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Summary Table

Category	Detail
Risk Factors	Vacuum-assisted delivery (strongest association), forceps delivery, prolonged or difficult labor, coagulopathy (hemophilia, vitamin K deficiency), prematurity
Etiology	Rupture of emissary veins bridging the dural sinuses to the scalp veins, causing blood to accumulate in the potential space between the periosteum of the skull and the galea aponeurotica
Patient Presentation	Neonate with a progressively enlarging, boggy scalp swelling after instrumental delivery; may show pallor, poor feeding, irritability, and signs of hemodynamic instability
Classic Physical Exam	Fluctuant, ballotable swelling that crosses suture lines and fontanelles; increasing head circumference over hours; periauricular ecchymosis; signs of hypovolemic shock (tachycardia, hypotension, delayed capillary refill)
Key Diagnostic Results	Dropping serial hematocrit; coagulopathy on PT/aPTT; ultrasound or CT confirming fluid collection in the subgaleal space
Management	Aggressive volume resuscitation, packed red blood cell transfusion, correction of coagulopathy (fresh frozen plasma, vitamin K), NICU monitoring with serial head circumference and hematocrit
Keywords	"Boggy swelling crossing suture lines," "vacuum-assisted delivery," "fluctuant scalp mass," "dropping hematocrit after birth," "ballotable head swelling in a neonate"

1. Pathophysiology

The scalp has five anatomical layers, classically memorized by the mnemonic SCALP: Skin, Connective tissue (dense), Aponeurosis (galea aponeurotica), Loose areolar tissue, and Periosteum (pericranium). Subgaleal hemorrhage occurs when blood collects in the loose areolar tissue layer, which lies between the galea aponeurotica above and the periosteum below.

This layer is critically important because it is a potential space with no anatomical boundaries that limit expansion. It extends from the orbital ridges anteriorly to the nuchal ridge posteriorly, and from one temporal fascia to the other laterally. Because of this vast extent, this space can accommodate up to 260 mL of blood, which is nearly the entire circulating blood volume of a term neonate (approximately 80 mL/kg).

The bleeding originates from the emissary veins that traverse this space, connecting the dural sinuses to the superficial scalp veins. During vacuum-assisted delivery, the negative pressure applied to the fetal scalp generates shearing forces that tear these bridging veins. This is why vacuum extraction is the single most important risk factor. Forceps delivery can also cause similar vascular disruption, though to a lesser degree.

Once the veins are torn, blood dissects freely through the loose connective tissue. Unlike a cephalohematoma, where the periosteum is tightly adherent to the skull at the suture lines and confines bleeding to a single bone, there is no such barrier in the subgaleal space. The hemorrhage spreads diffusely, leading to progressive swelling that crosses suture lines and fontanelles. This uncontained bleeding is what makes subgaleal hemorrhage a life-threatening emergency: the neonate can lose a fatal volume of blood into the scalp before the clinician realizes the severity.

The downstream consequence is hypovolemic shock. As blood volume drops, the neonate becomes tachycardic, pale, and hypotensive. The consumption of clotting factors at the bleeding site can trigger disseminated intravascular coagulation (DIC), which worsens the hemorrhage and creates a dangerous feedback loop of bleeding and coagulopathy.

2. Classification and Clinical Manifestation

Subgaleal hemorrhage does not have formal staging in the way that many diseases do, but it is clinically useful to understand it in terms of severity based on estimated blood loss, which drives presentation and urgency.

Severity	Blood Loss	Clinical Features
Mild	< 25 mL	Localized boggy swelling, stable vital signs, normal hematocrit, minimal change in head circumference
Moderate	25 to 100 mL	Swelling crossing suture lines, rising head circumference over hours, mild tachycardia, falling hematocrit on serial measurement
Severe	> 100 mL (up to 260 mL)	Diffuse fluctuant scalp swelling, frank hypovolemic shock (tachycardia, hypotension, poor perfusion, pallor), rapidly dropping hematocrit, coagulopathy (prolonged PT/aPTT, low fibrinogen, thrombocytopenia), periauricular and posterior auricular ecchymosis

It is also essential to understand where subgaleal hemorrhage fits among the three extracranial neonatal hemorrhages, as this is one of the most commonly tested comparisons:

