Massive upper gastrointestinal bleeding due to a gastric ulcer in a newborn

Abstract

Usually, swallowing of maternal blood is the cause of bloody vomiting in healthy term newborns. Other reported causes include gastritis, esophagitis, gastric ulcer, and duodenal ulcer. We report a newborn girl born by cesarean at 37^2/7 weeks who had hematemesis on postnatal day 1 and hematochezia on day 2. An erythrocyte transfusion was given on day 3. Gastroscopy performed on day 4 showed multiple gastric ulcers. Antacid treatment was given. On day 12, the newborn had a good general condition and stable vital signs and was discharged. Gastric ulcer needs to be considered as the etiology of hematemesis in healthy term newborns.

Massive upper gastrointestinal (GI) bleeding is rare in newborns. Reported causes include gastritis, esophagitis, gastric ulcer, and duodenal ulcer.¹ In the neonatal period, causes such as preterm labor, stress, birth asphyxia, prolonged labor, cesarean delivery, respiratory distress syndrome, medications, nasogastric tube trauma, coagulopathy, and sepsis increase the risk of stomach ulcers. GI bleeding is common in newborn babies with these risk factors. However, bleeding due to gastric ulcer is very rare in term newborn babies who are healthy and do not have the risk factors mentioned above.^1,2 The etiology of upper GI bleeding in healthy term newborns is unclear.¹ Here, we present a newborn with massive GI bleeding that presented as hematemesis and hematochezia.

CASE DESCRIPTION

A 2660 g baby girl born by cesarean from a primigravida 25-year-old mother at 37^2/7weeks was discharged 24 hours after birth. Her 1- and 5-minute APGAR scores were 8 and 9. She had bloody vomiting half an hour after being fed at home, and an hour later bloody vomiting recurred. Her physical examination upon presentation at the emergency service was unremarkable. There were no significant features in the patient or family history, except for a crack in the mother’s breast. The patient was admitted to the neonatal intensive care unit. Her body weight, height, and head circumference were in the 10th to 25th percentile. Her axillary body temperature was 36.3°F; blood pressure, 65/35 mm Hg; pulse, 130 beats/min; and respiratory rate, 50 beats/min. Examination of systems was normal.

Oral intake was discontinued. The stomach was drained freely with an orogastric tube. Fluid and ranitidine treatment were initiated. Her hemoglobin was 13 g/dL and thrombocyte count, 254,000/mm³; liver and kidney function tests, coagulation tests (prothrombin time, partial thromboplastin time), and tests of acute-phase reactants (C-reactive protein, interleukin-6) were normal. Blood continued to come from the orogastric catheter during follow-up. Hematochezia was seen on day of life 2. A red blood cell suspension was given to the patient on day 3 due to the progressive decrease in hemoglobin. Trophic breast milk was started on the same day because of the absence of hematemesis and hematochezia. Abdominal Doppler and transfontanel ultrasonography and echocardiography were normal, as were a TORCH panel, urine cytomegalovirus polymerase chain reaction test, thyroid function test, bleeding time, factor 13, and serum gastrin hormone levels.

Gastroscopy performed on day of life 4 revealed six to eight ulcers in the corpus mucosa, deeper than the surface, approximately 2 × 3 mm in size (Figure 1a, 1b). No adverse event occurred due to gastroscopy and/or during gastroscopy. Ranitidine was discontinued and replaced with omeprazole and antacid (Gaviscon). Nutrition was gradually increased. On day 12, the patient was discharged in good general condition with stable vital signs. A control gastroscopy performed at the age of 2 months was normal (Figure 1c, 1d). The patient is now 8 months old and her height, weight, and head circumference are in normal percentile ranges.

Figure 1.

(a, b) On gastroscopy, multiple ulcers deeper than the surface, approximately 2 × 3 mm in size, were detected in the corpus mucosa. (c, d) Control gastroscopy at the age of 2 months showed normal gastric mucosa.

DISCUSSION

Gastric acid production starts immediately after birth in term and preterm babies and probably contributes to the pathophysiology of stress ulcers.³ Stress increases gastric acid secretion and plays a key role in ulceration in older children and adults.⁴ Stomach ulcers are rare in the neonatal period. They usually occur secondary to an underlying disease.² Except for cesarean delivery, no other factor increased the risk of upper GI bleeding in our patient. Most upper GI bleeding cases in newborns are benign and self-limiting, but mortality approaches 40% when stress ulcers cause massive GI bleeding.^2,5 Hematochezia due to bleeding severity can be seen in bleeding due to stomach ulcerations. Since the bleeding was massive in our patient, hematochezia and low hematocrit in need of blood transfusion were observed. The most common cause of suspicious GI bleeding in newborn babies is the swallowing of maternal blood during labor or through cracks in the nipples during breastfeeding.⁶ Our patient’s mother had a cracked nipple, and at first we thought this was the cause of the bleeding. Because of the persistence of upper GI bleeding after gastric lavage, we excluded this cause.

It has been shown that histamine-2 receptor blockers and proton pump inhibitors (PPI) used in the neonatal period lead to earlier recovery compared to placebo.⁷ PPIs have been shown to be superior to histamine antagonists in healing bleeding ulcers.⁸ We first started histamine-2 receptor blocker (ranitidine) treatment for our patient. After seeing multiple ulcers on endoscopy, we replaced ranitidine with a PPI and antacid. After these treatments, the stomach ulcers completely healed. In conclusion, it is vital to consider stomach ulcers in the differential of healthy term newborns who present with bloody vomiting.