A fully functional 90-year-old Hispanic male presented to the emergency department with 1 day of nausea and vomiting. He had non-radiating, periumbilical and upper abdominal pain with non-bilious, non-bloody emesis. He has no blood or coffee-ground material in his vomitus. He denied any diarrhea or constipation. He had been unable to tolerate oral intake of any amount or consistency. These symptoms occurred acutely without any notable inciting factors. He denied subjective fevers, night sweats, or subjective weight loss, but had a recorded five pounds weight loss over 1 month. He had a good appetite prior to the onset of his symptoms, but he had been unable to eat or drink due to nausea and vomiting.
The patient has a past medical history of coronary artery disease, hypertension, hyperlipidemia, aortic regurgitation, mitral regurgitation, hypothyroidism, asthma, and pre-diabetes. He has a family history of thyroid disease, but he does not have a family history of cancers. He denies tobacco, alcohol, or recreational drug use. On presentation, his vital signs were within normal limits. On examination, he appeared lean and comfortable without evidence of distress or diaphoresis. He was alert and oriented to person, time, and place. His heart and lung exams were unremarkable. He had a soft abdomen with normoactive bowel sounds and mild tenderness to palpation of his periumbilical region and bilateral upper quadrants of his abdomen. He has no rebound tenderness and no guarding. His lower extremities had 2+ pitting edema to the mid-calves. Laboratory testing revealed no significant abnormalities on basic metabolic panel, complete blood count, and thyroid function panel. His CT of the abdomen and pelvis with intravenous contrast showed a mild ileus with diffuse wall thickening, edema and mucosal thickening of small bowel loops and colon concerning for enterocolitis, significant diverticulosis, and moderate ascites. He was started on intravenous piperacillin-tazobactam and metronidazole with some improvement in symptoms, and he was able to tolerate oral intake with decreased emesis. He was discharged on oral ciprofloxacin and metronidazole, but returned to the hospital the same day and was readmitted hours later for recurrent symptoms.
The patient was started on several antiemetics, including scheduled ondansetron and prochlorperazine with as needed metoclopramide, trimethobenzamide, and promethazine for symptomatic control. Despite that, he was still unable to tolerate any oral intake and continued to have nausea and vomiting of clear-yellow fluid and feeding materials without hematemesis and coffee-ground contents. Gastroenterology consultation was obtained on hospital day three. It was thought that he most likely had viral gastroenteritis. The team therefore discontinued antibiotics and monitored him clinically.
By hospital day 5, the patient showed no improvement, and a repeat CT of the abdomen and pelvis with intravenous contrast was performed, which showed persistent gastric antral wall thickening and narrowed lumen suspicious for gastric malignancy, diffuse omental infiltration, and concerns for linitis plastica (Figure 1). He subsequently underwent esophagogastroduodenoscopy (EGD), which showed severe reflux esophagitis from recurrent emesis, a 2-cm hiatal hernia, delayed gastric emptying, extrinsic compression on lesser curvature of stomach, and white nummular lesions in the gastric antrum. Biopsy of the stomach was performed, which later showed no malignant cells. Serial abdominal x-ray found no obstruction.
The patient's hospital course was complicated by intermittent, self-limiting fevers, and his vomiting progressed to copious bilious emesis. Blood culture, urinalysis, and chest x-ray showed no source of infection. An abdominal ultrasound showed no biliary obstruction or cirrhosis but again demonstrated ascites. Due to his fever and ascites, paracentesis was performed to evaluate for spontaneous bacterial peritonitis. His ascites fluid analysis was unremarkable for infection, with a serum-ascites albumin gradient of 0.4 g/dL and total protein of ascitic fluid of 3.2 g/dL, which was concerning for either tuberculosis or peritoneal carcinomatosis. His ascites fluid, however, did not show any organisms on acid-fast bacilli smear and culture and had no malignant cells on cytological analysis. His clinical status continued to decline, with ongoing emesis and inability to have oral intake. A nasogastric tube was placed for enteral feeding, which was intermittently held due to ongoing emesis that occurred shortly after being on enteral feeds. CT enterography demonstrates progressive dilatation of the second and third duodenal segments with transition to a nondilated, thick-walled distal fourth duodenal and jejunal segments suspicious for possible primary bowel malignancy. Along with the multifocal liver lesions, moderate ascites, and distinctive reticular infiltration of the omentum also seen on CT, this was highly suggestive of enteropathic non-Hodgkin's lymphoma (Figure 2). Given the rapid progression over a period of 3 weeks, however, these findings were thought to be more consistent with an infectious or inflammatory process rather than an aggressive neoplastic process with metastasis.
Repeat esophagogastroduodenoscopy with push enteroscopy showed Grade D esophagitis, gastritis, and jejunal inflammation with edema and erythema (Figure 3). The obtained biopsy from this procedure demonstrated a transition from normal jejunal mucosa to pathologically-involved and distorted mucosa, which was characterized by diffuse infiltrate of large neoplastic cells with highly irregular nuclei, moderate amount of cytoplasm, and centroblastic morphology. Immunohistochemistry identified sheets of B cells expressing CD45, CD20, CD79a, and BCL6 (subset), but not CD10, MUM1, CD138, cyclin D1, and cytokeratin AE1/AE3. This therefore affirmed the diagnosis of DLBCL, specifically the germinal center B cell type based on the Hans algorithm. The proliferation index (Ki-67) was approximately 90% (Figure 4).
Due to the patient's continued emesis, he developed a fever and was found to have aspiration pneumonia on chest x-ray. He was treated with a 7-day course of ampicillin-sulbactam and was started on partial parenteral nutrition. Palliative care and hematology/oncology consultation services were involved in his care. After a discussion with the patient and his family, it was decided that due to his poor nutritional status and deconditioned state, he would not pursue aggressive therapies such as surgery or chemotherapy. The patient received a peripherally inserted central catheter for total parenteral nutrition on hospital day 24 and was discharged the following day for home hospice. He did not receive any follow-up after discharge and eventually expired.