Feature	Caput Succedaneum	Cephalohematoma	Subgaleal Hemorrhage
Layer of bleeding	Subcutaneous tissue (above the aponeurosis)	Subperiosteal (between periosteum and bone)	Subaponeurotic (between aponeurosis and periosteum)
Crosses suture lines?	Yes	No (limited by periosteal attachments at sutures)	Yes
Onset	Present at birth	Hours after birth	Hours after birth, progressive
Character	Pitting edema, soft, poorly defined	Firm, well-circumscribed, non-pitting	Fluctuant, ballotable, diffuse
Severity	Benign, self-limiting	Usually benign (risk of jaundice from resorption)	Life-threatening, risk of hemorrhagic shock
Associated with	Prolonged labor, vertex presentation	Forceps, prolonged labor	Vacuum extraction
Management	Observation only	Observation (monitor for jaundice)	Emergency resuscitation

3. Diagnostic Workup

Test	Role	Expected Finding
Serial head circumference	Best initial monitoring tool	Progressive increase (each 1 cm increase corresponds to approximately 40 mL of blood loss)
Complete blood count (CBC)	Assessing blood loss	Falling hematocrit/hemoglobin on serial measurements
Coagulation panel (PT, aPTT, fibrinogen, platelets)	Detecting coagulopathy/DIC	Prolonged PT/aPTT, low fibrinogen, thrombocytopenia
Cranial ultrasound	Best initial imaging test	Hypoechoic or mixed-echogenicity fluid collection in the subgaleal space; can also rule out intracranial hemorrhage
CT scan of the head	Confirmatory imaging if diagnosis is uncertain or intracranial injury suspected	Well-defined hyperdense collection external to the skull, between the aponeurosis and the periosteum; can identify associated skull fractures

Clinical diagnosis is paramount. In the exam setting, the vignette will describe a neonate born via vacuum-assisted delivery who develops a progressively enlarging, fluctuant scalp swelling crossing suture lines within hours of birth. This clinical picture alone should trigger the diagnosis.

The best initial step is not imaging but rather clinical recognition and monitoring. Serial head circumference measurements are the most practical bedside tool. A commonly tested correlation is that each 1 cm increase in head circumference corresponds to roughly 40 mL of accumulated blood. This means a 2 to 3 cm increase may signal the loss of 80 to 120 mL, which in a 3 kg neonate (total blood volume around 240 mL) represents a loss of 33 to 50% of circulating volume.

Simultaneously, serial hematocrit measurements will show a progressive decline. The coagulation panel is ordered not only to detect DIC but also to identify underlying coagulopathies (such as factor deficiencies or vitamin K deficiency bleeding) that may have predisposed the infant to the hemorrhage in the first place.

Cranial ultrasound is the best initial imaging modality because it is portable, radiation-free, and can be performed at the bedside in the NICU. It visualizes the fluid collection well and can also evaluate for intraventricular or subdural hemorrhage. CT scan is reserved for cases where the diagnosis is unclear, where intracranial pathology is suspected, or when surgical intervention is being considered. CT provides superior anatomical detail and can detect skull fractures.

4. Management and Treatment

Phase	Intervention	Details
Immediate stabilization	Airway, Breathing, Circulation	Secure airway, ensure adequate ventilation, establish IV access
Volume resuscitation	Normal saline bolus	10 to 20 mL/kg IV, may repeat; goal is restoring perfusion
Blood transfusion	Packed red blood cells (pRBCs)	10 to 15 mL/kg IV; transfuse to maintain hematocrit above 30 to 35%; may need multiple transfusions
Correct coagulopathy	Fresh frozen plasma (FFP)	10 to 15 mL/kg IV for prolonged PT/aPTT
	Cryoprecipitate	5 to 10 mL/kg IV if fibrinogen is low (< 100 mg/dL)
	Vitamin K	1 mg IM/IV (if not already given at birth or if vitamin K deficiency bleeding is suspected)
	Platelet transfusion	10 to 15 mL/kg if platelet count is below 50,000/mcL with active bleeding
Monitoring	NICU admission	Serial head circumference every 4 to 6 hours, serial hematocrit every 6 to 8 hours, continuous cardiorespiratory monitoring
Supportive care	Phototherapy if needed	For hyperbilirubinemia from resorption of the hematoma

Acute stabilization is the priority. The "next best step" when you recognize a neonate in hemorrhagic shock from subgaleal hemorrhage is volume resuscitation with isotonic crystalloid (normal saline) followed immediately by packed red blood cell transfusion. Do not wait for lab confirmation before initiating resuscitation if the clinical picture is clear.

