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A 39-year-old previously healthy woman was referred to our emergency department by a primary care doctor on suspected to be acute enteritis, complaining of fever, anorexia, lower abdominal pain, and frequent diarrhea. The day after admission, although frequent diarrhea stopped, the abdominal distension worsened. An abdominal radiograph revealed several dilated loops of the small bowel, suggested that small bowel obstruction (SBO) had developed. White blood cell count and c-reactive protein were markedly increased, and abdominal contrast-enhanced computed tomography scan showed localized severely edematous bowel mucosa, increased adipose tissue concentration in the pelvis, and a beaded low absorption area in the uterus. Gynecological examination revealed the presence of a pus-filled plastic intrauterine device (IUD) in the uterus. The patient confided that she had sex with her husband 2 days before the onset of symptoms. A diagnosis of SBO due to pelvic peritonitis caused by IUD infection during sexual activity was made. The SBO was cleared in 12 days with fasting, peripheral parenteral nutrition, antibiotic treatment, and insertion of an ileus tube. This case reminds us that it needs to consider disorders associated with the uterine appendages, in women of reproductive age with lower abdominal pain.

A 73-year-old man with severe intellectual disability, malnutrition, and hypoalbuminemia presented to our hospital after experiencing vomiting following dinner. Electrocardiography revealed a sinus rhythm. Plain abdominal radiography showed branching radiolucency in the liver. Abdominal computed tomography (CT) revealed branching gaseous foci of low density in the portal vein and its tributaries, suggesting the presence of hepatic portal venous gas (HPVG). Abdominal contrast-enhanced CT showed a segmental lack of contrast enhancement in the intestinal wall despite the absence of vascular occlusion in the main trunk and branches of the mesenteric artery. The patient was diagnosed with non-occlusive mesenteric ischemia (NOMI) accompanied by HPVG. Peripheral parenteral nutrition, antibiotic treatment, and human serum albumin were administered. The HPVG disappeared approximately 20 h after hospitalization. Intravascular dehydration associated with hypoalbuminemia was considered to be the cause of NOMI; the latter improved through the early correction of dehydration and hypoalbuminemia. The presence of HPVG is usually considered a diagnostic clue in patients with abdominal catastrophe and is associated with high mortality. However, the current case demonstrates the pitfalls of assessing the severity of the underlying condition based solely on the presence of HPVG.

A 60-year-old man with an unruptured cerebral aneurysm and family history of moyamoya disease was admitted to our hospital with epigastric pain since the previous day. Serum levels of pancreatic enzyme were elevated and abdominal contrast-enhanced computed tomography showed localized enlargement of the pancreatic tail in the arterial phase and revealed numerous areas of fine mesh-like vascular hyperplasia consistent with an enlarged pancreatic tail. We diagnosed pancreatic arteriovenous malformation (P-AVM) with acute pancreatitis. Furthermore, in the pancreatic body, endoscopic ultrasonography showed lobularity (honeycombing type) and hyperechoic foci (non-shadowing), which suggests chronic pancreatitis. Acute management was performed with conservative treatment including administration of replacement fluids and proteolytic enzyme inhibitor. Distal pancreatectomy for P-AVM was performed because P-AVM is associated with acute pancreatitis recurrence, development of portal hypertension, progression of chronic pancreatitis, and refractory duodenal bleeding. Histological findings on the resected specimens revealed the anastomosis of abnormal arteries and veins, which suggested P-AVM. In addition, inflammation accompanied by fat necrosis due to ischemic infarction in the pancreatic tail, which suggested acute pancreatitis, and mild fibrosis in the pancreatic body, which suggested chronic pancreatitis, were shown. Although P-AVM is associated with various complications, symptomatic P-AVM should be considered a chronic and progressive disease.

Since diffuse hepatic hemangiomatosis (DHH) is an extremely rare disease especially in adults, the etiology and natural course of adult-onset DHH has not been well understood. We report a case of DHH complicated with multiple organic dysfunction and Kasabach-Merritt syndrome (KMS) in an 83-year-old female. She presented with mild abdominal distension and laboratory findings revealed thrombocytopenia and abnormal coagulation, indicating disseminated intravascular coagulation (DIC). Enhanced computed tomography revealed diffuse, hypodense hepatic nodules with delayed enhancement involving the whole liver, and multiple hypodense splenic legions. To obtain a definitive diagnosis, laparoscopic-guided biopsy was performed. Histological findings revealed irregularly dilated non-anastomotic vascular spaces, which were lined with flat endothelial cells without cellular atypia. We diagnosed this as DHH complicated with splenic lesions and KMS. Although the patient was treated with symptomatic treatment, such as anti-coagulation therapy, hemangiomatous lesions, especially in the spleen, progressed rapidly, leading to worsening of DIC. Finally, the patient died of multiple organ failure at 12 months after diagnosis. A postmortem examination demonstrated diffuse hemangiomatosis of not only the liver and spleen, but also the adrenal glands and bone marrow. Despite no malignant histologically, DHH can be fatal if it progresses rapidly within a short period of time.

An 80-year-old man was admitted to our hospital with iron deficiency anemia and exertional chest pain. Coronary artery angiography showed 90% stenosis in the middle left anterior descending branch; abdominal computed tomography (CT) showed enlarged mesenteric lymph nodes. Although his past medical history and results of imaging studies did not suggest intestinal stenosis, assessment of intestinal patency with the PillCam® patency capsule (tag-less PC) was performed. Thirty-three hours after administration, excretion of tag-less PC was not confirmed; an abdominal contrast-enhanced CT showed arrest of tag-less PC in the small bowel and thickening of the bowel wall, suggesting a small bowel tumor. Four days after administration of tag-less PC, he developed abdominal pain and vomiting. Intestinal obstruction was diagnosed by abdominal radiograph. A diagnosis of small bowel tumor with intestinal obstruction was made, and surgical resection was performed. The tumor was histologically an adenocarcinoma. It is necessary to carefully evaluate gastrointestinal patency before small intestine endoscopy especially in elderly people with reduced cardiopulmonary function and many underlying diseases.