Neonatal Massive Upper GI Bleeding Managed With Gastric Devascularization :- Medznat
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Gastric Devascularization for Severe Upper Gastrointestinal Bleeding in Neonates

eonatal upper gastrointestinal hemorrhage, Diffuse hemorrhagic gastritis eonatal upper gastrointestinal hemorrhage, Diffuse hemorrhagic gastritis
eonatal upper gastrointestinal hemorrhage, Diffuse hemorrhagic gastritis eonatal upper gastrointestinal hemorrhage, Diffuse hemorrhagic gastritis

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Poster abstract

In children, severe upper gastrointestinal bleeding is rare and potentially life-threatening. This case describes a 3-day-old male neonate who presented with hematemesis and melena as a result of diffuse hemorrhagic gastritis. Despite intensive medical therapy—including vitamin K, H2-receptor antagonists, gastric lavage, coagulation support, and blood transfusion—the bleeding persisted. Emergency laparotomy confirmed diffuse hemorrhagic gastritis.

Gastric devascularization, achieved through selective arterial ligation while preserving short gastric vessels, provided rapid and sustained hemostasis. The infant recovered smoothly, tolerated feeding early, and remained free of symptoms at 1-year of follow-up. A literature review of 29 reported neonatal cases underscores the diagnostic challenges and highlights gastric devascularization as a viable option when conservative and endoscopic measures fail.

Complaints

A 3-day-old male neonate presented with repeated episodes of hematemesis, coffee-ground vomiting, and passage of fresh and altered blood in stools, accompanied by clinical signs of hypovolemia.

Anamnesis

Introduction

Upper gastrointestinal (UGI) bleeding refers to blood loss from the esophagus, stomach, or duodenum above the ligament of Treitz and commonly presents with hematemesis (vomiting blood) or melena (black stools). Although UGI bleeding is a recognized emergency in pediatrics, massive UGI bleeding in infants—especially neonates—is extremely rare but potentially life-threatening. Reported etiologies encompass stress gastritis, gastric or duodenal ulcers, esophagitis, gastrointestinal (GI) duplication, vascular malformations, gastric polyps, cow’s milk protein allergy, coagulopathy, and nasogastric tube injury.

Maternal drug exposure during pregnancy—such as tolazoline, indomethacin, dexamethasone, sulindac, or ketorolac—may also contribute to neonatal UGI bleeding risk. Initial management often involves conservative therapy using proton pump inhibitors (PPIs) and H2 receptor antagonists. When bleeding persists or fails to respond to medical therapy, GI endoscopy is the preferred diagnostic and therapeutic approach. If endoscopic intervention is unavailable or unsuccessful, surgical exploration becomes essential.

In this case study, a neonate with hematemesis and melena caused by diffuse hemorrhagic gastritis achieved successful recovery following surgical stomach devascularization. The intervention effectively controlled bleeding and resulted in a favorable clinical outcome.

Medical History

The male neonate was born via vaginal delivery at 36 + 2 weeks’ gestation to a 30-year-old second-gravid mother following a spontaneous conception. The antenatal period was uneventful, with no exposure to medications known to increase neonatal bleeding risk. The baby’s Apgar score was 10 at 1 minute post-delivery. Birth weight was about 2.9 kg, appropriate for gestational age. Notably, 18 hours after birth, the infant exhibited poor responsiveness, raising suspicion for hypoxic-ischemic encephalopathy, prompting transfer to the pediatric department for further evaluation and management.

Examination

Upon admission, the neonate’s vital signs were as follows:

  • Body temperature 36.1 °C
  • Heart rate 140 beats per minute (bpm)
  • Respiratory rate 42 breaths/min

Physical examination depicted poor responsiveness, cyanosis (bluish discoloration) of the lips, and hypotonia of the limbs. No other congenital abnormalities or systemic issues were noted. On the second day of life, the infant developed coffee-ground vomiting, prompting suspicion of UGI bleeding. Laboratory investigations revealed:

  • White blood cell (WBC): 20.8 × 10⁹/L (mild leukocytosis)
  • Red blood cell (RBC): 5.53 × 10¹²/L
  • Hemoglobin (Hb): 220 g/L (polycythemia)
  • Hematocrit (HCT): 59.3%
  • Platelet count: 215 × 10⁹/L

By day 3, symptoms progressed to hematemesis of fresh blood and large-volume melena, indicating active and severe UGI hemorrhage. Repeat labs showed:

  • RBC: 4.50 × 10¹²/L
  • Hb: 59 g/L
  • HCT: 45.3%
  • Platelets: 162 × 10⁹/L
  • Prothrombin time (PT): 28.6 s
  • Activated partial thromboplastin time (APTT): >180 s
  • Thrombin time: >120 s

These findings reflected acute blood loss anemia, coagulopathy, and risk of hemodynamic instability, with heart rate dropping to 124 bpm.

