Hemorrhage

GI hemorrhage, in this case from duodenal and/or gastric ulceration, is the most common emergent complication of peptic ulcer disease, accounting for 73% of cases. Acute presentation is characterized by signs/symptoms of significant blood loss/hemorrhagic shock. Biochemical testing reveals marked anemia and, potentially, thrombocytopenia. If associated end organ ischemic time is short, hypokalemic, hypochloremic alkalosis may be incidentally noted. This finding is suggestive of underlying hypergastrinemia and may help guide resuscitation strategy.

The management of shock is not unique to hypergastrinemia-mediated GI hemorrhage. All patients presenting in shock should be treated emergently using a basic resuscitative algorithm designed to abrogate progressive life-threatening multiorgan failure. Such algorithms have been thoroughly described in the critical care/trauma literature and include airway stabilization, ventilatory support, resuscitation, and transfusion, in the context of frequent/real time vital sign monitoring. Following successful resuscitative treatment, the underlying source(s) of bleeding must be identified. This requires diagnostic imaging, which may include CT arteriography, upper and lower endoscopy, catheter angiography and, potentially, tagged red cell scintigraphy and/or capsule endoscopy. For bleeding peptic ulcer disease, these imaging techniques, when positive, will reveal evidence of upper GI hemorrhage. In addition, CT scanning may identify one or more incidental abdominal soft tissue masses (gastrinomas) when ZES is present.

Endoscopy is always indicated when upper GI bleeding is suspected or is identified by nonendoscopic imaging. Associated sensitivity and specificity for bleeding ulcer identification exceed those of all other imaging modalities, approaching 98% and 100%, respectively. In addition, endoscopic intervention for active ulcer hemorrhage is generally employed simultaneously, including thermal coagulation, mechanical clipping, hemostatic spray/powder application, and/or epinephrine injection, thus making upper endoscopy both diagnostic and therapeutic. ZES is most commonly characterized by a solitary ulcer, usually less than 1 cm in diameter, localizing to the first portion of the duodenum (75% of cases). Nonetheless, a thorough upper endoscopic assessment is required, as multiple ulcers may be present and may localize to other portions of the upper GI tract, including the stomach, other domains of the duodenum, and/or the proximal jejunum.

Following emergent resuscitation, endoscopic intervention, as above, is the first-line treatment for bleeding peptic ulcers, achieving hemorrhage control in over 90% of cases. In the acute setting, ulcer discovery in general should also prompt IV treatment with a proton pump inhibitor and, if at all possible, any baseline anticoagulation should be reversed. Should endoscopic management fail to control ulcer bleeding, either during initial assessment or in the context of recurrence, surgical or endovascular approaches are indicated. These second-line options are generally considered equally effective, relative to one another. Catheter angiography with transarterial embolization is less invasive than surgery and success rates for initial bleeding control range between 52% and 98%. Surgical interventions include laparotomy, with enterectomy to oversew the ulcer and tamponade associated bleeding vessel(s), or ulcer resection with appropriate GI tract reconstruction, if the patient is stable. In each case, vagotomy and pyloroplasty should also be performed.

Perforation

GI perforation is a second life-threating manifestation of ZES ( Table 16.1 ). Like GI hemorrhage, perforation in this context is the result of advanced ulcer disease. These ulcers eventually erode through the full thickness of the stomach/bowel wall, ultimately allowing spillage of GI contents (including GI flora) into the peritoneal space. As such, acute presentation is the result of peritoneal irritation and, potentially, septic shock. Patients most often complain of sudden onset severe abdominal pain, with physical examination findings generally consistent with peritonitis, including rebound pain, focal epigastric tenderness, and guarding. Biochemical testing may reveal leukocytosis.

Immediate management focuses on resuscitation, especially if hemodynamic instability is present. Subsequent diagnostic imaging will reveal evidence of GI perforation. Upright abdominal plain film radiography may show subdiaphragmatic free air. More commonly, abdominal CT scanning is the initial diagnostic imaging performed, revealing free air and extraluminal fluid in the vicinity of the perforation. If oral contrast is used, this may be seen extravasating into the adjacent peritoneal space. Evidence of gastric/duodenal GI perforation requires prompt broad-spectrum IV antibiotic and proton pump inhibitor administration, as well as ongoing fluid resuscitation. In general, emergent surgery to address the perforation and remove the associated peritoneal soilage is then indicated, although nonoperative management, with or without percutaneous drainage, is an option for elderly patients having small, sealed perforations and who are poor surgical candidates.

Operative management most commonly involves laparotomy, although laparoscopic approaches have been described. Surgical options for perforated gastric ulcers include total gastrectomy (if underlying gastric malignancy cannot be excluded and the patient is stable, without significant peritoneal soilage), as well as gastric wedge resection or omental (Graham) patch repair, with vagotomy and pyloroplasty in both cases. Perforated duodenal ulcers may be managed with patching, especially in hemodynamically unstable patients, or by pyloroplasty (with perforation incorporation) and vagotomy. More complex procedures/resections are generally not required but may be necessary if a large perforation is present in a hemodynamically stable patient.

Gastric Outlet Obstruction

Inflammation and edema associated with progressive peptic ulcer disease involving the distal stomach and/or duodenum may cause gastric outlet obstruction ( Table 16.1 ). In the emergent setting, presenting signs and symptoms include intractable nonbilious vomiting, epigastric pain, abdominal distention, and dehydration. Biochemical testing may reveal hypochloremic, hypokalemic alkalosis, in the setting of prolonged vomiting and gastrinemia-mediated chronic HCl secretion. Diagnostic plain film imaging may demonstrate gastric distention (if the stomach has not been decompressed by nasogastric tube suctioning or excessive vomiting) and CT scanning with oral contrast will identify severe restriction/failure of contrast progression at the gastroduodenal junction, with bowel edema involving the gastric outlet.

Initial management focuses on fluid resuscitation, IV proton pump inhibitor administration, and basic biochemical testing, with correction of identified electrolyte abnormalities. Nasogastric tube placement with gastric decompression should be employed if abdominal distention is noted or when imaging reveals gastric outlet obstruction. Following resuscitation, upper endoscopy should be performed to delineate the cause of obstruction. For underlying peptic ulcer disease, an endoscopic balloon dilation is generally attempted. This requires advancement of the endoscope beyond the obstruction and is associated with a low rate of perforation, depending on the size of the balloon used. Recurrence rates in the context of ZES are unacceptably high, however, and successful initial balloon dilation is thus considered a temporizing measure in this context. Surgical management is therefore often required to definitively relieve the obstruction and treat the underlying ulcer disease. Options include open or laparoscopic distal gastrectomy/antrectomy with vagotomy, or bypass drainage with vagotomy.

Outcomes

Management outcomes for emergent manifestations of gastrinoma depend on specific presentation (upper GI hemorrhage, GI perforation, or gastric outlet obstruction), as well as on the extent of patient comorbidity. Mortality rates in the acute setting may be as high as 18% for peptic ulcer hemorrhage and 20% for peptic ulcer perforation, whereas these rates are exceedingly low in cases of peptic ulcer-related (benign) gastric outlet obstruction. Regardless, formal workup for gastrinoma is vitally important following successful acute management in these patients, as failure to establish this underlying diagnosis will increase the probability of recurrence in each case and may allow disease progression if malignant gastrinoma is present. Diagnosis is based on marked elevation in serum gastrin level (greater than 1000 pg/mL) or, in cases with less marked hypergastrinemia, on positive secretin stimulation testing.