What is the management approach for a newborn with a subgaleal hematoma?

Management of Neonatal Subgaleal Hematoma

Immediate Recognition and Monitoring

Subgaleal hematoma is a neonatal emergency requiring immediate recognition and aggressive monitoring to prevent hemorrhagic shock and death. 1, 2

Clinical Diagnosis

• Identify the characteristic fluctuating hemorrhagic mass that crosses suture lines and extends toward the neck, distinguishing it from cephalohematoma (which does not cross sutures) or caput succedaneum (which resolves quickly) 3
• The subgaleal space can accommodate 260-280 mL of blood in a term infant, representing the entire blood volume, making massive hemorrhage possible 4
• Monitor for posterolateral extension of the hematoma, as the subgaleal space extends from orbital ridges anteriorly to the nuchal line posteriorly with minimal anatomical barriers to restrict blood flow 5

Critical Monitoring Parameters

Implement systematic close monitoring immediately upon diagnosis: 1, 3

• Vital signs every 1-2 hours looking specifically for hypotension and tachycardia as early shock indicators 3
• Serial hematocrit measurements to detect ongoing blood loss (falling hematocrit is a key diagnostic feature) 1, 4
• Head circumference measurements serially to track hemorrhage progression 1
• Signs of tissue hypoperfusion including capillary refill time, urine output, and mental status 1
• Blood gas analysis to detect metabolic acidosis, which predicts poor outcome 3

Laboratory Evaluation

Obtain coagulation studies immediately in all infants with subgaleal hematoma, as coagulopathy is common and associated with mortality 1, 2, 4

• Complete blood count with serial hematocrit monitoring 4, 3
• Prothrombin time, partial thromboplastin time, fibrinogen, and platelet count 2, 3
• Renal function tests (creatinine, BUN) as renal impairment predicts poor prognosis 3
• Blood type and cross-match for potential transfusion 4

Acute Management

Volume Resuscitation and Blood Product Support

Treat hypovolemic shock aggressively with blood products rather than crystalloid alone, as severe volume loss with anemia and coagulopathy are the primary causes of mortality 4, 3

• Transfuse packed red blood cells for significant anemia (hematocrit <30-35%) or signs of shock 4, 3
• Administer fresh frozen plasma for coagulopathy correction 2, 4
• Give platelet transfusions if thrombocytopenia is present 2
• Consider vasopressor support if hypotension persists despite volume resuscitation (need for pressors predicts poor outcome) 3

Supportive Care

• Provide respiratory support including mechanical ventilation if needed for shock or encephalopathy 2, 3
• Treat metabolic acidosis with appropriate fluid resuscitation and correction of underlying shock 3
• Monitor for and treat seizures if they occur, as seizures are associated with poor outcome 3

Neuroimaging

Obtain CT or MRI of the brain in all clinically symptomatic cases to evaluate for associated intracranial hemorrhage and skull fractures 4, 3

• Intracranial hemorrhage occurs in 50% of cases (subdural, subarachnoid, intraventricular, or intraparenchymal) 4
• Skull fractures occur in 19% of cases, with half being depressed fractures 4
• While intracranial hemorrhage does not correlate with SGH severity or mortality, skull fractures predict poor prognosis 4, 3

Predictors of Poor Outcome

Transfer to intensive care immediately if any poor prognostic factors are present: 3

• Hypotension requiring pressors 3
• Seizures 3
• Severe anemia requiring transfusion 3
• Coagulopathy 2, 3
• Metabolic acidosis 3
• Renal impairment 3
• Skull fracture 3
• Need for mechanical ventilation 3

Common Pitfalls

• Delayed recognition in infants transferred from other hospitals is associated with significantly worse outcomes (P < 0.001), emphasizing the need for immediate diagnosis at the delivering hospital 3
• Underestimating blood loss because the scalp swelling may appear deceptively benign initially while massive hemorrhage accumulates 1, 2
• Failing to obtain coagulation studies in all cases, missing treatable coagulopathy that contributes to mortality 1, 2
• Conservative management in severe cases when aggressive intervention is needed—mortality rate is 11.8% overall but approaches 100% in untreated severe cases 4, 3

Long-Term Follow-Up

Arrange long-term neurodevelopmental follow-up for all survivors, particularly those with poor prognostic factors, as complications include epilepsy, cerebral palsy, and auditory dysfunction 3

• Short-term neurological outcome in survivors is generally good, with minor abnormalities in only 12% at discharge 4
• However, 31% of infants with poor prognostic factors develop significant long-term sequelae including epilepsy, severe auditory dysfunction, and cerebral palsy 3