Intraoperative findings

A laparotomy via upper midline incision revealed:

  • Large volumes of blood within the colon and ileum
  • Petechial hemorrhages on the gastric mucosal wall
  • No evidence of duodenal ulceration

A 3-cm gastrotomy on the anterior gastric greater curvature illustrated:

  • Diffuse active bleeding
  • Severely congested, edematous mucosa
  • Appearance consistent with acute diffuse hemorrhagic gastritis

Treatment

1. Initial Supportive Measures

Upon transfer, the infant received:

  • Oxygen inhalation
  • Thermal support
  • Fluid replacement
  • Neurotrophic medications: Vitamin B6, Coenzyme A, and Adenosine triphosphate

2. Management of Suspected UGI Bleeding

Following coffee-ground vomiting on day 2, treatment included:

  • Placement of a nasogastric tube
  • Intravenous vitamin K
  • Gastric lavage
  • Cimetidine injection (H2-receptor antagonist)

Despite these measures, bleeding progressed. The infant developed fresh hematemesis and massive bloody stool. To control life-threatening hemorrhage, the following were administered:

  • 160 ml concentrated RBCs
  • 100 ml fresh frozen plasma
  • Cold normal saline gastric lavage
  • Thrombin administered through the nasogastric tube
  • Intravenous hemocoagulase
  • Intravenous dopamine (2.5 mg)
  • Bleeding remained uncontrolled, and emergency surgery was required.

3. Surgical Intervention

The surgeon performed ligation of:

  • Branches of the left gastroepiploic artery
  • Left gastric artery
  • Right gastric artery
  • Right gastroepiploic artery

The short gastric arteries remained intact, ensuring optimal gastric perfusion. The gastrotomy was closed using a two-layer suture technique via 4-0 absorbable sutures. Intraoperative transfusions included:

  • 100 ml concentrated RBCs
  • 60 ml fresh frozen plasma

4. Postoperative Course

On postoperative day 1, blood parameters improved:

  • RBC: 4.19 × 10¹²/L
  • Hb: 128 g/L

The infant experienced respiratory arrest episodes at the 7th and 16th hour after surgery, presenting with:

  • Cyanosis
  • Bradycardia
  • Oxygen saturation 70–80%

Both episodes were reversed with successful cardiopulmonary resuscitation. Breastfeeding began on postoperative day 3, and feeding was well-tolerated. The infant was discharged on postoperative day 14 in stable condition.

5. Follow-Up

At the 1-year follow-up, the kid:

  • Weighed 10 kg
  • Had no recurrent UGI bleeding
  • Demonstrated normal growth and recovery

Results

Discussion

Massive UGI bleeding during the neonatal period is exceptionally rare yet clinically significant, as even minimal blood loss can rapidly destabilize an infant. The differential diagnosis is broad and includes stress-related mucosal injury, gastritis, peptic ulcer disease, vascular abnormalities, medication exposure, and coagulation disorders. A review of the literature encompassing 29 reported cases shows that stress-related gastric lesions—such as diffuse gastritis and ulceration—represent the majority, accounting for approximately two-thirds of diagnoses. Most affected neonates present within the first three days of life, a pattern that aligns closely with the presentation in our case.

Initial management typically centers on hemodynamic stabilization followed by conservative medical therapy. Acid-suppression agents, including PPIs and H2-receptor antagonists, are frequently employed to mitigate mucosal injury and reduce ongoing blood loss. Although these measures may control mild forms of bleeding, they are often insufficient in cases characterized by diffuse or severe mucosal involvement.

Endoscopy is regarded as the gold standard for both diagnosing and treating significant UGI bleeding, offering direct visualization of the mucosa and the opportunity for immediate hemostatic intervention. However, neonates with profound hemorrhage often cannot tolerate endoscopy, and logistical constraints—such as the unavailability of pediatric-sized equipment or specialized expertise—may further limit its use. When the child is hemodynamically unstable or when endoscopic measures fail to achieve hemostasis, early surgical intervention becomes essential. Surgical exploration continues to hold an important role in the management of refractory neonatal UGI bleeding. Among operative strategies, gastric devascularization provides a valuable, organ-preserving option for diffuse mucosal hemorrhage. This approach offers several advantages:

  • Prompt reduction of mucosal blood flow, allowing rapid control of diffuse bleeding.
  • Selective adjustment of gastric perfusion without compromising tissue viability.
  • Avoidance of radical operations, such as partial or total gastrectomy, which carry substantial morbidity in infants.

In the present case, the neonate illustrated severe hematemesis and melena secondary to diffuse hemorrhagic gastritis. Conservative therapy was ineffective, and endoscopic intervention was not feasible given the clinical instability. Surgical devascularization was therefore undertaken and resulted in immediate cessation of bleeding. Postoperative recovery was rapid, and no recurrence was observed during one year of follow-up, illustrating the procedure’s effectiveness and durability. 

This case underscores the importance of a structured, tiered management approach for neonatal UGI bleeding—beginning with stabilization and medical therapy, progressing to endoscopic evaluation when appropriate, and transitioning without delay to surgical intervention when less invasive methods prove inadequate. Early recognition of treatment failure and timely operative management remain key to improving outcomes in this rare but potentially life-threatening condition.

Learning

  • Diffuse hemorrhagic gastritis should be considered in children with massive hematemesis and melena.
  • Conservative treatment may fail in rapidly progressive mucosal bleeding; early surgical consideration improves outcomes.
  • Gastric devascularization is a safe and effective life-saving intervention when endoscopic or medical measures are insufficient.
  • Close postoperative monitoring is fundamental due to the risk of respiratory or circulatory instability.

Source:

BMC Pediatrics

Article:

Gastric Devascularization In a Neonate With Massive Upper GI Bleeding: A Case Report and Literature Review

Authors:

Xinxing Liu et al.

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