient for acute onset abdominal pain and hypotension. On arrival of rapid response (RRT) personnel, the patient was a 65-year-old male with a known history of chronic obstructive pulmonary disease (COPD), active smoking, and chronic back pain for which he was taking ibuprofen daily. The patient was admitted two days before for a COPD exacerbation and was receiving prednisone 60 mg daily. He had received a dose of 125 mg of IV methylprednisolone at the time of admission.
Temperature: 98 °F, axillary
Blood Pressure: 80/55 mmHg
Heart Rate: 135 beats per min (bpm)
Respiratory Rate: 25 breaths per min
Pulse Oximetry: 97% on 2 L nasal cannula
Focused Physical Examination
A quick exam showed a severely distressed man who appeared tachypneic and was attempting to lay in bed motionless. His abdominal exam showed diffuse guarding and rigidity. Significant tenderness was noted on palpation of all quadrants. Bowel sounds were hyperactive. Lungs had mild expiratory wheezing. His cardiac exam was unremarkable.
A cardiac monitor and pads were attached immediately. A 16-G intravenous (IV) access was established, and a 1 L IV fluid bolus was started. In addition, 1 mg IV hydromorphone was administered for pain. A stat lactate level, troponin level, complete metabolic panel, complete blood count (CBC), and lipase level were ordered. Electrocardiogram (EKG) was obtained, which showed sinus tachycardia; no acute ST changes were seen. An upright abdominal X-ray was ordered but could not be completed given the patient’s severe distress. Blood pressure showed improvement with the fluid bolus, and emergent computed tomography (CT) scan of the abdomen was obtained ( Fig. 53.1 ). Findings were consistent with acute duodenal perforation. Based on the patient’s clinical history, a perforated duodenal ulcer seemed like the most probable cause. The patient was immediately given a dose of IV pantoprazole, and a stat consult was placed for surgery. The patient was transferred to the intensive care unit for further management and treatment planning.
Duodenal perforation from peptic ulcer disease (PUD).
Perforation of an abdominal viscus requires full-thickness injury to the wall leading to the expulsion of the contents into the peritoneal cavity. This leads to irritation of the peritoneum and presents as severe acute abdominal pain. As peritoneal inflammation worsens, it leads to the development of severe abdominal tenderness, guarding, and rigidity.
The most common cause of gastric and duodenal perforation is PUD and is seen in about 3-6.5 per 100,000 individuals suffering from the disorder. Despite the widespread use of aggressive acid-lowering therapies such as proton pump inhibitors, the incidence of peptic ulcer perforation has remained the same over the years. Perforated peptic ulcers carry a high mortality rate (10%–40%), and most of these patients require surgical intervention.
Helicobacter pylori infections and non-steroidal anti-inflammatory drugs (NSAIDs) (especially in combination with medications like steroids) are most commonly associated with the development of complications related to PUD (see Table 53.1 for the risk factors of PUD. Table 53.2 describes other causes of gastric and duodenal perforation.