A male 59-year-old patient was admitted to the Dr. Soetomo General Hospital with hematemesis and melena. The patient complained of hematemesis for 6 h before admission. He vomited three times with an amount of 200–300 mL and had lower abdominal pain. Defecate black liquid twice since 6 h before admission with a very bad smell. The patient complained of dizziness accompanied by nausea and had no appetite since 5 days. There had been shortness of breath when performing heavy activity, reduced when resting and absence of fever.\nThe patient had a history of diabetes mellitus since 3 years. He was under insulin and oral medication but irregularly. History of hypertension, heart, lung, and kidney diseases was denied. There was a history of consuming medicinal herbs for myalgia. The patient consumed it every day. He felt weak when he did not drink. He used this drug for the past 5 months. Psycho-social history: he works as a construction worker and is smoking three packs a day since youth.\nOn physical examination, it was found with compos mentis GCS 456 that his blood pressure was 125/75 mm Hg, heart rate was 96 ×/min regular, strong pulse, adequate content, respiratory rate was 20 ×/min, the axillary temperature was 36.5°C, and SpO2 was 99% of free air. The examination of head and neck conjunctiva anemic was present, no jaundice, no cyanosis, no dyspnea, no enlarged lymph nodes, jugular venous pressure does not increase. The thorax was normal, the abdomen appeared flat and there was no palpable mass, liver and spleen enlargement were not palpable, he had normal bowel sounds, and abdominal pain in the umbilical region. Extremities were warm, dry acral, capillary refill time <2 s. No edema was found on both legs.\nLaboratory tests showed that his Hb was 8.3 g/dL, hematocrit was 23.6%, MCV 78.1; MCH 27.5; MCHC 35.2; platelets were 356,000 mm3, leukocytes were 14,369 mm3, neutrophils were 79.1%, lymphocytes were 14.5%, sodium was 132 mmol/L, potassium was 4.4 mmol/L, chloride was 106 mmol/L, HbA1C was 11.2%, random blood sugar was 202 mg/dL, SGOT was 16 U/L, SGPT was 27 U/L, blood urea nitrogen (BUN) was 28 mg/dL, serum creatinine was 1.14 mg/dL, and albumin was 3 g/dL. The examination of chest radiograph showed normal heart and lungs.\nThe patient was treated with a B1 soft diet 2,100 kcal/day, infusion of NaCl 0.9% 1,500 mL in 24 h i.v., injection of omeprazole 40 mg every 8 h i.v., sucralfat syrup 15 mL every 8 h orally, novorapid injection 4 units every 8 h sc ac 15 min, transfusion of packed red cells (PRC) 1 bag/day until Hb >10 g/dL, metoclopramide 10 mg every 8 h i.v., amlodipin 10 mg every 24 h orally, lactulac syrup 15 mL every 8 h orally, Ceftriaxon 1 g every 12 h i.v., and paracetamol 500 mg every 8 h orally.\nThe patient had been given PRC transfusion until Hb reached 10.3 g/dL, and the upper gastrointestinal EGD showed that the cause of bleeding to this patient was a gastric ulcer which was suspected and caused by consumption of medicinal herbs. At EGD, double pylorus was accompanied by giant white ulcer with a partially covered in clotting without any sign of active bleeding. It could be concluded that there was a double pylorus with giant ulcer, Forrest IIb (Fig. ).\nAfter 1 week of treatment at Dr. Soetomo General Hospital, the patient's complaints were improved and he had no nausea nor vomiting, there were no hematemesis and melena, and his appetite was improved. The patient was discharged from hospital. Planning therapy was B1 soft diet 2,100 kcal/day, omeprazole 20 mg every 12 h per oral, sucralfat syrup 15 mL every 8 h orally, novorapid injection 4 units every 8 h sc ac 15 min, amlodipin 10 mg every 24 h orally. Biopsy revealed chronic inactive gastritis, and no H. pylori was detected. The patient underwent checkup at the Gastroenterology department after 1 week of hospital discharge with complaints of decreased appetite, abdominal pain, and no nausea and received sucralfate syrup and lansoprazole orally.
A 42-year-old woman without a history of vomiting in infancy presented to the emergency department with postprandial abdominal distension and repeated vomiting but no abdominal pain. Laboratory examination showed normal results, including a normal serum Helicobacter pylori antibody level, except for mild anemia. Abdominal computed tomography (CT) showed gastric dilatation and wall thickening of the distal stomach (Fig. , asterisk, arrow). Endoscopy and contrast gastrography revealed gastric outlet obstruction due to stenosis of the antral and pyloric region (Fig. ), and a deep ulcer in the stenotic antrum (Fig. ). She was admitted to our hospital and treated with nasogastric tube drainage, fasting, and administration of a proton pump inhibitor. Three days later, her symptoms improved and she could start to take a liquid diet. Ten days after the initiation of treatment, she was asymptomatic and could eat a normal diet. Follow-up endoscopy performed on hospital day 12 showed a healing ulcer in the prepyloric region (Fig. ) and a distinct opening to the duodenum at the edge of the healing ulcer that was different from the original pylorus. Endoscopic ultrasonography (EUS) revealed circumferential thickening of the muscularis propria layer of the pylorus with a maximum thickness of over 10 mm (Fig. , arrowheads). Pathological examination of multiple biopsy specimens taken from the ulcer and surrounding mucosa showed no evidence of malignancy. Since the patient was asymptomatic, she was discharged from the hospital on hospital day 21. Additional follow-up endoscopic examinations revealed a clear double pylorus (Fig. , arrows). The endoscope could easily pass through both channels to the duodenum. Based on her clinical course and findings of clinical images, she was diagnosed as having gastric outlet obstruction due to AHPS that was improved by spontaneous double channel pylorus formation. Six months after onset, CT showed residual wall thickening of the distal stomach without gastric dilatation (Fig. , arrow) and EUS revealed residual circumferential thickening of the muscularis propria layer of the pylorus, indicating that she still had AHPS although she did not have any abdominal symptoms.\nOur patient's clinical and imaging findings suggested that the double pylorus formed in our patient in the following manner. When we retrospectively reviewed the endoscopic images from the EGD examination that the patient had undergone 1 year prior to the current admission, antral narrowing was observed. She may have had asymptomatic AHPS at that time. When the patient came to the emergency room, endoscopy and contrast gastrography revealed gastric outlet obstruction due to stenosis and a deep ulcer in the stenotic antrum. During the hospital admission, the deep ulcer made a fistula with the duodenum that would eventually become a double pylorus. After double pylorus formation, the patient no longer had symptoms of AHPS and she was discharged from the hospital.