Neonate with Hematemesis

DEFINITION & PRESENTATION

Hematemesis: Expulsion of blood in vomitus during first 28 days of life.
Source: Upper gastrointestinal (UGI) tract; proximal to ligament of Treitz.
Appearance: Bright red (fresh hemorrhage) or “coffee-ground” (heme degraded by gastric acid).
Hemodynamic Status: Varies from asymptomatic to life-threatening hypovolemic shock.

Neonatal UGI bleeding etiology differs significantly from older children.

Category	Specific Etiologies
Maternal Source	Swallowed maternal blood (during delivery or from cracked nipple during breastfeeding).
Mucosal Injury	Stress gastritis/ulcers (sepsis, hypoxia, mechanical ventilation), reflux esophagitis.
Hematologic	Hemorrhagic disease of the newborn (Vitamin K deficiency bleeding), disseminated intravascular coagulation (DIC), alloimmune liver disease.
Allergic	Cow’s milk protein allergy/sensitivity.
Anatomic/Vascular	Gastrointestinal duplication, vascular malformations, duodenal/gastric web, teratoma.

Mechanism: Fetal ingestion of maternal blood during parturition or via cracked maternal areola during nursing.
Clinical Nuance: Infant typically well-appearing; normal vital signs.

Mechanism: Vitamin K deficiency impairs gamma-carboxylation of coagulation factors II, VII, IX, X.
Risk Factors: Poor placental transfer, sterile neonatal gut (no bacterial synthesis of Vitamin K2), low Vitamin K content in breast milk.
Presentation: Bleeding from GI tract, umbilicus, or mucosal surfaces; elevated PT/INR.

Mechanism: Mucosal ischemia secondary to severe systemic stress (hypoxia, sepsis, congenital heart disease, mechanical ventilation).
Presentation: Often occurs in neonatal intensive care unit (NICU) setting. Can cause massive, fatal hemorrhage.

Apt-Downey Test: Mandatory test to differentiate fetal from adult (maternal) hemoglobin. Fetal hemoglobin resists alkali denaturation (remains pink); adult hemoglobin degrades (turns yellow-brown).
Nasogastric (NG) Lavage: Normal saline instillation and aspiration. Confirms UGI source; assesses active vs. resolved bleeding.
Hemogram & Coagulation: Complete blood count (CBC) to assess anemia (may initially underestimate blood loss) and thrombocytopenia. Prothrombin time (PT), partial thromboplastin time (PTT), and INR to assess coagulopathy.
Hepatic Panel: Transaminases, bilirubin, albumin to exclude congenital liver failure (e.g., Gestational Alloimmune Liver Disease).

Abdominal Radiography/Ultrasound: Identifies obstruction, free air (perforation), or vascular malformations.
Esophagogastroduodenoscopy (EGD): Diagnostic procedure of choice for identifying mucosal lesions (ulcers, erosions). Requires hemodynamic stability prior to procedure.

Apply “REO” protocol: Resuscitate, Evaluate, Operate.

Airway & Breathing: Secure airway; provide oxygen.
Intravenous Access: Establish dual large-bore IV lines.
Volume Expansion: Administer isotonic crystalloid bolus (Normal Saline) for hypoperfusion/shock.
Blood Transfusion: Transfuse packed red blood cells (PRBCs) for severe anemia or ongoing hemorrhage. Target hemoglobin: 7–9 g/dL.

Intervention	Indication & Dosage
Vitamin K	1 mg Intravenous (IV) or Intramuscular (IM); corrects VKDB rapidly.
Fresh Frozen Plasma (FFP)	Reverses severe coagulopathy or active life-threatening hemorrhage unresponsive to Vitamin K alone.
Acid Suppression	IV Proton Pump Inhibitor (e.g., Pantoprazole 2 mg/kg loading dose). Stabilizes clot formation; promotes mucosal healing in gastritis/ulcers.
Dietary Modification	Withhold breastfeeding temporarily if maternal nipple source confirmed. Use extensively hydrolyzed formula if cow’s milk protein allergy suspected.

Endoscopic Hemostasis: Utilized for active ulcer bleeding or vascular lesions. Modalities include epinephrine injection, electrocoagulation, or hemostatic clips.
Surgical Consultation: Indicated for hemodynamic instability refractory to medical/endoscopic management, suspected perforation, or intestinal obstruction.