1. HEMATEMESIS GROUP 6 :  AHMAD TIO (14700038)  ANITA RHEZA (14700030)  FEBBRYANI (14700086)  NIKOLAS BELL (14700046)  NURAINI IKQTIARZUNE (14700006)  RANI  TRI WAHYUNI (14700014)

2.  Hematemesis is the vomitus of bright red blood or “coffee-ground” material.

4.  Hematemesis &/or melena are caused by acute bleeding from the upper GI tract or the mouth or pharynx.  Profuse hematemesis is a very common hospital emergency that still caries an 8%- 14% hospital mortality  Among adults, hemorrhage from gastric or duodenal ulceration & esophageal varices are the most frequent causes.

5. o Duodenal Ulcer & Erosive Duodenitis o Gastric Ulcer (GU) o Hemorrhagic Erosive Gastritis o Esophageal Varices o Portal Hypertensive Gastropathy o Mallory-Weiss Tears o Erosive Esophagitis o Malignancies o Unusual Causes of Hematemesis or Melena

6. Minimal blood loss  If this is not the case, the patient is generally administered a proton pump inhibitor (e.g. omeprazole), given blood transfusion (if the level of hemoglobin is extremely low, that is less than 8.0 g/dL or 4.5–5.0 mmol/L), and kept NPO, which stands for “nil per os" (Latin for "nothing by mouth", or no eating or drinking) until endoscopy can be arranged.  Adequate venous access (large-bore cannulas or a central venous catheter) is generally obtained in case the patient suffers a further bleed and becomes unstable.

7.  In a "hemodynamically significant" case of hematemesis, that is hypovolemic shock, resuscitation is an immediate priority to prevent cardiac arrest.  Fluids and/or blood is administered, preferably by central venous catheter, and the patient is prepared for emergency endoscopy, which is typically done in theatres.  Surgical opinion is usually sought in case the source of bleeding cannot be identified endoscopically, and laparotomy is necessary.  Securing the airway is a top priority in hematemesis patients, especially those with a disturbed conscious level (hepatic encephalopathy in esophageal varices patient.) A cuffed endotracheal tube could be a life saving choice.

8. In no other situation is the medical history more important than in an acute GI bleed. Not only does the history usually point to the diagnosis, more importantly it determines prognosis because patientsrarely die from exsanguinations, but more frequently from co-morbid conditions or complications.

10. The most important items of the physical examination are the vital signs, pulse, blood pressure,respiratory rate & body temperature. The examining physician needs to obtain these measurements personally or to verify their accuracy as well as to evaluate the patient for postural changes in pulse or BP indicative of blood volume depletion. It takes at least 24 hours for a brisk GI bleed to be fully reflected by decreased hematocrit & hemoglobin levels.

12. EXAMPLE : A 62-year-old man was admitted to our hospital complaining of hematemesis. He had been diagnosed with an incipient hepatocellular carcinoma (HCC) 5 years before this admission. Since that time, he had been repeatedly treated for recurrence of HCC by transarterial chemoembolization and radiofrequency ablation. Bone metastases of HCC were detected 30 months before the present admission, and adrenal metastases of HCC were detected 10 months before the present admission. At admission, he was anemic, but not jaundiced, and had slightly unstable vital signs. On physical examination, he was seen to have flapping tremor, although his consciousness was clear. Laboratory data revealed that the hemoglobin level was 6.1 g/dL (normal, 14.0–16.0 g/dL), and the total bilirubin, albumin, and creatinine values were 1.0 mg/dL (normal, 0.3–1.2 mg/dL), 2.4 g/dL (normal, 3.5–5.0 g/dL), and 2.75 mg/dL (normal, 8–20 mg/dL), respectively. Antigens for serum hepatitis C antibodies were positive. The serum α-fetoprotein level was 6404 ng/mL (normal, 0– 28.5 ng/mL).

13. When the patient suffered from hematemesis, he underwent an emergency endoscopic examination under the impression of variceal bleeding. Upper endoscopic examination revealed esophageal varices without bleeding, a few whitish pedunculated polypoid lesions, and a blood clot in the stomach (Figure A); however, the bleeding site was not detected. For hemostasis, abdominal angiography was performed. Computed tomography during celiac angiography revealed a hypervascular tumor in the stomach with extravasation (Figure B, arrow indicates hypervascular tumor). Embolization was performed successfully against a branch of the gastroepiploic artery via the splenic artery. Although a biopsy was not performed because of fear of causing further bleeding, we diagnosed gastric metastasis of HCC for the following 2 reasons. First, this polypoid lesion was not detected 5 months before hematemesis, and it had emerged during the short term. Second, this tumor showed hypervascular imaging on computed tomography scan. Successful hemostasis allowed temporary stabilization of the patient. However, the patient died of hepatic failure 1 month after hematemesis. Autopsy was performed, and histologic evaluation revealed trabecular proliferation of the large cell forms with multinucleated tumor cells adjacent to normal gastric glands, consistent with metastatic HCCs to gastric mucosa (Figure C).

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