Correction of coagulopathy runs in parallel. Fresh frozen plasma replaces the consumed clotting factors, and cryoprecipitate is added if fibrinogen is critically low. Vitamin K should be confirmed or re-administered. These interventions break the cycle of consumptive coagulopathy and ongoing hemorrhage.

There is no role for surgical evacuation in most cases. The hemorrhage is venous and diffuse, not a localized arterial bleed amenable to ligation. Management is entirely supportive and resuscitative. However, if there is an associated intracranial hemorrhage or depressed skull fracture, neurosurgical consultation is warranted.

Long-term considerations are generally favorable for survivors. Once the acute phase is managed, the hematoma resorbs over days to weeks. During resorption, the breakdown of red blood cells produces unconjugated bilirubin, so the infant should be monitored for hyperbilirubinemia and treated with phototherapy as needed. Follow-up should include neurodevelopmental assessment, particularly if the infant experienced prolonged hypotension or required prolonged resuscitation.

Contraindication to note: In a neonate with suspected or confirmed coagulopathy, avoid any procedures that could worsen bleeding (such as unnecessary scalp punctures or aggressive scalp manipulation). Also, if DIC is present, platelet transfusion alone without FFP/cryoprecipitate is insufficient because the coagulation cascade itself is disrupted.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Caput succedaneum	Also crosses suture lines; also associated with labor and delivery	Caput is pitting edema (not fluctuant blood), is present at birth, and resolves within 24 to 48 hours without hemodynamic compromise. Subgaleal hemorrhage is fluctuant, worsens over time, and causes hemodynamic instability.
Cephalohematoma	Also a post-delivery scalp swelling; also associated with instrumental delivery	Cephalohematoma does not cross suture lines (confined to one bone), is firm and well-circumscribed, and does not cause shock. It is subperiosteal, not subaponeurotic.
Epidural hematoma	Can present with signs of increasing intracranial pressure in a neonate after difficult delivery	Epidural hematoma is intracranial (between the skull and dura), typically associated with a skull fracture and middle meningeal artery injury. Imaging shows a biconvex (lens-shaped) collection. Subgaleal hemorrhage is extracranial.
Subdural hematoma	Can occur after traumatic delivery; neonate may present with altered mental status and focal neurologic signs	Subdural hematoma is intracranial (between dura and arachnoid), produces neurological signs (seizures, bulging fontanelle from raised intracranial pressure), and imaging shows a crescent-shaped collection. Subgaleal hemorrhage is extracranial with diffuse scalp swelling.
Birth molding	Head may appear elongated or misshapen after vaginal delivery	Molding is a normal physiological process due to overriding of skull bones during passage through the birth canal. There is no fluid collection, no swelling, and it resolves spontaneously within days.

6. Traps and High-Yield Pearls

The most common way students lose points on subgaleal hemorrhage questions is by confusing it with cephalohematoma. Both are post-delivery scalp swellings, and both are associated with instrumental delivery. The critical discriminator is whether the swelling crosses suture lines. If the vignette says the swelling crosses suture lines and the baby is becoming hemodynamically unstable, it is subgaleal hemorrhage, not cephalohematoma. If the swelling is confined to one bone and the baby is otherwise stable, it is cephalohematoma.

A second common trap is confusing subgaleal hemorrhage with caput succedaneum because both cross suture lines. The key here is timing, character, and trajectory. Caput is present at birth and resolves; subgaleal hemorrhage develops after birth and worsens. Caput is pitting edema; subgaleal hemorrhage is fluctuant collected blood.

Another tested pearl: exam writers love to test whether you know the volume significance of the subgaleal space. When a vignette provides a head circumference that has increased by several centimeters over hours, you should immediately calculate approximate blood loss (1 cm = ~40 mL) and recognize the severity of the situation.

Finally, do not forget the association between subgaleal hemorrhage and underlying coagulopathy. A vignette may describe a neonate without a history of instrumental delivery who develops diffuse scalp swelling. In this scenario, the question is testing whether you will investigate for an inherited bleeding disorder such as hemophilia or for vitamin K deficiency bleeding as the underlying cause.

The core competency being tested is your ability to localize the anatomical layer of bleeding (subcutaneous vs. subperiosteal vs. subaponeurotic), connect that localization to clinical behavior (crossing suture lines, hemodynamic compromise), and initiate the correct sequence of resuscitative management.

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